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Semester 3 Medical School > Mini 1 - Fund 2 pt.1 > Flashcards

Mini 1 - Fund 2 pt.1 Flashcards

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USMLE® Step 1 flashcards
1
Q

What is MALDI-TOF?

A

Automatic, measures exact masses of numerous proteins and produces protein ‘fingerprint’ for microorganisms. Can identify CULTURED organisms quickly.

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2
Q

What is karyorrhesis?

A

Fragmentation of pyjnotic nucleus (see nuclear dust in interstitium).

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3
Q

What is the outer layer of fungi and parasites?

A

Rigid cell wall with chitin, flexible membrane.

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4
Q

What is a Thayer-Martin agar?

A

A selective version of chocolate agar to isolate Neisseria gonorrhoeae.

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5
Q

What is the D antigen?

A

Rhesus.

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6
Q

What does cytotonic mean?

A

Alter cellular pathways but don’t kill the cells of the host.

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7
Q

Describe Triple Sugar Iron agar.

A

Determines in a tube if organism is a sugar fermenter (turns yellow if ferments). If only glucose is fermented then only the butt turns yellow. H2S production makes a black precipitate.

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8
Q

For a 70kg person, what does a Vd of >50L mean?

A

Stored within specific cells or tissues.

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9
Q

What kind of integrins do monocytes have and what are their ligands?

A

LFA-1, MCA-1 - ligands ICAM-1, ICAM-2 VLA-4 - ligand VCAM-1

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10
Q

What are the two steps of bacterial attachment?

A

Docking (nonspecific) and Anchoring (specific).

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11
Q

What is biofilm?

A

Collection of aggregated bacteria bound to a surface and embedded in self-made polymeric matrix. Good for resistance, can communicate through it.

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12
Q

What is the protein secretion mechanism for gram(+) and gram(-) bacteria?

A

Shared GSP, the gram(-) one only gets to the periplasmic space. Gram(-) have additional mechamisms on their OM called injectisomes.

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13
Q

What is a western immunoblot?

A

Mostly used for HIV. Ag separated and blotted to membrane (commercially prepared). Membrane is inculated with patient serum.

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14
Q

What are the antiapoptotic members of the BCL2 family and what do they do?

A

BCL2, BCL-XL, MCL-1. Block proapoptotic (BAX and BAK).

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15
Q

What is a titer?

A

The highest dilution of serum able to agglutinate a particular antigen.

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16
Q

What is a NET?

A

Neutrophil extracellular trap - nuclear chromatin meshwork to capture pathogens and then kill then with bactericidal granular content.

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17
Q

How is bioavailability measured mathematically?

A

AUCotherroute/AUCiv For a plasma concentration over time graph.

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18
Q

What are the anatomical sterile sites?

A

Blood, BM, CSF, serous fluid (sputum), tissues, bladder, lower respiratory tract.

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19
Q

What kind of drugs need to enter through endocytosis?

A

Very large ones (>5000D)

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20
Q

What type of temperature/acidity restrictions do pathogens have?

A

Mostly mesophiles/neutrophiles.

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21
Q

What do glycopeptides target and what is a common example?

A

Vancomycin. Binds stem peptide D-ala D-ala to prevent transpeptidation and transglycosylation.

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22
Q

Describe Enzymatic fat necrosis.

A

Focal areas of fat destruction resulting from an abnormal release of activated pancreatic enzymes into pancreas and peritoneal cavity. Chalky-white calcium deposits, shadowy outlines of necrotic adipocytes, basophilic amorphous calcium deposits.

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23
Q

What are susceptibility and permissiveness?

A

Host specificity. Susceptibility = possesses surface receptors allowing attachment. Permissiveness = contains all components required for virion production.

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24
Q

What are the types of antagonism?

A

Pharmacological (drug acts on same receptor), pharmacokinetic (prevents absorption or increases elimination), physiological/functional (antagonist acts on different receptor), or chemical (combines with drug to inactivate).

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25
Q

How does aspirin interact with anticoagulants?

A

Increases anticoagulation effect.

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26
Q

When are flocculation tests used?

A

When the antigen is particulate.

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27
Q

What is a noncomposite transposon?

A

An insertion sequence with genes beyond tp in the insertion sequence.

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28
Q

What is Vd defined as?

A

Volume of distribution - measures passage from systemic circulation to body tissues.

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29
Q

What are some features of drug allergy?

A

<10% of all ADEs, related to frequency of exposure and can be influenced by associate illness, not dose-dependent. Only in drugs MW>6000 or ones that form a hapten.

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30
Q

Describe acetaminophen.

A

Good COX inhibitor in CNS, antipyretic and analgesic. No effects on inhibition of peripheral PG synthesis. Very few ADEs (liver toxicity when overdose or in risk patients)

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31
Q

What does glutathione peroxidase do?

A

Breaks down peroxide and hydroxide. GSH + one of them forms GSSG and water

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32
Q

Describe eosin methylene blue agar.

A

Inhibits gram(+) bacteria. Lactose fermenters appear blue-black, and non-fermenters appear clear. Strong fermenters (like E.coli can have a shiny green metallic sheen).

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33
Q

Describe analgesic nephropathy.

A

Renal papillary necrosis and chronic interstitial nephritis - back pain, hematuria, decreased concentrating capacity of the kidney. Usually in 30-40y/o 5:1 females, due to chronic antipyretic analgesic use.

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34
Q

What does ‘naturally competent’ mean? Give two examples.

A

Can do transformation. Streptococcus pneumoniae and Haemophilius influenzae

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35
Q

What caspases are used in the apoptotic pathways?

A

Intrinsic - 8
Extrinsic - 9

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36
Q

What is a drug’s intrinsic activity?

A

Ability to initiate changes that lead to a biologic response.

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37
Q

What is the most common conjugation of xenobiotics?

A

Glucuronidation. Occurs in liver, catalyzed by glucuroosyl transferase, generally an inactivation reaction.

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38
Q

What is a ‘slow acetylator’?

A

An autosomal recessive trait of acetylating enzyme deficiency - impairs drug biotransformation.

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39
Q

What’s the most common agglutination test?

A

Latex agglutination.

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40
Q

What are the methods of envelopment?

A

Simultaneous (capsid forms as viral particle buds through membrane) Sequential (capsid forms, accessory proteins and envelope added in stepwise fashion)

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41
Q

What is a Gell&Coombs type III sensitivity?

A

Immune complex mediated reaction - immune complex deposits/aggregates on basement membrane of blood vessels, causing complement activation/inflammation. IgM or IgG involved but IgE can play a role.

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42
Q

What is an absolute contraindication of beta blockers?

A

AV block.

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43
Q

When does glucuronide reach adult values?

A

Age 3-4.

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44
Q

What are blastoconidia?

A

Conidia formed by dimorphic fungi in their yeast stage.

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45
Q

After what amount of time is a drug said to be effectively eliminated from the body?

A

Four half lives.

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46
Q

Where are Leishmaniasis amastigotes found?

A

Macrophages.

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47
Q

What is SOAP?

A

Subjective, Objective, Assessment, Plan.

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48
Q

What is Fibrinous inflammation?

A

A type of acute inflammation. Fibrin is found with leukocytes and necrotic tissues. Caused by increased vascular permeability. Outcome is resolution or organization.

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49
Q

Describe Caseous necrosis.

A

Loss of tissue architecture and cell outlines, firm in consistency. Caused by tuberculosis and others. Eosinophilic and structureless. Gross - ‘cheese-like’

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50
Q

How do fungi and parasites replicate?

A

Bud or mitose, mitose.

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51
Q

What are the types of parasites?

A

Protozoa - complex unicellular organisms with defined nucleus and other organelles. Helminths - multicellular

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52
Q

What is a viral envelope made of?

A

Host membrane’s lipids, host and viral proteins and glycoproteins.

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53
Q

Why are samples taken at the outer margins offungal lesions?

A

Because hyphae undergo apical growth.

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54
Q

What is xanthoma and xanthelasma?

A

Accumulation of cholesterol in the skin. Xanthelasma is it around the eyes.

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55
Q

What is the difference between acute and chronic inflammation?

A

Acute - mediated by neutrophils, repair done by regeneration. Chronic - mediated by lymphocytes and macrophages, repair done by healing (CT formation).

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56
Q

What determines whether an injury will scar or regenerate?

A

Basement membrane integrity.

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57
Q

What cells contribute to chronic inflammation?

A

MPS, blood monocytes, rissue macrophages, also lymphocytes, maybe other PMNs.

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58
Q

What is a caseating vs noncaseating granulom?

A

Caseating is a central area of caseous necrosis surrounded by epithelioids/Langhans cells, then lymphocytes, plasma cells, fibroblasts. TB causes this. A noncaseating granumola (ie sarcoidosis) does not have the central area of caseous necrosis.

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59
Q

What NSAIDs inhibit PLA2?

A

Indomethacin.

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60
Q

What does bacitracin target?

A

Prevents bactoprenol-PP recycling.

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61
Q

What does PDGF promote?

A

Migration/proliferation of monocytes, fibroplasts, pericytes, smooth muscle cells.

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62
Q

What are the types of fungi?

A

Yeasts (single-cell, bud) or Moulds (grow by extending filamentous hyphae and reproduce asexually by releassing spores from specialized hyphae called condiophores/spongiophores).

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63
Q

Describe sublingual/buccal administration

A

Absorption usually rapid, through oral mucosa. First pass effect avoided as oral veins flow directly to cava veins.

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64
Q

What kind of integrins do neutrophils have and what are their ligands?

A

LFA-1, ligands ICAM-1, ICAM-2

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65
Q

What is chemically defined vs complex media?

A

Chemically defined - you know the exact composition of the media. Complex you don’t. Most obligate human pathogens need complex media.

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66
Q

What DNA viruses do not replicate in the nucleus?

A

Poxviridae.

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67
Q

What is ergosterol and what drug(s) target(s) it?

A

Distinguishing feature of cell membranes of fungi. Azoles and polyene antifungals target it.

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68
Q

What is an indirect ELISA?

A

Ag-coated wells looking for the presence of a specific antibody.

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69
Q

What are ‘clear profiles’?

A

ER swelling in damaged cells.

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70
Q

What are chlamydiaceae?

A

Unrelated to gram(-) and unreactive to stain. Has an OM with LPS but no PG (instead Cys-rich envelope proteins).

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71
Q

What is Reye’s syndrome?

A

In kids under 18, microvesicular fatty infiltration of liver and other organs. Respiratory infection, after 4 days nausea/vomiting, sudden change in mental status, lab signs of liver damage. May be mild OR may progress to fatal toxic encephalopathy.

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72
Q

What is the definitive host of toxoplasmosis?

A

Cat.

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73
Q

What are phases of bacterial growth?

A

Lag, log, stationary, death.

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74
Q

What is the theta model of replication?

A

Replicates semiconservatively at ori.

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75
Q

What vitamins are ROS scavengers?

A

E, C, retinoids. E is terminal electron acceptor, C directly inactivates superoxide and hydroxide radical, retinoids block free radical chain reactions.

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76
Q

What is the urease test?

A

Sees if organism breaks down urea (amides), producing ammonia. If positive changes from yellow to pink.

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77
Q

What kind of viruses generally do sequential assembly?

A

Icosahedral

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78
Q

What is direct vs indirect Coombs test?

A

Direct tests presence of blood Abs bound to erythrocytes, indirect tests ones in serum.

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79
Q

What do drug clearances of 100-150, >150, and <100 mean?

A

<100 = reabsorption/protein binding 100-150 = filtration >150 = secretion

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80
Q

What is the oral bioavailability and Vd and half life of salicylic acid?

A

100% and 12L and dose-dependent half life.

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81
Q

What do beta-lactams target?

A

Transpeptidases - results in weak PG.

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82
Q

What are arthroconidia?

A

Conidia formed by fragmentation of hyphae (may occur in tissues or environment).

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83
Q

What are C3a, C5a, LTB4, and HETE involved in?

A

Chemotaxis, leukocyte recruitment and activation.

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84
Q

What is an ulcer vs a wound?

A

Ulcer - defect on an organ surface made by shedding of inflamed necrotic tissue Wound - Defect produced by mechanical force.

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85
Q

What percent of patients chronically treated with NSAIDs experience occult GI bleeding?

A

>70% - aspirin is the worst for this probably because of its irreversible mechanism

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86
Q

Describe Hektoen enteric agar.

A

Inhibits growth of gram(+) bacteria. Fermenters appear yellow-orange and non-fermenters appear green/transparent. Organisms that produce H2S from sulfate will form a black precipitate.

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87
Q

What kind of drugs can reach systemic circulation by bulk flow transport through capillaries? What about ones that don’t fit that?

A

Ones <15000-16000D. Ones that are too big can enter systemic circulation through bulk flow transport through lymphatic vessels.

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88
Q

What is OARS?

A

Open-ended questions (well timed) Affirmations Reflective listening statements Summarize to communicate understanding

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89
Q

What is a desmoid/aggressive fibromatosis?

A

Rare tumor-like CT growth.

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90
Q

What are bacterial essentials for growth?

A

C, water, N, P, O, S, ions (especially Fe)

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91
Q

What are these terms as they relate to virus infection? Eclipse, latent phase, yield.

A

Eclipse (no virions), Latent (time to release of first virion), Yield (# of virions released by cell).

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92
Q

What RNA viruses do not replicate in the cytoplasm?

A

Retroviridae, Deltaviridae, Orthomyxoviridae.

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93
Q

What is karyolysis?

A

Nuclear dissolution (can follow karyorrhexis or develop ab novo).

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94
Q

What are some special contraindications for indomethacin?

A

Same ones as for other NSAIDs, Parkinson’s seizure disorders, depression, renal disease, HF, DM, SLE, EC volume depletion, elderly, 3rd trimester pregnancy.

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95
Q

What is a composite transposon?

A

Genes flanked by insertion sequences.

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96
Q

What is a viable plate count?

A

CFUs/mL

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97
Q

What are conidia?

A

Airborne fungal spores.

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98
Q

What is fibrosis?

A

Excessive collagen and other ECM components in visceral organs. Caused by chronic inflammation and immune diorders associated with loss of tissue.

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99
Q

What are Acid-fast bacteria? Name 3.

A

Gram(+) but more complex because of mycolic acids - helps them resist chemicals including phagolysosomes and some antibiotics. Mycobacteria, Nocardia, Corynebacteria.

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100
Q

What are coxibs?

A

Selective COX2 inhibitors. Highly effective antiinflammatory effect, lack of effect on platelet aggregation. Have very low incidence of gastric ulceration and intolerance!

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101
Q

What are the types of helminths?

A

Cestodes (flatworms), Nematodes (roundworms), Trematodes (flukes).

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102
Q

What are myelin figures?

A

The result of damaged membranes in cells (concentric circle looking things).

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103
Q

How is bradykinin produced? What’s it a mediator for?

A

Cleavage of kininogen by kallikrein. Pain.

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104
Q

What is the catalase test?

A

Sees if organism can break down hydrogen peroxide. If positive, produces bubbles.

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105
Q

What is tropism?

A

Specificity.

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106
Q

What are the BH3 sensors members of the BCL2 family and what do they do?

A

BAD, BIM, BID, Puma, Noxa. Sense cellular stress and damage, regulate balance between anti and proapoptotic groups.

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107
Q

What genera have sialic acid in their capsules (molecular mimicry)?

A

Neisseria, Haemophilius.

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108
Q

What are some stomach and liver effects of aspirin?

A

Erosive gastritis, prolonged gastric emptying, decreased PG synthesis, increased gastric acid secretion, decreased mucus and bicarbonate. Direct stimulation of bile secretion, possible Reye’s, inhibition of Vit K dependent hemostasis.

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109
Q

What kind of cells are found in chronic nonspecific vs chronic purulent inflammation?

A

Mainly mononuclear cells vs neutrophils.

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110
Q

What are the two types of analgesics and to which type do NSAIDs belong?

A

Antipyretic (peripheral, nonopioid, aspirin-like) and narcotic (central, opiate, opioid, morphine-like).

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111
Q

What’s the main mechanism of NSAIDs?

A

COX inhibition. Aspirin does it irreversibly.

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112
Q

What are adhesins?

A

Molecules on pathogens that bind eukaryotic receptors.

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113
Q

What’s the difference between exudate and transudate?

A

Exudate is high specific gravity, high protein content, has cells. Transudate is the opposite - very few cells maybe some lymphocytes.

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114
Q

Are fungi and parasites motile?

A

No and mostly

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115
Q

How is calcification identified?

A

IC or EC deposits of amorphous basophilic material - or large round laminated psammona bodies. Identified in the von Kossa stain.

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116
Q

Name some chemoattractants.

A

Bacterial N-formyl methionine, IL-8, IL-1, TNF, C3a, C5a, LTB4, 5-HETE.

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117
Q

What are some areas of the brain outside the BBB?

A

Posterior pituitary, ME of hypothalamus (ventral part), supraoptic crest, subfomical region, area postrema.

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118
Q

What is tachyphylaxis?

A

Rapid tolerance.

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119
Q

What does VEGF promote?

A

Casodilation via NO production stimulation, angiogenesis.

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120
Q

What is fatty change?

A

Abnormal triglyceride accumulation in cytosol of parenchymal cells. Mostly liver, heart, muscle, and kidneys affected. See clear vacuoles in cytosol of water and glycogen.

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121
Q

Describe the two main modes of viral entry.

A

Endocytosis (RME), membrane fusion (only if enveloped).

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122
Q

What is transformation, transduction, conjugation?

A

Transformation is uptake of naked DNA across a cell wall, Transduction is uptake of DNA via phage, Conjugation is uptake of DNA via sex pilus.

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123
Q

What are the three principles of motivational interviewing?

A

1: express empathy 2: develop discrepancy 3: roll with resistance

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124
Q

What is the presentation of a myeloperoxidase deficiency?

A

95% asymptomatic, 5% recurrent fungal infections.

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125
Q

Describe MacConkey Agar.

A

Selective - bile salts and crystal violet inhibit growth of gram(+) bacteria. Differential - lactose metabolizers turn red (neutral red indicator) and nonmetabolizers remain colourless.

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126
Q

What are spirochetes? Name three.

A

Gram(-) thin spiral bacteria that must be visualized with a dark field or fluorescence microscopy. Has endoflagella between PG and OM. Treponema, Borrelia, Leptospira.

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127
Q

What is DnaB?

A

Helicase.

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128
Q

What’s the 50S subunit made of?

A

5S rRNA, 23rRNA, 34 polypeptides.

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129
Q

What are Penicillin-binding proteins (PBPs)?

A

Do lots of jobs in the PG biosynthesis process.

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130
Q

What do Th2 cells do?

A

Secrete IL-4 (and IL-5 and IL-13) to activate M2 macrophages.

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131
Q

What NSAIDs inhibit ox. rad production?

A

Diclofenac, piroxicam.

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132
Q

What is DnaA?

A

Directs replication initiation.

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133
Q

What are gyrase and topoisomerase IV?

A

Type II topoisomerases (relax supercoiling). ALso topoisomerase IV decatenates/unlinks replicated molecules.

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134
Q

What are major causes in contraction in wound healing?

A

Burns, MMP deficiency.

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135
Q

What are the CNS protozoa?

A

Naegleria fowleri and Acenthamoeba culbertsoni (less aggressive).

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136
Q

How much of aspirin is biotransformed and excreted?

A

85% transformed in liver, 15% excreted in acid urine, 85% in alkaline urine.

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137
Q

What are some predisposing factors to adverse drug effects?

A

<1y/o. >60 y/o, being female, liver/kidney disease.

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138
Q

Describe Gangrenous necrosis.

A

Coagulative or liquefactive of organs which contact the environment. Dry - ischemic/coagulative of limbs (usually lower), may progress to wet. Wet - secondary bacterial infection and digestion of already dead tissue. Gas - infectious disease.

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139
Q

What kind of viruses release through lysis vs budding? What are the other ways of viral release?

A

Lysis usually naked, some enveloped. Budding usually enveloped. Exocytosis (some enveloped) and direct transfer to other cell - often just part of the virus.

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140
Q

What are the relative speeds of ion channels, TM/GCPRs, IC receptors?

A

Ion channels - milliseconds, TM/GCPRs - sec/mins, IC receptors - hours/days.

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141
Q

What is the difference between a hypertrophic scar and a keloid?

A

Hypertrophic stays within wound marginc, regresses with time. Keloid does neither.

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142
Q

What is the Fenton reaction?

A

Fe2+ + H2O2 -> Fe3+ + hydroxide + hydroxide radical

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143
Q

Describe Cys-Tellurite agar.

A

For isolation of Corynebacterium diphtheriae. Appears grey/black with a brown halo. Potassium tellurite inhibit gram(-) bacteria.

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144
Q

What is metaplasia vs dysplasia?

A

Replacement of one mature cell type with another vs expansion of immature epithelial cells.

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145
Q

What are the two main monooxygenases and what do they need?

A

Cyt P450 and NADPH-cyt P450. Need NADPH and molecular oxygen.

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146
Q

Describe non microsomal drug metabolizing enzymes.

A

Found mainly in cytosol or mitochondria byt also the ECF. Substrate specificity variable. Catalyze mainly conjugations (except glucuronidation), hydrolyses, and some ox/red. Can be inhibited but not induced by drugs.

147
Q

Where do carbon particules accumulate in inhalation and what’s it called?

A

In the lymphatics/regional lymph nodes (taken there by alveolar macrophages). Anthracosis.

148
Q

What dose causes salicylate toxicity?

A

400-800mcg/mL mild, >800mcg/mL severe Toxicity in pregnancy.

149
Q

How does aspirin interact with probenecid?

A

Decreased renal urate excretion.

150
Q

What is zymosan?

A

Found in fungal cell wall, resembles endotoxin and triggers TNF production.

151
Q

What is pyknosis?

A

Nuclear shrinkage and increased basophilia.

152
Q

What is the effect of spare receptors?

A

Increase the sensitivity of a tissue to a drug.

153
Q

Describe the three intestina sporozoa. How are they diagnosed?

A

Isospora belli, Cyclospora cayetanensis (get through fruit), Cryptosporidium parvum/hominis (get through swimming pools).

Have sporogony and schizogony phases. Diagnost with acid-fast oocyte in feces.

154
Q

What are some endogenous pyrogens?

A

IL-1, IL-6, TNF

155
Q

What is hyaline? What are three types.

A

Amorphous intracellular homogenous eosinophilic material. Russell Bodies - Ig containing globules in plasma cell cytosol (common in multiple myeloma and chronic inflammation) Mallory Bodies - cytosol of hepatocytes, contain intermediate cytokeratin filaments (alcoholic liver disease) alpha1AT deposits - abnormal folding, RER accumulation, formation of PAS(+) globules.

156
Q

What foes FGF promote?

A

Angiogenesis, migration of epithelial cells to creaste a new epidermis, migration of macrophage, fibroblasts, endothelial cells in damaged tissues?

157
Q

Describe gas administered drugs absorption.

A

Systemic effects, the most rapid absorption, proportional to partial pressure of drug in alveoli, absorbed via lipid diffusion in the alveolar membrane.

158
Q

What is an Hfr bacterium?

A

F plasmid integrated into its chromosome.

159
Q

What is the oral bioavailability and Vd and half life of aspirin?

A

70% and 11L and 15 mins.

160
Q

Describe remodelling in healing.

A

Deposition of CT - migration and proliferation of fibroblasts into injury site, production and deposition of ECM proteins collagen and fibronectin. Reorganization/proper remodelling - degradation of ECM by MMPs and then synthesis of new ECM.

161
Q

What are the NSAID propionic acid derivatives? Describe them.

A

Ibuprofen, Naproxen, Ketoprofen, Fenoprofen, Flurbiprofen. Inhibit COX1 and 2 reversibly, very good oral bioavailability, distributed in all tissues including brain. Naproxen markedly inhibits leukocyte migration.

162
Q

How can yeasts be classified?

A

By structure or by clinical syndromes.

163
Q

What do Th17 cells do?

A

Secrete IL-17 which induces chemokine production.

164
Q

What are the three steps in leukocyte accumulateion?

A

Margination (concentrate along endothelium, leave central axial column), Rolling (mediated by selectins), and Adhesion (mediated by integrins).

165
Q

What kind of selectins do endothelium, leukocytes, and platelets have?

A

E-selectins, L-selectins, P-selectins (stored in Weikel-Palade bodies).

166
Q

What is in the bacterial plasma membrane?

A

Proteins in a phospholipid bilayer. No sterols, has cardiolipin.

167
Q

What is Sabourad’s medium?

A

Good for growing fungi - 5.6 pH to inhibit bacterial growth.

168
Q

What is TxA2 a mediator for?

A

Vasoconstriction.

169
Q

What is atherosclerosis?

A

Lipoproteins and cholesterol accumulation in intima of large and medium vessels.

170
Q

What is healing by second intention?

A

A wound with separated edges. There’s a larger clot than in first intention, more intense inflammation, epithelial cells cannot cover defect, lots more granulation tissue. Scar formation with wound contraction via myofibroblasts, acquisition of tensile strength takes weeks but never reaches 100%.

171
Q

What % of medical visits, hospital admissions, and deaths of hospitalized patients are caused by drug adverse effects?

A

2-3%, 0.4%, 0.3% respectively.

172
Q

What does sandwich ELISA measure the presence of?

A

An antigen.

173
Q

What does DNA Pol I do?

A

Removes RNA primers on lagging strand and fills in Okazaki segments. Also has bidirectional exonuclease activity.

174
Q

What is Serous inflammation?

A

A type of acute inflammation, low protein content (but still exudate), some neutrophils/lymphocytes, single fibrin strands. Caused by physical injury (heat, viruses) Outcome is resolution.

175
Q

What are the prozone and postzone phenomena?

A

Prozone - excess antibody in precipitation test, postzone - excess antigen in precipitation test. Give false negatives.

176
Q

Are oral/sublingual/buccal/rectall administrations for systemic or local effects?

A

Systemic and rarely local.

177
Q

What is Chediak-Higashi syndrome? How does it present?

A

autosomal recessive defects in lysosomal trafficking regulator, fusion of phagosome and lysosome, phagocyte function. Presents as giant granules in leukocytes, albinism, photophobia, recurrent bacterial infections (mainly S. aureus).

178
Q

What drugs is placebo effect present for?

A

All drugs! Always present in any drug effect!

179
Q

What is direct vs indirect chemical injury?

A

Direct is interaction with molecules, indirect is metabolic transformation to toxic derivatives (by cytP450 mixed function oxidases in liver/lungs SER).

180
Q

Describe a CSF-India Ink (Nigrosin) Wet Mount.

A

Only for suspected cryptococcal meningitis (common in AIDS patients). CSF sediment mounted in india ink - ink does not penetrate the yeast capsule so look for ‘holes’ around budding yeasts. A rule-in test only.

181
Q

Describe Fibrinoid necrosis.

A

EC (not IC) degeneration, accumulation of deeply eosinophilic material within injured/necrotic vessel walls. Usually indicates severe vascular injury. Irreversible, can cause inhibition of metabolite transport and rupture of blood vessel wall (hemorrhage).

182
Q

What is an abscess?

A

A localized collection of pus in tissues with destruction of the tissue architecture. Resolution is impossible - will fix by healing.

183
Q

What is the periplasmic space?

A

Space between the PM and PG or between PG and OM

184
Q

What is purulent/suppurative inflammation?

A

A type of acute inflammation. Pus is semiliquid white/yellow material with dead/viable neutrophils. Green means too much MPO or some microorganisms. Causes are mainly cocci but minorly M. tuberculi, S. typhi, fungi. Outcomes are resolution, orgnaization, repair, or progression to chronic inflammation.

185
Q

What is the thioglycollate test?

A

Thioglycollate removes oxygen - a tube of semisolid medium containing it is inocculated with the test organism, producing oxygen gradient. Obligate aerobes only grow at the top, facultative aerobes grow better at the top, etc.

186
Q

What are the major US dimorphic fungi genera?

A

Histoplasma, Blastomyces, Coccidioides, Sporothrix.

187
Q

Distinguish between generalized and specialized transduction.

A

In generalized, a random fragment of host DNA gets packaged in the phage and with a low success rate. In specialized, the host DNA flanking the prophage is taken into the phage and with a high success rate.

188
Q

What is potency?

A

Dose needed to achieve 50% of max effect.

189
Q

What NSAIDs block PMN migration?

A

Naproxen, Indomethacin.

190
Q

How does aspirin interact with bilirubin?

A

Cases kernicterus in infants.

191
Q

Describe a bacterial capsule.

A

Usually high molecular weight, made of polymerized simple sugars (rarely proteins and AAs). Prevents phagocytosis, good for adherence and colonization, prevents dessication, prevents complement and Ab deposition.

192
Q

Describe radial immunodiffusion.

A

Ab-coated well has holes punched in it. Ag is added to holes and diffuses outwards depending on how much there is.

193
Q

Where are drugs reabsorbed in the nephron?

A

All along the nephron via lipid diffusion.

194
Q

What’s the difference between physiologic or pathologic adaptation?

A

Whether or not the cell responds beyond homeostatic limits.

195
Q

How do viruses attach?

A

Adhesin-receptor binding. Naked viruses usually through the capsid or added protein, enveloped usually through VAP (generally glycoprotein).

196
Q

What does DNA Pol III do?

A

Synthesizes DNA 5’ to 3’, but also has 3’ to 5’ exonuclease activity.

197
Q

What are the types of helminths?

A

Platyhelminths(flat) - (trematodes/flukes and cestodes/tapeworms)

Nelahelminths(round) - Intestinal and tissue worms.

198
Q

What kind of drugs are more readily reabsorbed by the tubule?

A

Lipid soluble.

199
Q

What embryonic stage is most susceptible to defects which may manifest later in life?

A

Histogenesis (81d and on)

200
Q

What are the effets of a partial agonist?

A

Agonist when full agonist concentration is low, antagonist when full agonist concentration is high.

201
Q

What is a Gell&Coombs type IV sensitivity?

A

Delayed/cell mediated reaction. On 2nd exposure T cells attach - most commonly manifests as contact dermatitis.

202
Q

What is chronic granulomatous disease and NADPH ox deficiency?

A

A group of X-linked and AR disorders including NADPH ox deficiency - inadequate neutrophil response, macrophage-rich chronic inflammatory reaction, granuloma formation. Increased susceptibility to bacterial and fungal infections. Confirmed by a negative Nitro Blue Tetrazolium test (NBT).

203
Q

What are oxicams?

A

COX1 mainly inhibitors. Piroxicam and Indomethacin. Piroxican also blocks PMNs and has a great antiinflammatory effect and a very long half life. Indomethacin also blocks PMN migration, and inhibits PL A&C. High incidence of adverse effects!

204
Q

What is an absolute contraindication of ACE inhibitors?

A

Pregnancy.

205
Q

What are the types of hyphae?

A

Septate (cross walls, more uniform) and Aseptate (AKA coenocytic, hollow and multinucleate, may have irregular width, grow rapidly, not common).

206
Q

What are the proapoptotic members of the BCL2 family and what do they do?

A

BAX, BAK. Allow leakage of cyt c into cytosol.

207
Q

How does aspirin interact with methotrexate?

A

Increases methotrexate effects.

208
Q

What molecular mimicry does S. pyogenes have?

A

A hyaluronic acid capsule.

209
Q

What is an oil/water partition coefficient?

A

Amount of drug in oil phase / amount of drug in liquid phase. Determines lipid solubility. *related to the degree of ionization in ionizable drugs.

210
Q

What are the salicylates?

A

Aspirin, Sodium salicylate, Mesalamine.

211
Q

How do apoptotic bodies stain?

A

Eosinophilic.

212
Q

What is in the cell walls of fungi? What drug(s) target(s) it?

A

Mannose-proteins, chitin with glucan (target of echinocandins).

213
Q

What is CRE?

A

Carbapenem-resistant Enterobacteriaceae - possessses NDM-1 which cleaves carbapenems.

214
Q

What is peptidoglycan?

A

Main component of bacterial cell wall. Alternating NAG (GlcNAc) and NAM (MurNAc) but referred to as monomer. Forms 3D multilayered net. Is a PAMP, induces IL-1, IL-6, GCSF, TNFalpha

215
Q

When does drug accumulation occur?

A

When the dosing interval is less than four half lives.

216
Q

What is a zero order vs first order drug?

A

A zero order drug is when a constant amount must be processed per unit time (e.g. alcohol). A first order drug is when a constant percentage must be processed per unit time.

217
Q

Describe Traumatic fat necrosis.

A

Female breast, mechanical trauma leads to inflammation leads to calcificaiton and scarring. Mimicks breast cancer.

218
Q

Describe RNA Pol I.

A

Binds promoter (-10, -35), unwinds DNA and immediately starts putting nucleotides on template strand. Needs sigma factor to be a holoenzyme.

219
Q

Where is mecA found?

A

In SCCmecIV, the MRSA gene

220
Q

What is Farmer’s Lung?

A

Illness caused by exposure to organic dust and spores of thermophilic fungi and Actinomyces.

221
Q

What is the advantage of wet mounts?

A

You can see bacteria alive.

222
Q

What’s the sensitivity difference between naked and enveloped viruses?

A

Naked are resistant to dying, acid, temperature, detergents, bile salts. Enveloped is sensitive to these. Both are sensitive to solvents.

223
Q

What is the ion trapping mechanism?

A

How a drug is non ionized in the gastric lumen, crosses into a cell, and then ionizes in the higher pH and is ‘trapped’.

224
Q

What are capsules/slime made of?

A

Sugars, AAs, or both.

225
Q

What is a radioimmunoassay?

A

Like immunofluorescence but with a radioactive conjugate.

226
Q

How do you treat a drug allergy?

A

With withdrawal, or if its serious with corticosteroids and/or antihistamines.

227
Q

What is coagulase and the coagulase test?

A

Coagulase converts fibrinogen to fibrin. Free coagulase is secreted from the bacterial cell - identified with a tube. Bound coagulase is attached to the bacterial cell wall - tested with slide coagulase or coagulase agglutination test.

228
Q

What does phosphomycin target?

A

Inhibits MurA.

229
Q

What are dimorphic fungi?

A

Can convert from filamentous form to yeast form in the body.

230
Q

Describe prokaryotic translation.

A

30S separated by IF1 and IF3, then binds to upstream purine-rich Shine-Dalgarno sequence to position itself (16S binds it). IF2 brings fmet-tRNA for start.

231
Q

What kind of viruses generally do concerted assembly?

A

Filamentous, some icosahedral.

232
Q

What dose causes acetaminophen poisoning? How does it work and how do you treat it?

A

150-250mg/kg - in children 250 will be fatal. NAPQI (N-acetyl-parabenzoquinone) is a metabolite - it reacts with SH groups of glutathione and inactivates it - with high doses glutathione is depleted and NAPQI reacts with SH of hepatic proteins and causes liver damage. Can cause liver centrilobular necrosis in about 10% of patients (10-20% of these die). Treated with acetylcysteine (many SH groups).

233
Q

What are the phases of the inflammatory reaction? What phase do NSAIDs affect?

A

Acute, transient vascular phase Delayed, subacute cellular phase Chronic, proliferative phase NSAIDs affect the acute phase.

234
Q

Describe transdermal administration drug absorption.

A

Systemic effects, absorption slow, first pass avoided.

235
Q

For a 70kg person, what does a Vd of 10-20L mean?

A

Distributed through ECF but can’t penetrate cells.

236
Q

What is the tnerapeutic window?

A

Between the minimum effective concentration and the minimum toxic concentration (1%)

237
Q

What are labile, stable, and permanent cells?

A

Labile (continuously dividing, can multiply but not become larger) Stable (usually in G0 but can enter cell cycle, can multiply or become larger) Permanent (pernanently in G0, can become larger but not multiply)

238
Q

How is hemosiderin identified?

A

With a Perl’s/Prussian0Blue stain.

239
Q

What are the types of calcificaiton?

A

Dystrophic - calcification of previously damaged.necrotic tissue (normal serum Ca++) Metastatic - normal tissues calcified due to hypercalcemia

240
Q

What is an absolute contraindication of retinoids?

A

Pregnancy.

241
Q

What is the oxidase test?

A

Tests for cyt c oxidase (if negative doesnt necessarily mean it doesnt have an ETC!) Positive means it uses oxygen for respiration, an will turn purple.

242
Q

Where is transendothelial migration done and what is the stimulus? What molecules are involved?

A

Post-capilary venules, stimulus is the chemokine gradient. CD31/PECAM-1 on both the endothelial cell and the leukocyte

243
Q

Describe microsomal drug metabolizing enzymes.

A

Found in the SER of mainly liver cells. Have low specificity and efficiency but are very abundant. Mainly monooxygenases, catalyze mainly oxidations and glucuronidations, only catalyze reactions of things that are lipid soluble. Can be inhibited or induced by drugs.

244
Q

What is a Gell&Coombs type I sensitivity?

A

1st exposure makes IgEs, 2nd exposure Ag-Ab rxn on sensitized cells triggers release of vasoactive/inflammatory mediators.

245
Q

Describe aerosol administered drugs absorption.

A

Local effects, absorption via lipid diffusion in alveolar membrane, slow. Local effect depends on proportion of drug reaching alveoli which depends on concentration, pulmonary ventilation, particle size.

246
Q

What is mycelium?

A

Hyphae of moulds form together into matlike structure.

247
Q

What are TNF and IL-1?

A

Cytokines made by macrophages, mast cells, T-lymphs and macrophages, endothelial cells respectively. Involved in chemotaxis, leukocyte recruitment and activation, and fever.

248
Q

What kind of hypersensitivity is a contraindication of celecoxib?

A

Sulfonamide

249
Q

What are PGD2, PGE2, and PGI2 involved in?

A

All involved in vasodilation. PGE2 also involved in fever and pain.

250
Q

What is confusing about chlamydias?

A

Small energy dependent bacteria that are obligate intracellular parasites and only grow in cell culture.

251
Q

What is healing by first intention?

A

A wound with opposed edges. 1st day neutrophils fill blood clot (scab), 2nd day movement of epithelial cells below scab with formation of continuous layer, 3rd day macrophages replace neutrophils (appearance of granulation tissue), 5th day is maximum of granulation tissue. 6-14th day CT deposition, reduction of inflammation and edema, restoration of epidermis. By end of a month, a scar has formed.

252
Q

Describe the outer membrane.

A

Found only in gram(-) and chlamydiaceae. LPS outer leaflet, phospholipid inner leaflet. Selective barrier. LPS has Lipid A anchored to the OM and a tail (O-antigen).

253
Q

What does cycloserine target?

A

Inhibits D-ala D-ala synthetase (and Ala racemase).

254
Q

What is SOLER?

A

Squarely face patient, Open posture, Lean towards patient, Eye contact, Relaxed manner.

255
Q

Describe bile esculin agar.

A

Inhibits gram(+) bacteria and most streprococci EXCEPT Group D and enterococci. They can hydrolyze esculin to esculitin, which interacts with iron to form black precipitate. Can be plate or tube.

256
Q

What is ambisense RNA?

A

Can be read as + or - RNA.

257
Q

What are the NSAIDacetic acid derivatives. Describe them.

A

Diclofenac, Ketorolac. Diclofenac has a particularly great antiinflammatory effect. Great for rheumatoid arthritis and ankylosing spondylitis. Ketorolac has a particularly great analgesic effect. Long term use is associated with peptic ulceration and renal impairment.

258
Q

What is the reward system in the brain?

A

Dopaminergic neurons from ventral tegmentum synapse with nucleus accumbens.

259
Q

Describe Coagulative necrosis.

A

Most commonly caused by ischemia - Cell outlines preserved for at least 2 days. Acidophilic coagulated anuclear cells. Gross - dead tissue dense.dry, cut surface white-grey.

260
Q

What happens at toxic doses of aspirin?

A

Respiratory center depression, respiratory and metabolic acidosis.

261
Q

What are viroids?

A

ssRNA, no capsid (self-replicates, no protein, known to be in plants).

262
Q

How can you measure bacterial growth?

A

By optical density (turbidity)/light scatter in liquid media. By growth in culture and counting CFUs.

263
Q

What are the human host plasmodium species?

A

falciparum, vivax, ovale, malariae.

264
Q

What is confusing about rickettsias?

A

Small bacteria that are obligate intracellular parasites.

265
Q

What is darkfield microscopy used to identify?

A

Spirochetes.

266
Q

What is K-antigen?

A

Capsule.

267
Q

What are multinucleated giant cells?

A

Fused epithelioids (>20 nuclei). Stimuli is IFNgama or IL-4 but uncertain. Langhans giant cells are horseshoe shaped, and Foreign body giant cels are centrically clustered.

268
Q

What’s the difference between capsule and slime?

A

Capsule organized and anchored to the lipid membrane or covalently onto the PG, slime is disorganized and not anchored.

269
Q

What are epithelioid cells?

A

Large fusions of macrophages (1-3) with pale pink granular cytoplasm, present in granulomas.

270
Q

What is FASD?

A

Fetal alcohol syndrome - occurs in organogenesis. CNS dysfunctions, slow growth, cluster of facial malformations, variable set of major and minor malformations, greater susceptibility to infectious disease.

271
Q

What is pseudoallergic?

A

If a drug produces a type I-like reaction but no antibodies are found.

272
Q

Describe blood Agar’s differentiability.

A

alpha hemolytic organisms reduce RBC Hb to metHb - green. beta hemolytic organisms have total hemolysis clearing around colonies. gamma hemolytic orgainsms have no hemolysis.

273
Q

What’s a telltale sign of cardiac hypertrophy?

A

Boxcar nucleus.

274
Q

What does it mean when a phage is ‘temperate’?

A

Can be lysogenic or lytic.

275
Q

What drugs will not be glomerularly filtered?

A

Ones bound to plasma proteins or MW>65000.

276
Q

What are Koch’s postulates?

A

Identify in all diseased subjects, Isolate, Introduce (recreate), Reisolate.

277
Q

What is the name for forms of protozoa found in tissue and found in blood plasma?

A

Amastigote and trypomastigote.

278
Q

What is H-antigen?

A

Flagella.

279
Q

What is leukoplakia?

A

Replacement of nonkeratinized with keratinized epithelium.

280
Q

What’s the difference between marasmus and cachexia?

A

Masasmus is severe protein-caloric deficiency, cachexia is muscular wasting caused by TNF release in patients with cancer and chronic infectious diseases.

281
Q

What kind of drugs are poor to cross the placenta?

A

Ones with MW>1000, ones with MW>200 that are highly ionized.

282
Q

What kind of ribosomes do bacteria, viruses, fungi, and parasites have?

A

70S, none, 80S, 80S

283
Q

What does myeloperoxidase do?

A

Makes HOCl from peroxide and chloride. It is a bactericidal system.

284
Q

What are some acquired causes of deficient leukocyte function?

A

Thermal burns, diabetes mellitus, hemodialysis, malnutrition.

285
Q

What are the causes of atrophy?

A

Reduced metabolic activity w/ decreased protein synthesis. Or inadequate degradation of cytosolic and nuclear proteins (lysosomal - lipofuscin accumulation or ubquitin/proteosome - protein accumulation).

286
Q

What is the difference between homo and heterofermentation?

A

Homo - no gas production, hetero - gas production.

287
Q

What are the characteristics of inflammation?

A

Rubor, tumor, calor, dolor, functio leasa.

288
Q

Describe subcutaneous or intramuscular drug absorption.

A

For systemic and rarely local effects. IM absorotion rapid, subq slower. Absorbed via bulk flow across IC pores of endothelium, limited by local blood flow and drug solubility into interstitial fluid.

289
Q

What does catalase do?

A

Breaks down peroxide.

290
Q

What is compliance?

A

The degree to which a patient adheres to a treatment plan.

291
Q

Describe the chromatographic immunoassay.

A

Like backwards sandwich ELISA - qualitative, antigen goes up bed to captured Abs.

292
Q

What does NO synthase do?

A

Maes peroxynitrite (ONOO-) from NO. It is a bactericidal system.

293
Q

What is ABPA?

A

Allergic bronchopulmonary aspergillosis.

294
Q

What is the adult dosage of aspirin for the different effects? What about kids?

A

80-325mg daily for antiplatelet 300-600mg every 4-6hrs for analgesic/antipyretic (6-10mg/kg for kids) 1000mg every 6hrs for antiinflammatory (10-15mg/kg every 4-6 for kids)

295
Q

What is the fate of glucuronide conjugates?

A

They can be excreted with bile, hydrolyzed in the intestine by beta-glucuronidase, and reabsorbed.

296
Q

What encodes the F-pilus?

A

The tra operon in the F plasmid.

297
Q

What increases a receptor’s affinity for beta-arrestin?

A

Phosphorylation.

298
Q

How does the NSAID antypyretic effect work?

A

Inhibits PG synthesis.

299
Q

Describe the Ziehl-Neelsen stain.

A

Heated aniline dye/carbolfuschin, acidified alcohol decolourizer (washes away lipids), methylene blue counterstain.

300
Q

What is the presentation for (and what are) LAD1 and LAD2 deficiencies?

A

Leukocyte Adhesion Deficiency 1 - defect in beta2 subunit of LFA-1 or MAC-1 integrins. LAD2 - absence of Sialyl-Lewis X (ligand for E and P selectins). Present as recurrent bacterial infections.

301
Q

Describe a KOH wet mount.

A

10% KOH added to glass slide, degrades human cells. Warm, let rest for 10 min to release fungal elements. View in reduced light to see unstained fungi. Can use calcofluor white and read with a fluorescent scope.

302
Q

Describe the gram stain.

A

Add crystal violet, iodine to fix colour, alcohol to wash away lipids, Safranin counterstain. Gram(-) pink, Gram(+) purple.

303
Q

For a 70kg person, what does a Vd of 40-50L mean?

A

Distributed through TBW, can pass most biologic barriers.

304
Q

What is a viral capsid?

A

Build from many copies of one or several self-assembling proteins. Packages and protects nucleic acids. Protein -> protomer -> capsomere (pentamer/penton) -> capsid (12 pentons + X hexons).

305
Q

What’s the 30S subunit made of?

A

16S rRNA, 21 polypeptides.

306
Q

Describe binary fission.

A

The chromosome splits, the two new chromosomes attach to the cell membrane, the bacterium divides at the septum.

307
Q

What do acidic and basic drugs mainly bind to?

A

Albumin and alpha1 acid glycoprotein respectively.

308
Q

What is indomethacin used for?

A

Rheumatoid arthritis, osteoarthritis, bursitis, tendinitis, ankylosing spondylitis, acute gout, to accelerate closure of ductus arteriosus in infants.

309
Q

What are the phases of PG biosynthesis?

A

I: monomer production from NAG/NAM - completed on Bactoprenol P. II: bridge peptide (if present) III: translocation across PM, transglycosylases incorporate new monomer into PG macromolecule - bactoprenol recycles. IV: transpeptidases cross-link strands through peptide tails/bridges. Final D-ala cleaved to provide energy for the reaction.

310
Q

How is Vd calculated?

A

DxF/Cp0 *Cp0 - plasma [drug] at time 0

311
Q

What are the apoptosis pathways?

A

Mitochondrial (intrinsic) or death receptor/extrinsic - Fas/TNF receptors.

312
Q

How does rectal administration absorption compare to oral?

A

Lower, often irregular (heavily influenced by degree of fullness of rectal ampulla).

313
Q

Describe M1 vs M2 macrophages.

A

M1 are proinflammatory and are stimulated by microbes and IFNgmama. M2 are antiinflammatory and are stimulated by IL-13 and IL-4. They activate fibrosis/CT.

314
Q

Describe Liquefactive necrosis.

A

Necrosis with loss of cell/tissue structure (neutrophil influx and digestion of cell carcasses). Comes from bacterial infection or preexisted coagulative necrosis. No cellular outlines, soft and wet tissue, colour depends on presence of blood (grey, red, brown, black).

315
Q

What is an absolute contraindication of osmotic diuretics?

A

Heart failure.

316
Q

What is the complement fixation test?

A

Patient serum is heated to destroy complement. Specific antigen and measured complement are then added, and then sheep erythrocytes. If there is no antibody to the specific antigen, the complement will not have been fixed and will lyse the sheep cells (negative test).

317
Q

How does amyloid differ from hyaline? Describe it. How is it identified?

A

It’s extracellular. It’s defective folding - beta pleated sheets instead of alpha helices. It’s identified with Congo red stain - fluorescent microscopy of which will generate apple-green birefringence.

318
Q

What % of patients report hypersensitivity to NSAIDs?

A

0.3 but 25% of middle aged patients with asthma, nasal polyps, chronic urticaria.

319
Q

What is drug biotransformation? Describe it.

A

Increases water solubility. Can result in inactivation, maintenance of activity, or activation. Has phase I (nonsynthetic) - ox, red, hydrolyses. Has phase II (synthetic) - conjugations. Can do I, II, or I then II.

320
Q

What does TGFbeta promote?

A

Fibroblast migration and proliferation, increased synthesis of collagen and fibronectin, inhibition of epithelial growth, inhibition of inflammatory response.

321
Q

What is an F’ plasmid?

A

An F plasmid that has been improperly excised and taken a piece of hte host chromosome with it.

322
Q

What do Quinolones target?

A

topoisomerases.

323
Q

Describe Histoplasma capsulatum.

A

Is a fungus, is inhaled, resists lung macrophage lysosomes. Grows intracellularly, bloodstream circulation, generally self-limiting pneumonia, disseminates in T-cell immunocompromised people.

324
Q

For a 70kg person, what does a Vd of 3-5L mean?

A

Restricted to the vascular compartment.

325
Q

What are the only groups of drugs that skin tests are reliable for when determining allergy?

A

beta lactam antibiotics and local anaesthetics.

326
Q

What are some causes of lipofuscin accumulation? What is lipofuscin?

A

Ageing, severe malnutrition, cancer cachexia. Lipofuscin is a yellow-brown pigment found in cytosol, it is the end product of free-radical injury (lipid peroxidation of polyunsaturated lipids of membranes).

327
Q

What are LTC4, LTD4, and LTE4 involved in?

A

Increased vascular permeability and vasoconstriction.

328
Q

Describe Cetrimide agar.

A

Isolates Pseudomonas aeruginosa. Has Mg and K that promote production of pyocyanin and fluorescin from some strains.

329
Q

What’s the difference between pathogenic hyperplasia and neoplasia?

A

Hyperplasia is reversible (resolves when stimulus is removed) and responds to regulatory mechanisms. Neoplasia is irreversible an doesn’t.

330
Q

What can happen after 2-3 years of aspirin use?

A

Renal lesions.

331
Q

What embryonic stage is most susceptible to teratogenesis?

A

Organogenesis (17-80d)

332
Q

What do Sulfomanides target?

A

They block nucleotide and folate synthesis.

333
Q

Name 3 acid-fast stains.

A

Ziehl-Neelsen, Kinyoun, Auramine.

334
Q

What is bioavailability?

A

A measure of drug absorption - measures the fraction of the drug reaching systemic circulation unchanged).

335
Q

What do Histamine and Serotonin do and what produces them?

A

Histamine (mast cells, basophils) and serotonin (platelets). Are involved in increased vascular permeability, histamine is also a vasodilator.

336
Q

What is the effect of O-acetylation of the OM?

A

Blocks its ability to impede lysozyme access.

337
Q

What are two good screning questions for depression?

A

Have you been feeling sad for the past two weeks? Have you lost interest in activities for the past two weeks?

338
Q

What drug is given with NSAIDs in patients prone to get a peptic ulcer to reguce the risk?

A

Misoprostol (PGE1).

339
Q

What is a Virus-like particle (VLP)?

A

Virion with missing component, non-infections, is up to 99% of viral particles.

340
Q

What is cholesterolosis?

A

Accumulation of cholesterol in the gallbladder mucosa.

341
Q

What is special about mycoplasma structure?

A

No cell wall, just exposed cell membrane.

342
Q

How does aspirin interact with alcohol and corticosteroids? How does it work with alcohol?

A

Increases gastric effects - moreso with alcohol. Alcohol induces CYP2E1 synthesis (which converts acetaminophen to NAPQI)

343
Q

What is an insertion sequence?

A

The smallest TE, encodes tnp and other proteins. Flanked by inverted repeats.

344
Q

What is a therapeutic index?

A

The ratio between a harmful/lethal and an effective dose.

345
Q

What’s distinctive about gram(+) peptidoglycan?

A

Has techoic and lipotechoic acids.

346
Q

What is a Gell&Coombs type II sensitivity?

A

Ab dependent - binds surface components of cell, making it appear foreign. IgM or IgG.

347
Q

Describe Mannitol-salt agar.

A

High salt concentration (inhibits all but osmotolerant organisms). Fermentation of mannitol causes colour change from red to yellow (neutral red indicator).

348
Q

What are siderophores?

A

Things many bacteria secrete - bind iron strongly and then are internalized.

349
Q

What are mollicutes?

A

Very small bacteria with no cell wall, membrane has sterols acquired from the host. Mycoplasma, Ureaplasma.

350
Q

How is drug secretion done in the nephron?

A

In the proximal tubule, two systems - one for cations and one for anions. There is competition within each system but not across systems. Incompetely developed in newborn and diminished in the elderly.

351
Q

What is the motility of amoebae and sporozoa?

A

Pseudopodal and gliding motility respectively.

352
Q

What does NADPH oxidase do?

A

Makes superoxide from oxygen and NADPH. It is a bactericidal system

353
Q

What are the mechanisms of reperfusion injury?

A

Additional calcium influx, oxygen influx, inflammatory response to necrotic tissue.

354
Q

What is special about Candida albicans?

A

Has 3 forms, can also form pseudohyphae when they invade tissues.

355
Q

What does the presenve of IgMs vs IgGs mean?

A

Current infection vs past infection/immunity.

356
Q

What does ‘pathognomic’ mean?

A

Characteristic or indicative of a disease.

357
Q

What NSAIDs inhibit LOX?

A

Diclofenacm, ketoprofen.

358
Q

What is direct vs indirect latex agglutination?

A

Direct tests for antigen, indirect tests for antibody.

359
Q

What do Th1 cells do?

A

Secrete IFNgamma to activate M1 macrophages.

360
Q

What is twitching motility?

A

Pilus mediated form of solid surface translocation. Occurs via grappling hook-like retraction and extension of pilus.

361
Q

What are some topical uses of NSAIDs?

A

Keratolytic, counterirritant, antifungal.

362
Q

How do drugs reach the CNS? What obstacles do they face?

A

By crossing cerebral capillaries (to the interstitial fluid) or choroid plexus (to BBB). They must cross occluding zonulae and P-glycoprotein in the choroid plexus epithelium.

363
Q

What are gapped viruses?

A

dsDNA but with gaps, uses an RNA intermediete.

364
Q

Do the NSAID analgesic and antipyretic effects undergo tolerance?

A

No

Semester 3 Medical School (5 decks)

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