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General 2 Flashcards

1
Q

What is assc. w/ leukoplakia besides EBV (secondary to HIV)?

A

Tobacco use

Can’t be scraped off unlike oral thrush

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2
Q

What should you think about when there’s oral thrush w/out any other complains (like dentures, DM, immunosuppression)?

A

HIV -> b/c this is how it commonly presents

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3
Q

First study found significant reduction in RR w/ good p vale. Second study found no significant reduction b/c they got the same RR but w/ bad p value. What’s the problem?

A

Sample size is!
Don’t think of p value as being the indicator of only type I error
The second study has type II error b/c they found no difference when difference truly exists, so this is related to power of the study, which is related to sample size

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4
Q

What kinds of transplant should you be thinking about GVHD instead of acute rejection?

A

BM, liver (or any other organ rich in lymphocytes), transfusion of non-irradiated blood
You’ll also see manifestations in skin, liver, GI tract outside of what’s transplanted in GVHD (vs. just infiltrates in graft vessels in acute rejection)
Both GVHD and acute rejection are mediated by T cells and develop at about 1 wk tho

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5
Q

What does it mean that genetic code is degenerate?

A

There are more codons than AAs

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6
Q

What are P bodies?

A

Foci w/in cytoplasm that serves in repression/decay of mRNA as well as mRNA storage

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7
Q

2 enzymes involved in methylguanosine capping at 5’ end? Why does this step matter?

A

Guanylyltransferase: adds guanine triphosphate to 5’
Guanine-7-methyltransferase: methylation of guanosine cap
This process protects mRNA from degradation by cellular exonucleases and allows it to exit nucleus

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8
Q

What is the eukaryotic equivalence of PABA?

A

Folic acid

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9
Q

Which protein synthesized by HIV needs to be glycosylated and cleaved into 2 smaller proteins in ER and golgi?

A

gp160 from env gene -> cleaved intto gp120 and gp41

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10
Q

How does HIV infection of CD4+ T cells cause cell damage?

A

Direct cytopathic effect

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11
Q

5 class of antibiotics that tx pseudomonas?

A

Penicillins: ticarcillin, piperacillin
Caphalosporins: ceftazidime (3rd gen), cefepime (4th gen)
Aminoglycosides
Fluoroquinolones: ciprofloxacin, levofloxacin
Carbapenems: imipenem, meropenem

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12
Q

What does TGF-B induce isotype switching to?

A

IgA

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13
Q

What Ig is best at complement fixation? What about opsonization of bacterial toxin?

A

Complement: IgM

Opsonization of bacterial toxins: IgG

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14
Q

What does it tell you when neoplasm expresses CD31?

A

CD31 = PECAM1 -> tells you that it’s endothelial origin

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15
Q

What are the 2 characteristics of drugs w/ high intrinsic hepatic clearance?

A

High lipophilicity

High Vd

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16
Q

What are the 3 characteristics of drugs that tend to be excreted unchanged in urine?

A

Low Vd
Highly plasma PB
Hydrophilic

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17
Q

2 molecules in death receptor pathway?

A

Type 1 TNF receptor

Fas (CD95)

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18
Q

What can minors consent to in most states w/out parental consent?

A

Prenatal care (but CAN’T consent to abortion in most states)
STDs
Contraception
Drug/alcohol rehabilitation

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19
Q

Diff steps of protein translation and antibiotics that target them?

A

Order pretty much goes w/ mnemonics buy AT 30, CCEL at 50.
Formation of initiation complex: aminoglycosides (30S)
Binding of aminoacyl-tRNA to A site: tetracyclines (30S)
Peptidyltransferase enzyme: chloramphenicol (50S)
Translocation: clindamycin and erythromycin (50S)

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20
Q

What do A, P, and E sites do on ribosome complex?

A

P site: binds starting AA (methionine)
A site: binds incoming aminoacyl-tRNA -> AA from P site gets transferred over to A site
E site: empty tRNA gets shifted here from P site

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21
Q

3 most common bacterial causes of acute otitis media, sinusitis, and bacterial conjunctivitis in childhood?

A
  1. Strep pneumo
  2. Nontypable H. influenzae (DON’T produce capsule -> the one that does causes meningitis)
  3. Moraxella catarrhalis
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22
Q

Why is histone H1 special?

A

The only one outside the nucleosome core -> helps package nucleosomes into more compact structures by linking DNA bet. adjacent nucleosomes

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23
Q

Steps of PI3K/Akt/mTOR pathway?

A

growth factor binds receptor tyrosine kinase -> PI3K activated -> PIP2 in plasma membrane turned to PIP3 -> PIP3 activates Akt (protein kinase B, serine/threonine-specific protein kinase) -> mTOR activated and translocated into nucleus to induce gene expression (promotes survival)

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24
Q

What’s the effector of JAK/STAT pathway?

A

STAT dimerize and translocate to nucleus

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25
Q

Major adaptive immune mechanism that prevents reinfection w/ influenza virus?

A

IgG against hemagglutinin in circulation
IgA against hemagglutinin in nasopharynx
NOT T cell response or anything like that

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26
Q

Best antibiotics for anaerobes above diaphragm (like lung abscess)? Below diaphragm?

A

Above diaphragm: clindamycin b/c it covers both anaerobic and aerobic
Below diaphragm: metronidazole (only covers anaerobic)

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27
Q

Which org has peritrichous flagella?

A

Proteus mirabilis -> highly motile (so flagella uniformly distributed over entire surface of cell)

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28
Q

What other sign signifies irreversible cell damage besides membrane lysis?

A

Vacuoles in mitochondria (implies permanent inability to generate ATP)
NOT mito swelling, which is reversible

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29
Q

What’s the effector of PLC pathway?

A

Protein kinase C

Activated by DAG and Ca2+ (which is released under IP3 influence)

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30
Q

Was told the % of absolute risk in standard tx and that FDA would only approve a new drug if it decreases the risk by a certain % compared to standard tx. How do you calculate % absolute risk of new tx?

A

Just take the percentage that FDA will accept and multiply it to %AR of standard tx
Ie. standard tx’s recurrent rate is 8%, FDA will only approve if new drug decreases the rate of recurrence by at least 40% -> so just take 60% of 8% -> meaning FDA will approve a new drug if the maximal rate of recurrence is 4.8%
More proper way to do it is RRR = (ARcontrol - ARtx) / ARcontrol
Plug in RRR = 0.4, ARcontrol = 0.08 and solve for ARtx

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31
Q

What’s the problem w/ RRR?

A

Overestimate effectiveness of intervention

RRR of 50% occurs whether a drug decreases incidence from 2% to 1% or from 50% to 25%

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32
Q

What molecule from N. meningitidis correlates w/ morbidity and mortality? What molec correlates w/ immunogenicity?

A

Morbidity and mortality: look at LOS (it’s like LPS but lacks repeating O-Ag) -> this is what causes sepsis, petechiae, Waterhouse-Friderichsen
Immunogenicity: capsular polysaccharide -> generates protective Ab (but remember that there’s no vaccine for B serotype)

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33
Q

Life cycle of strongyloidiasis? What’s the complication?

A

Laevae penetrate skin (might see larva currens on thigh and buttocks) -> migrate hematogenously to lungs -> go up pharynx and swallowed -> lay eggs which hatch in intestinal mucosa -> so dx is seeing rhabditiform (noninfectious) LARVAE in stool
B/c of autoinfection, worm burden might cause hyperinfection and septic shock

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34
Q

What is the mechanism that generates infectious virus from 2 noninfectious viruses that don’t have segmented genomes? What about segmented genomes?

A

Non-segmented genomes: recombination (crossing over w/in homologous regions)
Segmented genomes: reassortment

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35
Q

Triad of congenital toxoplasmosis? How do you dx?

A

Chorioretinitis, hydrocephalus, intracranial calcification

Serology, bx (tachyzoite)

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36
Q

Nematodes that you get from ingestion?

A

“you’ll get sick if you EAT these!”

Enterobius (pinworm), Ascaris (giant roundworm), Toxocara (visceral larva migrans from dogs and cats)

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37
Q

Nematodes that penetrate your skin?

A

“these get into your feet from the SANd”

Strongyloides (threadworm), Ancylostoma (hookworms), Necator (hookworms)

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38
Q

Nematodes that you get from bites?

A 
"lay LOW to avoid getting bitten"
Loa loa (deer fly, horse fly, mango fly), Onchocera volvulus (female blackfly bite, river blindness), Wuchereria bancrofti (female mosquito, elephantitis)
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39
Q

What 4 orgs cause food poisoning assc. w/ exotoxin formed AFTER ingestion?

A

ETEC and cholera

EHEC and Shigella

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40
Q

Lipid A is present on LPS outer membrane of what group of orgs? What does it do?

A

All Enterobacteriaceae

For acivation of macrophages -> cytokines causing septic shock

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41
Q

What organisms show up green on EMB agar?

A

Anything fermenting lactose -> like E. coli

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42
Q

O Ag is on the outer membrane of what group of orgs?

A

G- -> EXCEPT neisseria spp

Used to classify G-

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43
Q

What is the increase in glycogenolysis assc. w/ muscle contraction mediated by?

A

Increase in cytoplasmic Ca2+!!! -> phosphorylates stuff and activates them
cAMP promotes glycolysis too but it’s not assc. w/ muscle contraction (just flight or fight response)

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44
Q

What gives rise to mammary glands and epidermis?

A

Surface ectoderm

Mammary glads are just modified sweat glands so consider them epidermis appendages

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45
Q

What gives rise to adenohypophysis?

A

Surface ectoderm

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46
Q

Best way to prevent neonatal tetannus?

A

Maternal vaccination (w/ tetanus toxoid) during pregnancy -> transfer of IgG antitoxin across placenta

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47
Q

What monosaccharide has the fastest rate of metab in glycolysis?

A

Fructose (enters glycolysis as G3P so bypass PFK-1 which is a major regulatory step)

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48
Q

What do diff monosaccharides enter glycolysis as?

A

Galactose: enters as glu 6-P
Mannose: enters as fruc 6-P
Fructose: enters as G3P

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49
Q

3 drugs that tx C. diff and when to use them?

A

First mild-moderate attack: metronidazole
First severe attack or recurrent: oral vancomycin (bacteriostatic)
Recurrent colitis or increased risk of recurrence: fidaxomicin

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50
Q

Patchy areas of skin anesthesia and hypopigmentation + bacteria invading Schwann cells. What’s the org?

A

Mycobacterim leprae (clinical manifestations depend on Th1 immune response)

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51
Q

What bac has PRP (polyribitol ribose phosphate)?

A

H. influenzae B -> part of its capsule (vaccine targets this)

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52
Q

What is “malignant pustule” and what causes it?

A

Painless ulcer w/ black eschar and local edema

B. anthracis

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53
Q

What do you use to stain Giardia cysts in stool?

A

Iodine

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54
Q

Diff precursor proteins responsible for LOCALIZED amyloidosis?

A

Cardiac atria: ANP -> increases risk to A-fib
Thyroid gland: calcitonin
Pancreatic islets: amylin (islet amyloid protein)
Cerebrum/cerebral blood vessels: B-amyloid protein (Alzheimer and cerebral amyloid angiopathy)
Pituitary gland: prolactin

55
Q

In what condition might you see intrasplenic lipid accumulation?

A

Lysosomal lipid storage disorders like Gaucher’s disease

56
Q

Probability that an unaffected person w/ unaffected parents & affected AR sibling is a carrier?

A

2/3! (exclude the aa because we know the individual is unaffected)
So if s/he marries an affected person, the probability of her child being affected is 2/3 (probability that she’s a carrier) x 1/2 (probability that she’ll pass on the one bad allele)

57
Q

2 signs of cyanide toxicity?

A

Altered mental status + lactic acidosis

58
Q

How is elastin different from collagen?

A

No triple helix or extensive hydroxylation (however still have non-polar AAs like glycine, alanine, valine)
Secreted as tropoelastin and interacts w/ fibrillin in extracellular space
The ability to recoil is from desmosine crosslinking bet. 4 diff lysine residues (4 diff chains) -> lysyl hydroxylase does this (EXTRACELLULAR not intracellular like the one used for collagen)

59
Q

What 6 biochem pathways occur in mitochondria?

A 
B-oxidation of FA
Ketogenesis
TCA
Urea cycle (only carbamoyl phosphate synthetase 1 and ornithine transcarbamoylase)
Pyruvate carboxylation
Heme synthesis (parts of it)

HMP is all in cyto!

60
Q

Diff bet. VDRL/RPR test and FTA-ABS? (besides the fact that one is screening and one is confirmatory)

A

VDRL/RPR -> evaluates presence of cardiolipin (byproduct of treponemal infection) -> so will be affected by therapy and can be used to follow disease progression
FTA-ABS -> not affected by therapy and remains positive for life

61
Q

What does H. ducreyi need in medium to grow?

A

X factor (hematin)

62
Q

What kind of immunity causes clinical manifestations in schistosomas?

A

TH2-mediated granulomatous response direct against eggs -> see infiltrating TH2 cells, eosinophils, M2 macrophages
S. haematobium: bladder
S. japonicum and mansoni: periportal “pipestem” fibrosis (pathognomonic for hepatic schistosomiasis)

63
Q

How is S. bovis endocarditis unique from S. viridans endocarditis? (sides colon cancer assc.)

A

S. bovis: pts w/ NO preexisting valvular abnormality

S. viridans: w/ existing abnormality

64
Q

Where is buccopharyngeal fascia and what’s the clinical significance?

A

Ant. to prevertebral fascia -> the two create retropharyngeal space -> infection in this space can extend directly to sup. mediastinum -> acute necrotizing mediastinitis!

65
Q

What do you call a drug that doesn’t have any effect on its own, but when used w/ another drug (which can produce some effect) causes that other drug’s effect to shoot up?

A

“Permissive” effect

Wouldn’t be considered additive or synergistic b/c that drug has no activity for that particular effect on its own

66
Q

How do you tell what the enzyme defect in urea cycle is that is responsible for hyperammonemia?

A

Get level of urinary orotic acid!
Defects in enzymes for the first step of urea cycle (carbamoyl phosphase synthetase and N-acetylglutamate synthease) -> high blood ammonia w/OUT high urinary orotic acid
Defect in ornithine transcarbamoylase -> high blood ammonia w/ high urinary orotic acid (b/c carbamoyl phosphate is converted into orotic acid)

67
Q

What does calcineurin do?

A

Dephosphorylates NFAT -> NFAT goes to nucleus and binds IL-2 promotor -> growth & differentiation of T cells
This is why it’s targeted by immunosuppressants

68
Q

What are the signals for intrinsic pathway of apoptosis process?

A

Phosphatidylserine or thrombospondin on plasma membranes

can occur w/ UV, heat, hypoxia, toxins, radiation

69
Q

What are “cysteine-aspartic-acid-proteases”?

A

Caspases (b/c they contain cysteine and are able to cleave aspartic acid residues)

70
Q

What enzyme plays a role in converting pro-carcinogens into carcinogens?

A

P450 oxidase system

Don’t be distracted by the oxidative burst enzymes. P450 is the only one that can convert stuff into good OR bad

71
Q

What glands are responsible for sweat stink?

A

Apocrine glands (in dermis and subQ fat) -> secretes sweat into HAIR FOLLICLES (as opposed to skin surface like eccrine aka merocrine glands do) -> these glands are not functional til puberty and odor is secondary t skin bacteria

72
Q

What are holocrine glands?

A

Secretion means the entire cells break down to release secretory products
Glands found in assc. w/ sebaceous glands

73
Q

What’s the site of viridans strep adherence?

A

Fibrin and platelets (not endothelial surface or anything like that)

74
Q

What kind of molecs should you assc. DAG-IP3 system w/?

A

Anything involving vessels -> a1, ARB, ADH

Also oxytocin

75
Q

Why is basic architecture of tissue preserved in coagulative necrosis?

A

B/c acute denaturation involves both structural and enzymatic cellular proteins (so proteolytic enzymes are also inactivated)

76
Q

Formula for calculating Vd? What does Vd tell you?

A

Vd = amount of drug given (mg) / plasma drug conc (mg/L)
Vd around 3-5 L -> drug has large molec weight, extensively bound to plasma proteins, or highly charged (hydrophilic) -> so limited to plasma (plasma vol is 3 L)
Vd around 14-16 L -> drug has small molec weigght but is hydrophilic -> so limited to plasma volume + interstitial volume
Vd around 41 L -> drug has small molec weight and is hydrophobic (uncharged) -> this is the vol of total body water
Vd > 41 L -> drugs avidly bound in tissues (so low plasma conc)

77
Q

Dx of fever + diarrhea + vomiting + muscle pain + erythroderma + tampons or nasal packing? What are involved cells?

A

Toxic Shock Syndrome -> from superAg (like enterotoxins, exfoliative toxins, TSST-1)
Involves T cells (releasing IL-2) and macrophages (releasing IL-1 and TNF)

78
Q

What is ecological study and what is it susceptible to?

A

When you study a frequence of characteristics (ie vit D intake) and a given outcome (MS prevalence) on a POPULATION level (not individual!)
Ecological fallacy: when conclusions made are applied to individuals

79
Q

What is nested case-control designs?

A

Start w/ cohort studies (ppl followed over time) -> whoever develop an outcome become cases for the case-control study

80
Q

What is qualitative study?

A

Use focused discussion groups, interviews, and other anthropologic techniques to obtain narrative info that can be used to explain quantitative results

81
Q

What does lepromin skin test tell you in ppl w/ skin manifestation?

A

Lepromin +: their TH1 response is strong (assc. w/ IL-2, IFN-g, IL-12) -> they’re just having tuberculoid leprosy
Lepromin -: their TH1 is bad -> so TH2 is predominant (assc. w/ IL-4, IL-5, IL-10) -> they’re having lepromatous leprosy (leonine facies and full blown stuff)

82
Q

If shown a graph of membrane potential (y) vs. time (x), where is the membrane most permeable to K+ ions?

A

The drop after peak -> this is where VOLTAGE-GATED K+ efflux happens (the leak channels responsible for resting membrane potential are NON-GATED K+ channels)
NOT at the peak -> this is called overshoot (K+ permeance comes a little later than this)

83
Q

What are Hutchison’s incisors and mulberry molars manifestations of?

A

Congenital syphilis (late manifestations)

84
Q

How is riboflavin deficiency dx? (besides low urinary riboflavin excretion)

A

Performance of the erythrocyte glutathione reductase assay

85
Q

Venous drainage of adrenal glands?

A

Like testicular vein

Right one drains directly to IVC, left one goes to renal vein first then IVC

86
Q

Formula for false positive rate? False negative rate?

A

False positive rate = 1 - specificity

False negative rate = 1 - sensitivity

87
Q

What bac goes from nasopharynx -> blood -> choroid plexus -> meningitis?

A

N. meningitidis

88
Q

What bac goes from pharynx -> lymphatics -> meninges?

A

H. influenzae

89
Q

What bac goes from middle ear -> contiguous tissues -> meninges?

A

S. pneumonia

90
Q

What bac goes from traumatic wound (skull trauma or neurosurgery) -> leaking CSF -> meninges?

A

S. aureus

91
Q

What bacs go from primary lung focus -> blood -> meninges?

A

S. pneumonia and TB (basal meningitis)

92
Q

What does PYR test replace?

A

Bacitracin

So PYR + in group A strep

93
Q

How do NK cells kill cells? How are they activated?

A

Don’t directly lyse cells -> kill by inducing apoptosis (have perforins and granzymes)
They’re activated by IFN-g and IL-12
Present in athymic pts (don’t require thymus for maturation even tho it’s lymphoid)

94
Q

Diff in pathogenesis of flushing from niacin vs. vancomycin?

A

Niacin: PG mediated -> so fix w/ aspirin
Vancomycin: histamine mediated

95
Q

Urine positive for copper reduction test but negative for glucose oxidase test?

A

There’s reducing sugar in urine (glucose, glyceraldehyde, galactose) but it’s not glucose

96
Q

What are endostatin and thrombospondin?

A

Anti-VEGF molecules (anti-angiogenic)

But if asked why tumor expresses increased VEGF, answer decreased PO2

97
Q

What’s unique about noncompetitive antagonist graph?

A

At low conc will shift dose-response curve right (looks like competitive antagonist)
At max dose will also shift dose-response curve down (decreases Vmax)

98
Q

What should be considered when genetic mutation is found in offspring but not parents?

A

Germline mosaicism
Probability of the next kid being affected depends on the proportion of mutated to wild type germ cells in the mosaic parents (if two kids were affected, we can deduce that this proportion is high)

99
Q

What cell jx is Ca2+?

A

CADherins = “Ca2+-dependent adhesion” -> so removes Ca2+ from cells would destroy this jx
Participate in desmosome formation (hemidesmosomes on the other hand are mediated by integrins)

100
Q

What’s palmitoylation?

A

Anchors carboxyl tail of many G-protein receptors to plasma membrane cysteine residue -> increases protein hydrophobicity
V2 receptor is an example

101
Q

Allelic heterogeneity vs. variable expressivity vs. genetic heterogeneity vs. penotypic heterogeneity?

A

Allelic heterogeneity: DIFFERENT mutations on the SAME genetic locus causes SIMILAR phenotypes (but some mutations can cause partial loss of protein and some can cause total loss -> ie Duchenne and Becker)
Variable expressivity: SAME mutation on the SAME gene causes DIFFERENT phenotypic severity
Genetic heterogeneity: mutations on DIFFERENT genes cause the SIMILAR phenotypes
Phenotypic heterogeneity: mutation on the SAME gene causes DIFFERENT phenotypes

102
Q

Yellowish crust on cutaneous wound. What’s the org?

A

Staph aureus

This is impetigo, which is commonly caused by S. aureus or group A strep

103
Q

Intrabacterial drug conc sharply increases when H+ is added to solution. What’s the mechanism of this bac resistance?

A

Membrane efflux pump
Know this b/c most efflux pumps use energy from H+ gradient -> co-transport of both H+ and drug out of cell -> so gradient eliminated from adding H+

104
Q

What does hydrophobic core sequence at the N-terminal of some proteins do?

A

These are signaling proteins for proteins destined for SER
Sequence gets translated in cytosol -> SRPs (signal recognition particles) recognize this sequence, stops translation, and drag the ribosomes over to protein pore in SER -> SRPs dissociate once the ribosomes are bound to SER -> protein synthesis continues in SER
So if this sequence gets deleted, you’ll get protein accumulation in cytosol

105
Q

What does safranin O stain?

A

Stain these structures red: cartilage, mucin, granules of mast cells

106
Q

What are the steps in that involve methylation?

A 
PNMT step (from NE to epinephrine)
COMT step (from epinephrine to metanephrine)
107
Q

What are the cofactors involved in catecholamine synthesis/tyrosine catabolism?

A

BH4: first 2 steps (phenylalanine -> DOPA)
Vit B6: 3rd step (DOPA -> dopamine)
Vit C: 4th step (dopamine -> NE)
SAM: 5th step (NE -> epinephrine)

108
Q

Diff bet. ras and proteins like c-myc, Rb, BRCA, p53?

A

Ras is actually involved in signal transmission from membrane to nucleus
The rest stay in nucleus and do their own thing there

109
Q

What happens to lineweaver burke plot in presence of competitive inhibitor?

A

y is 1/V; x is 1/[S]
So competitive inhibitor will result in the same y intercept, but x intercept is shifted RIGHT so closer to 0 (b/c you get higher Km w/ competitive inhibition, and x intercept is equal to -1/Km)

110
Q

PharmacoDynamic drug interactions vs. pharmacoKinetic drug interactions?

A

PharmacoDynamic drug interactions: drug alters the action of another drug at target tissues -> like vit K noncompetitive antagonism of warfarin
PharmacoKinetic drug interactions: P450 enzyme induction or inhibition

111
Q

What virus infecting epithelium replicates in nucleus using host enzymes?

A

Papovaviridae -> this includes polyomaviruses (BK and JC) and papillomavirus (HPV)

112
Q

Where do paramyxoviruses replicate?

A

Cytosol

113
Q

What’s a Quellung rxn?

A

When Strep pneumo is exposed to Ab against its capsular Ag, its capsule swells (can see under microscope)

114
Q

What protein dictates cell differentiation?

A

Transcription factors!

NOT growth factors, growth factor receptors, cytokines, etc.

115
Q

Where are ethmoid sinuses?

A

Medial to orbits above nasal turbinates

116
Q

What’s a ROC (receiver operating characteristics) and how do you interpret it?

A

It’s a graph of sensitivity (y) vs. 1-specificity (x, false positive rate)
Area under the curve represents accuracy -> so most useful test will have a graph resembling a rectangle (AUC close to 1), whereas test that’s as good as guessing will have a straight line going up as you move right

117
Q

Hallmark ions of ischemic injury?

A

Accumulation of Ca2+ INSIDE cells

You’ll also have increased K+ outside cells from impaired Na+/K+ ATPase and K+ leakage from dying cells

118
Q

What does protein binding mean to Vd?

A

Inverse relationship -> more PB, less Vd -> so liver and kidney disease can alter apparent Vd of PB-bound drugs

119
Q

Main bac factor for establishing infection in N. gonorrhea?

A

Pili! -> what undergoes Ag variation

don’t confuse N. gonorrhea w/ N. meningitides. Gonorrha actually doesn’t have capsule like meningitides

120
Q

What’s complementation?

A

Homozygous mutations in more than one genes cause distinct phenotypic trait

121
Q

What’s contact inhibition?

A

Normal cells would grow until they over the surface of petri dish then stop -> cues mediated by catenins and cadherins
Malignant cells lose this ability and will pile up in mounds

122
Q

Where are ApoB-100 and ApoB-48 synthesized?

A

100: in hepatocytes
48: in intestine

123
Q

New test involves adding urine to glass containing anti-hCG Ab. Then hCG-coated latex particles are added and agglutination occurs. Pregnant or not pregnant?

A

NOT pregnant
This is considered agglutination INHIBITION rxn -> so positive result would be NO agglutination (if there was hCG floating around in her urine, the SOLUBLE hCG Ab in the glass would react to it and when hCG-coated latex is added, there won’t be any soluble Ab to agglutinate)

124
Q

DNA was taken from 2 ppl in the family and run thru bacterial restriction enzyme and probe. Mom shows up w/ 2 fragments while the son shows up w/ 1 fragment (thicker band). What’s the mechanism?

A

This is called RFLP -> restriction fragment length polymorphism
Single nucleotide polymorphism is the most common cause of RFLP (change in a single base pair -> restriction site altered)

125
Q

Injecting recombinant protein and found that certain ppl w/ particular HLA don’t mount effective IgG response against Ag. What process is defective?

A

Ag presentation by B lymphocytes
NOT Ag recognition by B or T lymphocytes
Keyword is unable to mount “effective IgG response” -> so the process under focus here is isotype switching, which is a T-cell mediated process. If your MHC II is defective and don’t bind Ag, the professional Ag cells can’t present this to T cells and can’t switch to IgG
Impaired Ag recognition by T lymphocytes implies defects at the level of TCR
Impaired Ag recognition by B lymphocytes implies that IgM synthesis would be ineffective

126
Q

What do you call alpha helix protein fragment w/ leucine residues at every 7th position?

A

Leucine zipper dimerization domain found in basic zipper proteins (it’s a TF, example is zinc finger motifs)
Dimerization -> TF that can bind DNA

127
Q

Dx of intracellular org situated peripherally w/in histiocytes?

A

Leishmaniasis (macrophages containing amastigotes)

128
Q

Where in the cell would incorporation of CO2 in the process of making DNA occurs?

A

First step of both de novo pyrimidine synthesis (CPSII) and purine synthesis happen in cytosol

129
Q

When does Karposi sarcoma occur?

A

At any stage of HIV infection! -> so can happen even if CD4+ count is still high

130
Q

Children w/ chronic headaches are recruited for study and are all treated w/ acupuncture in addition to their usual therapy, then you evaluate feasibility of acupuncture. What do you call this kind of study?

A

Case series

B/c there’s no control

131
Q

Pts are informed they would be treated w/ a new drug, are assigned to each dose of drug, and tx efficacy is later determined. What kind of study is this?

A

Open-label clinical trial

132
Q

How do you calculate carrier prevalence (risk that someone is a carrier of an AR gene) from disease prevalence?

A

Disease prevalence since it’s AR is q^2 -> so solve for q

Carrier prevalence is 2 x q

133
Q

Proteins for retrograde and anterograde transport by microtubules?

A

Anterograde: kinesin -> think neurotransmitters
Retrograde: dynein -> think cilia and flagella

Question Bank (10 decks)

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