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STEP 1 > ID and LC > Flashcards

ID and LC Flashcards

1
Q

describe the mneumonic for live attenuated vaccines

A

Music and lYRICSS are best enjoyed Live

M= MMR

Y= Yellow fever

R= Rotavirus

I= Influenza nasal

C= Chickpox (VZV)

S= Smallpox

S= Sabin polio virus

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2
Q

what does catalase distinguish between

A

catalase = positive makes bubbles in the presence of hydrogen peroxide

staph= catalase +

and

strep= catalase -

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3
Q

describe the mneumonic for oxidase + organisms

A

oxidase positive = changes the paper color (turns blue or pink with that black dot)

spell punch with a “v”

PVNCH

P= Pseudomonas

V= Vibrio

N= neisseria

C= Campylobacter

H= H pylori

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4
Q

what is the treatment for neisseria gonorrhea

A

ceftriaxone= 3rd generation cephalosporin = because theyre great for serious gram negative infections and neisseria is a gram negatvie diplococci

also give a macrolide or tetracycline =azithromycin or doxycycline for possible chlamydial coinfections

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5
Q

what does coagulase test distinguish between

A

coagulase positive test causes clumps/clots

different strains of staph

staph aureus is coag + (golden hemolytic… clumping factor= turns fibrinogen into fibrin to make a clump that is protective from phagocytosis)

the rest are coag -
(more than >90% of the time its a contaminant… but be wary if there is metal or plastic in the body… staph epidermidis)… coag neg= 31 + staph species, white, non hemolytic

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6
Q

describe alpha and beta hemolysis

A

alpha= partial hemoglobin reduction causes a green brown color without clearing
(strep pnu [optochin sens] and strep viridans [optochin resistant])

beta= complete lysis of RBCs causes a clearing around bacteria
(staph aureus [cat +], strep pyogens GAS [bacitracin sens], strep agalactia GBS [bacitracin resistant])

both are gram + cocci

gamma hemolysis is no hemolysis

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7
Q

what is the “danger hypothesis”

A

that our bodies recognize pathogens because they cause damage to us

PAMPs are now MAMPs (Microorganism) and DAMPs (Damage/Danger)

example- innate immune response to mitochondrial DNA or uric acid s/p trauma

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8
Q

what is the 5th sign of infection

A
  1. tumor
  2. rubor
  3. dolor
  4. calor
  5. loss of function (functio laesa)
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9
Q

Describe what grows and what you will see with different bacteria on McConkey agar

A 
McConkey agar=
lactose fermenters turn pink (ex- ecoli)
non fermenters are colorless
- contains bile salts
- inhibits growth of gram + bugs
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10
Q

what is protein A

A

a virulence factor on staph aureus cell wall which binds Fc of IgG and prevents compliment activation

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11
Q

what are the two superantigens that cause shock

A

toxic shock syndrome toxin (TSST 1) = staph aureus

binds to MHC2 and TCR and causes an overwhelming release of IL1 and IL2… (presents as fever, rash, shock)

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12
Q

what are the toxins of staph aureus

A

Toxic shock syndrome toxin (TSST 1)= fever, rash, shock

exofoliative toxin A or B= scalded skin syndrome (proteases digest desmosome in the skin causing separation at the granular layer… causes bullae and sloughing, no scarring)… also called Ritter’s disease of the newborn or staph scarlet fever in older kids… bullous impetigo (most common bacterial skin infection in kids) is the localized version of scalded skin syndrome

heat stable enterotoxin = food poisoning

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13
Q

what is important about the MEC-A gene

A

it confers resistance to penicillins

it codes for PBP2A which decreases beta lactam’s ability to bind cell wall and inhibit formation

seen in MRSA

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14
Q

what is a positive D-test

A

when erythromycin is placed next to clindamycin and the clearing around clindamycin is blunted from the erythromycin

what happens is “erythromycin induced resistance to clindamycin”

due to the plasmid gene erm

thus you do not give a patient clindamycin if there was a positive D test

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15
Q

what is a furuncle

A

a boil

commonly caused by staph aureus

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16
Q

what is osteomyelitis

A

a bone abscess

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17
Q

what is chronic granulomatous disease

A

aka Bridges Good Syndrome or Quie Syndrome

x linked recessive inherited neutrophil defect

cells have problems making reactive oxygen species for killing (hydrogen peroxide)

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18
Q

what is Job’s syndrome

A

Hyper IgE, recurrent colds, rash

defect in neutrophil chemotaxis

AD (STAT3 mut…. affects JAK STAT pathway)

mneumonic: FATED
F= Facies (coarse)
A= cold Abscesses
T= Teeth (primary teeth retained)
E= increased IgE
D= Dermatologic problems
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19
Q

Describe Toxic shock syndrome

A 
macular erythema (widespread red rash that looks like a sunburn... later it peels on the palms and soles)
acute high fever
organ failure (kidneys and liver)
confusion
diarrhea
low blood pressure
muscle aches
nausea and vomiting
redness of facial mucosa
seizures

TSST1 enterotoxin of staph aureus
genetically predisposed with no pre existing ab to the toxin

20
Q

what are lancefield (A-U) groups

A

ways to identify different beta hemolytic strains of strep (complete lysis)

GAS pyogens [virulence factor is M proteins which has a neg charge to repel phagocytes)
Group B
Group C and G
Group D= now enterococci

21
Q

what is the spreading patterns of staph vs strep

A

staph likes to localize (and build fibrin walls)

strep likes to spread out (they break down fibrin)

22
Q

Describe the eagle effect

A

In cases of extremely high bacterial burden (such as with Group A Strep), bacteria may be in the stationary phase of growth. In this instance since no bacteria are actively replicating (presumably due to nutrient restriction) penicillin has no activity. This is why adding an antibiotic like clindamycin, which acts ribosomally, kills some of the bacterial and returns them to the log phase of growth

23
Q

what are some ways to differentiate viral from bacterial sore throat

A

viral (2/3rd) =
cough
runny nose

bacterial=
tender lymph nodes
close contact
(biopsy = tonsillar #1, second best is posterior wall of pharynx… neg rapid test then do culture)

24
Q

what are complications of strep pharyngitis

A

scarlet fever

toxic shock syndrome

ARF (3-6 weeks later, JONES criteria)

reactive arthritis (assume its a less severe ARF in high prevalence areas)

PSGN (glomerulonephritis) 2-4 weeks after

PANDAS (pediatric autoimmune neuropsychiatric disorders associated with strep)

if you suspect ARF or PSGN you can do strep serology (ASO or ADB- anti Dnase B)

25
Q

what can a mom be colonized with that infects a baby at birth and they get pneumonia and sepsis

A

Group B strep

high mortality rate

give intrapartum abx (penicillin)

its neisseria gonorrhea that makes babies blind :(

26
Q

what bug do you get from dental procedures when you have damaged valves

A

strep viridans

27
Q

which bug smells like butterscotch and causes brain abscesses and orbital cellulitis

A

strep anginosis (milleri)

28
Q

what is SRY

A

the Sex determining Region of Y chromosome

on the short arm (p for petite) of Y chromosome (YP11)

the pseudoautosomal region is right next to SRY (crossover can occur around here and SRY can get lost as a consequence of crossover mistake)

29
Q

what structures are derived from the mesonephric wolffian duct

A

SEED

S= seminal vesicle

E= Epididymis

E= Ejaculatory duct

D= Ductus deferens

(all internal structures except the prostate)

30
Q

what are the remnant structures left behind in the female and male

A

female= appendix testis

male= gartner duct

31
Q

what are some genes on the pathway to a normal male testis vs normal female ovaries

A

WNT1, NR5A1 needed to make the bipotential gonads before further differentiation

male= SRY, SOX9, FGF9, one copy DAX1

female= FOXL2, two copies DAX1…. (also WNT4, RSPO1, FOXL2, beta catenin)

32
Q

What is Rokitansky syndrome

A

absent or underdeveloped mullarian structures (uterus, tubes, vagina)

in 46XX female

still have ovaries because of the XX chromosomes

but there are no uterus/cervix, tubes, or upper vagina

primary ammenorrhea

puberty is fine because there are ovaries but there are no periods

33
Q

what would cause persistent mullerian ducts in 46 XY male

A

if they could not make MIF (aka AMH) or there was a problem at the receptor

34
Q

what does each of these indifferent structures become

genital tubercle

urethral folds

labial scrotal swellings

A

genital tubercle= glans penis or clitoris

urethral folds= penile urethra or labia minora

labial scrotal swelling= scrotum or labia majora

35
Q

Leydig Leads to (blank)… Sertoli Shuts down (blank)

A

Leydig Leads to male

Sertoli Shuts down female

36
Q

Where is Testosterone produced for the first 13 weeks of the baby’s life

A

The placenta (which also makes aromatase)

thats why there is normal external genitalia in an HPG axis problem

37
Q

what do the genitals look like for a baby 46XX with CAH

A

clitoromegaly

normal girl external structures because of XX and mom supplying the T and aromatase

but then the baby’s adrenals develop and make too many androgens which enlarge the clitoris thinking its a penis

38
Q

what is the difference between gender identity and gender role

A

identity= self defined

role= society defined

39
Q

what is the normal penile length and clitoral length/diameter of a newborn

A

penis >2.5cm stretched

clitoris <1cm length and <0.06cm diameter

40
Q

What do the prader stages refer to

A

1= female

middle is ambiguous

5= male

41
Q

what test do you use to look for SRY gene

A

FISH

frozen in situ hybridization

42
Q

what is the most common enzyme deficiency in CAH

A

1= (95%) 21 hydroxylase (both aldo and cortisol pathway)… [hyperpigmentation from too much ACTH]…. suspect in a baby with aldo def

next most common is (5%) 11 beta hydroxylase (aldo pathway only)… 11 beta hydroxylase has some MC activity in itself so theres not as much salt wasting)

43
Q

what form of screening for CAH is on the newborn screen

A

They screen for 17 hydroxy progesterone

because in the cortisol pathway, 17 OH progesterone —-(21 hydroxylase)—-> –> cortisol

so high levels could indicate CAH

44
Q

what is lipoid CAH

A

where there is deficiency in the StAR protein (used in the first step of steroidogenesis)

cholesterol esters accumulate in adrenocortical tissues

AR

fatal if not detected early

both boys and girls have female external genitalia because no androgens were made

45
Q

memorize the numbers in the steroid pathway of the adrenal cortex

A

Ok I’ll do it now!

46
Q

describe

“mini puberty”

“juvenile pause”

and “gonadarche”

A

minipuberty= normal pubertal ranges of testosterone and estrogen in a baby 1-2m old
FSH dominant

juvenile pause= after that 2m old, the HPG axis becomes quiet again due to inhibitory GABA actions

gonadarche= re-emergency of HPG axis function at puberty
LH sominant
due to stimulatory kisspeptin/kiss-1 neuron

STEP 1 (11 decks)

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