Review Questions 3

Medical Sciences Medical School Gts with Ghanem at Johns Hopkins University

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By: Alex Jenson
Created: 2011-02-12
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What organisms cause diarrhea within 3 hours?

Staph Aureus and B Cereus (both have preformed toxins)

What organisms cause diarrhea within 10 hours?

Clostridium perfingens (8-16 hours)

What are vomiting + diarrhea suggestive of?

Listeria/toxin producing infection (like cholera) - also viral

MOA of cholera toxin?

increases cAMP with its toxin. This incites increases in Cl secretion which brings along with it sodium secretion out of the bowel mucosa and into the lumen. This creates an osmotic gradient increasing water secretion into the lumen, causing massive diarrhea

what diarrheal agents can be transmitted from person-to-person

Shigella + STEC - low innoculum

what is the physological basis of oral rehydration therapy

the remaining function of the Na/gluc symporter allows the reflux of glucose back into the cells. because it is a symporter, it also drags with it sodium, decreasing the salt gradient across the mucosa and decreasing the pressure to increase secretion, decreasing diarrhea and maintaing enough electrolytes in the body

2 bacteria that come from undercooked pork

Yersinia entercolitica + Clostridium perfingens

MOA of sulfonimides?

sulfonamides act by mimicking PABA - this makes them bind to DTPase in the formation of FH2 in bacterial folate synthesis. this eliminates an essential nutrient for bacterial action

toxicities with sulfonamides

1. fever rash LAD joint pain - mostly hypersensitivity 2. w/neonates - kernicterus - bumps bilirubin off by binding to serum albumin - accumulates @ basal ganglia 3. skin rash - steven's john syndrome

MOA of trimethoprim

blocks FH2 reductase on the way to FH4 - only impacts bacterial FH2 reductase however

toxicities of trimethoprim

1. rash/nausea/vomiting 2. folate deficiency in humans - supplement with vitamins (but bact can't take up b/c they have to make their own - and thats blocked by SMX)

benefits of adding TMP with SMX

1 synergistic impact on folate synthesis 2. synergy decreases dosage - decreases toxicit 3. increase spectrum 4. combats resistance 5 makes them cidal when each is static individually

MOA quinolones

inhibit DNA gyrase (TopoII) in gm - bacteria or topo IV in gm + bacteria - create the cleavable complex by binding when the gyrase is attached to the DNA - then causes DNA cleavage and then apoptosis of bacteria via SOS repair

spectrum of coverage for each of different quinolones

1st generation - gm- UTI 2nd generation - gm - 3rd generation - gm- and gm+ 4th generation - gm- gm+ anaerobes

most important causes of resistance to FQ

1. change in DNA gyrase/TopoIV 2. membrane changes (changes in efflux to allow them in) 3. plasmid mediated DNA homolog (comes via plasmid and creates a DNA like protein that binds into the gyrase instead - preventing the cidal action)

renal and liver failure impact on dosing of floroquinolones?

the only one that has any adjustment is moxifloxacin - because it is entirely excreted by the liver - means that in renal failure you don't need to make a dose adjustment. the rest of them you have to make a renal failure dose adjustment, but no liver failure dose adjustment

O antigen of LPS is the least variable portion

F - the Lipid A moiety of LPS is the least variable (O antigen varies in length)

O antigen is most virulent portion

F - Lipid A is the most virulent

Lipid A is most conserved part of LPS

T - is the most conserved and most virulent

Clostridium produces spores

T - all 5 types produce spores

Bacillus produces spores

T - both B cereus and B anthracis produce spores

Spores are heat sensitive

F - spores allow the organism to survive strong environments, such as extreme heat

spores are important for cell division

F - they are metabolically inert (like a hybernation stage)

coarse temp control is achieved by behaviour

F - controlled by preoptic area of the hypothalmus controls body temp by heat loss and heat raising responses based on current body temperature

during fever temp "set point" is elevated

T - physiologic understanding within the body to raise the normal temp set point - adjusts with themroregulation

basal metabolic rate raises 10% for every 1 C increase in temp

T - particular problem for persistant fever among neonates in 3rd world - die of malnutrition more

Macrophages are main source of these pyrogens

T - respond to endotoxin and fungal cell ways by secreting these

decreased albumin production by liver - part of acute phase response?

T - liver stops making albumen - switches to other proteins found in plasma but increased (include increase CRP)

increased production of fibrinogen and haptoglobins - part of APR?

T - liver stops making albumen - switches to other proteins found in plasma but increased (include increase CRP)

increase production of CRP - part of APR?

T - liver stops making albumen - switches to other proteins found in plasma but increased (include increase CRP)

Sepsis, for the most part is a host mediated response

T - sepsis is caused by host reaction to agens - TNF a and IL1 mediated it and produce overwhelming inflammation that cause it

sepsis is due to bacterial infections only

F - sepsis is 85% of the time due to bacterial infections, but can be due to other things too

Sepsis is the result of small vessel injury leading to hypovolemia and hypotension

T - due to inflammation we have vasodilation and obstruction of vessels with platelets and pmn's - this shunts blood away from tissues and flood loss - leading to organ ischemia and dysfunction

what is not an early manifestation of shock: fever, tachypnea, delerium or hypotension

hypotension - this is a late indicator. Early on the heart compensates for the vasodilation by increasing the HR but eventually it fails leading to late stage hypotension

parameters of septic shock:

increased cardiac output, decreased systemic vascular resistance, decreased oxygen extraction in peripheral tissues, increased lactate production due to ischemia, and acidosis (due to lactate production)

in early sepsis, cardiac output is high to help compensate for low vascular resistance

T - early on get tachypnea - this eventually progresses to hypotension as the heart can't overcome the decreasing vascular resistance due to vasodilation

in late sepsis, periph vsc resistance increased due to catecholamine production

F - catecholamine doesn't increase periph vasc resistance - just continue with hypotension

most common cause of death in sepsis is hyperthermia

F - due to organ failure b/c of ischemia - eventually cardiac arrest

mortality of TREATED sepsis is 30%

F - about 50% (but protein C is pretty expensive)

most significant advancement in sepsis management was antibiotics

F - didn't change all that much for mortality just prolonged it - really what is key is management

Protein C has decreased mortality of sepsis to less than 10%

F - still at about 25%

use of antibacterial antibiotics may cause Cdiff

T - especially clindamycin - kills alot of native flora

cdiff is a benign disease

F - c.diff can produce large amounts of diarrhea causing loss of electrolytes and even bowel and colonic perforation

cdiff is mediated by toxins

T - Toxin A - enterotoxin toxin B - cytotoxin

treatment of Cdiff - stopping antibiotics and starting oral vancomycin

T - only time using oral vanc - b/c doesn't invade tissue - has no oral bioavailability but cdiff is in the lumen

clindamycin is LEAST likely offending antibiotic to cause cdiff

F - clindamycin is the MOST likely cause of cdiff

C matching: genital elephantiasis

Clamidya L1-L3 (LGV)

C matching: asymptomatic but able to transmit sexually

L1-L3 and D-K - both can be asymptomatic/undetected

C matching: rectal pain and bleeding

D-K (L1-L3 allows for rectal infection but not bleeding)

C matching: conjunctivitis

A-C - trachoma

C matching: trichiasis

A-C - late stage of trachoma

C matching: pneumonia

C Pneumoniae

C matching: azithromycin effective for treatment

D-K and A-C

C matching: doxycycline effective for treatment

All (L1-L3, D-K, A-C, pneumonia, and psitacci)

C matching: LGV

L1-L3

C matching: painful LAD

L1-L3 - secondary to original lesion that is painless

C matching: painless ulcer

L1-L3 - primary infection - painless ulcer lesion usually not seen

C matching: pneumonia in pet store owner

C. psytaci

What is the epi of C. trachomatis D-K in the US

more in women than in men - increasing rates recently in the us. Decreased socioeconomic status and multiple sexual partners are individual and independant risk factors for infection

what does actinomyces species look like @ gram stain

its a gm + rod that are pleiomorphic

where doe actinomycetes live and what disease?

live on skin as normal flora - in avascular areas - like areas that are far away from oxygen. When infect that cause tissue crossing progressive infections that are purulent and produce sulfur granules!

what organism causes gas gangrene, virulence factor and treatment?

C. perfingens causes gas gangrene. it is the result of an alphatoxin that causes cell lysis with gas production. treatment occurs with PCN or clindamycin as well as surgical debridement

what causes botulism, treatment how get it symptoms and treatment

c. botulinum. You get it from 2 ways - if an adult you get it from food in bad cans. if a child you get it from bad honey (esp neonates) causes botulism -> Early symtpoms are nausea/vomiting, late symptoms include double blurry vision, CNS!, decreased swallowing - also DESCENDING paralysis treatment - horse antiserum and human botulism Ig

what causes tetanus and how does it do it - how do you get and how do you treat? how do you prevent?

C tetani - acts via toxin called tetanospasmin - neuro related impacts on the CNS - causes muscle spasms the smile and the arched back. treatment = tetanoid Ig and metronidazole. vaccine = DTAP

what is bacteroides fragilis - where found - disease and treatment?

Bacteroides fragilis is a gm-rod anaerobe that is normal gi flora - it causes intraabdominal infections and decubitous ulcers and perirectal abscesses. it is treated with metronidazole

a person is infectious during syphilis incubation period

F - infectious via sexual route up trhough primary and secondary syphillis, infectious to child through latent stage of syphillis

incubation period of syhpillis is 205 days

F - incubation period is about 3 weeks

most people who are not treated for syhpilis will develop late complications

F - only 30% of those will develop late complications

syphilis may infect CNS right from onset of infection

F - only infects the CNS at late neurosyhpilis

mucous patches are hallmark of primary syhpilis

F - hallmark is chancre like painless ulcer

skin lesions occur only during primary and 2ndary stages of syphilis

F - at 3rd stage of syphilis can get gummatous lesions - also type of skin lesion

patchy alopecia occurs in primary syphilis

F - never

late syphilis can involve blood vessels, CNS heart kidneys and skin

T - 3 types 1. cardiovascular - aortitis sacular aneurysm, 2. gummatous - lesions 3. CNS - meningovascular or parenchymous

late syphilis can be stroke or aortic aneurysm

T - aortitis in CV late syphilis, or CNS meningovascular

if you test someone and have positive RPR you must confirm with treponemal

T - b/c 30% = false positives

test of choise to diagnose genital lesions is darkfield microscopy

T - and there are lots of spiroketes - easier to see

anyone with positive syphilis should be tested for HIV and others

T - STIs run in packs!

reason start with RPR is because its sensitie cheap can be done quickly and provides titer

T - but 30% = false positive so verify with treponemal test@

treponemal test give titer so we can decide if treatment is appropriate

F - only qualitative - yes no - no titer

late latent syphilis can transmit to a partner via sex

F - only in early stage can it go sexually - in late latent only blood transfusion

What are the causes of Painful genital ulcers

Herpes, chancroid

Causes of painless genital ulcers

LGV, syphillis and klebsiella granulomatous (GI)

gay man complaining of rectal pain, bleeding and pain on defecation what is it?

Clamydia, gonnohrea, herpes, chancroid

4 diseases that cause penile discharge or cervical discharge

clamidya, gonnohrea, mycoplasma genitalium, trichimonas vaginalis

7 diseases from haemophilous

epiglotitis, sinusitis, otitis (media), pneumonia, bacteremia, arthritis, endocarditis

unique about hamophilous growth requirnments

requires X and V factors for growth - unique proteins required in envt for it to grow

pertussis syndrome - complications? prevention?

Pertussis is caused by bordetella pertussis - get via respiratory droplets. Catacorral symptoms - fever rhinorea malasie, paroxysmal stage - whooping cough vomit and apnea - complications are neuro from persistant dsypnea, pulmonary hemmorage from coughing - prevention = DTAP

epi of legionella

aquatic air droplets transmit it - first found in 1970s - lives in aquatic amoeba - like schistosomiasis

what are some risk factors for legionella - presentation?

risk factors - immunocompromised, CVD, ESRD Age diabetes presentation - flue and pneumonia with neuro changes and bradycardia

how do we diagnose legionella

sputum culture - grow on a selective media - because a fastidious gm - rod

mycobacteria grow rapidly

F - grow slowly

mycobact grow at same rate

F - grow at different rates - slow growers and rapid growers (slow growers = marinum avium kansassii ulcerans)

if you have a ppd thats negative, can't have TB

F - esp in immunocompromised - if not mounting immune response to TB, cant have positive PPD

positive PPD = active disease

F - only shows that they have or have had the disease or the vaccine (esp if grew up outside US)

cavity presence increase likelihood of positive sputum smear may organisms

T - tons of organisms in the cavity

BCG is efficacious at preventing TB

F - at best 80% effective and only for 15 years

non TB mycobacteria aren't transmitted person to person

T - unlike leprosy and TB - from envt

skin lesious in lower extremities for 2-3 months and fishing history has mycobacterium marinum

T - mycobacterium marinum = skin lesions presentation

major immunological defense mechanism against TB is antibody

F - intracellular bacteria - its T cell and hormonal immunity - Th1 response

MAC causes disseminated disease in patients with AIDS

T if CD4 less than 50

M kansasii mimic TB if underlying lung disease

T - all we know about kansassi

kansasii causes hot tub lung

F - MAC causes hot tub long - sob, cough fever etc

m ulcerans produces toxin - painless ulcerations in kids at swampy water

T - causes enormous buruli ulcers

Nocardia look like on gram stain

aerobic gm + rod on gram stain stains better on acid fast however

disease of nocardia

1. cutaneous @ immunocompromised host - mycetoma abscesses and cellulitis 2 pulmonayr and disseminated nocardiasis @ AIDS and decrease T cell immunity - nodular infiltrates - difficult to diagnose

NTMycobacteria vs nocardia

Same - acid fast, lung disease, impacts on CMI, mycobacteria different - gm stain, person-person soil/envt - not humans

pathophys of primary vs post primary TB

primary TB - ghon focus - site of infection, ghon complex - focus + local lymph node - both get granulomas => TH1 response eventionally - then migrates to Simon focus @ apex and posterior lung - granuloma there post rpimary - LN explosion or eriosion - 3 impacts 1. bronchopneumonial TB 2. empyema TB (@pleural space) 3. Miliary TB

current epi of TB in US

recurred in HIV patients, had dereased until mid 1980s - HIV caused it to increase much more quickly

Ghon focus/Complex - definition

focus - site of first infection of TB - original granulloma - ghon complex = focus + nearest lymph node

Simon focus

simon focus @ primary infection - at apex and posterior side of lung that is infected -2nd site for granuloma to occur

TB bronchopneumonia vs. miliary TB

both occur in progressive primary and progressive post primary TB - @ progressive primary result from LN that opens up into different things. if it opens up into airway creates bronchopneumonia TB - tons of infiltrate into airway - nodules vary in size. If opens up into pulmonary vein near the hylum = miliary TB - equal in size and spread evenly

manifestations of progressive post primary

when the cavitation opens 4 options 1. vein = miliary TB 2. airway = bronchopneumonial TB 3. cavity = emyema TB 4. artery - arterial bleeding!

HIV + TB - differences

1. occurs much quicker than opportunistic infections 2. more often extrapulmonary - non atypical and non cavitary 3. bad granulomas 4. drug resistant TB 5. negative PPD

NTM - early or late on HIV timeline

Early - bfore other opportunistic infections

compare and contrast primary vs secondary drug resistance

primary - what you have when the drug regimen is started - why you take multiple drugs - 2ndary = drug resistance that accumulates due to poor drug management and adherence to regimen - why you take them and observed

MDR vs XDR TB

MDR - resistant to INH and Rifampin XDR - resistant to all know anti TB - S africa and Russia

About this deck

By: Alex Jenson
Created: 2011-02-12
Size: 158 flashcards
Views: 0

About StudyBlue

“I have used this website for three exams, and I see a huge difference in my test results.”
Naj