TEST 1

Virulence Factor
P fimbrae (or pili) pyelonephritis associated pili
LPS
EHEC Verotoxin (Shiga-like toxin)
Heat-stable / Heat-labile enterotoxins
K1 capsular polysaccharide
E. coli virulence factors:

Mechanism
Allows adhesion to uroepithelium
activaton causes widespread release of: IL-1, IL-6, TNF-
Inactivates the 60S ribosomal s.u.-//-> protein synth=cell death
Promotes fluid & e- secretion from intestinal epithelium
Prevents phagocytosis & complement-mediated lysis

Presentation
UTI
Bateriemia & Septic shock
Gastroenteritis (bloody)
Gastroenteritis (watery)
Neonatal meningitis

Each tRNA molecule contains a specific anticodon that is complementary to one or more mRNA codons. Translation of mRNA template
proceeds in the 5 3 direction. Bc complementary sequences align in antiparallel fashion, during translation tRNA anticodons will be
oriented in the opposite 3 5 direction. The AUG codon initiates protein synthesis and the UAG, UGA, UAA codons halt protein
synthesis (stop codons)
Glucose transport occurs along its
[ ] gradient (high low) however,
it cant passively diffuse and
requires carrier proteins to aids
its crossing (which undergo
conformational changes as the
substrate is transported, unlike
channel proteins). This is termed
carrier-mediated transport, a
type of facilitated diffusion.
The GLUT family prefers catalyze
the entrance of D-glucose rather
than L-glucose
A case-control study is used to compare the exposure of people with the disease (cases) to the exposure of people w/o the disease
(controls) The main measure of association is the EXPOSURE ODDS RATIO:
Odds of exposure of people with the disease (cases)
Odds of exposure of people w/o the disease (controls)
Recent hx of viral esophagitis and pneumocystis pneumonia is dx of HIV infx. CNS infx in an HIV(+) pt is
Cryptococcus neoformans; opportunistic fungus that causes meningitis or meningoencephalitis. Latex
agglutination test detects the polysaccharide capsule Ag of Cryptococcus and is dx. India ink staining of CSF:
round or oval budding yeast. Tx = Acute meningitis: Amphotericin B & Flucytosine. Prophylaxis: Fluconazole
Huntington Disease: AD, complete penetrance, 4ch, CAG trinucleotide repeat on HD gene that codes for the abnormal protein
huntingtin; which decrease the expression of other genes by -//-> transcription (called: transcriptional repression or silencing). This
occurs bc of the presence of histones. Hypertmethylation of histones bind DNA and prevent transctiption of certain genes.
The cause of rapid plasma decay (and brain clearance) of thiopental and other related lipid soluble barbiturates is the rapid
redistribution of the drug to other tissues throughout the body (skeletal & adipose tissue, within 5-10 of administration)
Its unethical to discuss information regarding the pts dx, tx, px, etc. with a physician who is not involved in the pts care. Likewise. The
physician should neither confirm nor deny whether the person of interest is, in fact, a pt.
Rejection
Hyperacute
ACuTe

Onset
minutes
1-4
w
after
transplant

Cause
Host preformed ABO antibodies against graft ABO Ags
Host T cells (CTL) sensitization against graft MHC Ags

Chronic
GVHD

Months-years
Varies

Host B & T cells sensitization against graft MHC Ags

Graft T cells sensitization against host MHC Ags (bone
marrow transplant: competent T cells transplanted to a pt w/o

Prevention / Tx
Screen ABO incomp
P: Cyclosporine, Tracolimus (calcineurin
inh)
T: Same + systemic corticosteroids
Same as above
Exact HLA matching, histoidentical siblings.
Wash donor cells w/ anti-thymocite immune

them)

globulin to remove T lymphocytes from graft

In silicosis, there may be a disruption of macrophage phagolysosomes by internalized silica particles. Macrophage killing of
intracellular mycobacteria may be impaired as a result, causing increased susceptibility of pts w/ silicosis to pulmonary TBC.
Acute intertstitial pancreatitis= Gross: edematous pancreas. LM: fat necrosis, calcium deposition & interstitial edema.
Necrotizing (hemorrhagic) pancreatitis= Gross: chalky-white areas of fat necrosis interspersed w/ hemorrhage.
Mesenteric ischemia= dusky red, congested bowel segment. Subserosal ecchymoses, edema, well-defined necrosis areas
Intestinal perforation= peritonitis + abdominal wall defect
Bacterial peritonitis= dull.appearing peritoneal surface + viscous white-yellow suppurative exudate.
Chrons D= mesenteric fat extends along serosa of affected segment (creeping fat). Dull-gray intestinal serosa, edematous, granular + fibrotic/edematous mesentery
Celiac disease= serosa & mesentery appear normal

Adhesion molecules: integrins, cadherins, selectins, Ig superfamily members They interact with the Extracellular Matrix (ECM)
by binding to: fibronectin, collagen, laminin.
Heparin sulfate (proteoglycan of ECM): contributes to vascular endothelial cell attachment to basement membrane
Hyaluronic acid (glycosaminoglycan of ECM): water retention in ECM, lubricant properties, viscous gel-like consistency.
Elastic fibers: elastin protein surrounded by fibrillin protein microfibirls.
Keratin sulfate (galactose-containing glycosaminoglycan): mantains type I collagen fibril organization in the cornea.

MC congenital anomalies seen in women & men are accessory nipples (polythelia): failure of appropriate involution of mammary
ridge. Usually asymptomatic. They may swell or become tender with other breast tissue bf menses. Can become symptomatic during
pregnancy and lactation. Can occur along the embryonic milk line at the lower chest & abdomen, bilateral 50% pts.
Attrition bias: type of selection bias; is the disproportionate loss to follow up between exposed & unexposed groups in
prospective studies. This form of bias doesnt occur if the losses happen equally and randomly between both groups (only the study
population becomes smaller. As a result, investigators try to achieve high pt follow up rates.
Exocrine pancreas insufficiency: due to chronic pancreatitis (alcoholism); inability to normally metabolize fat, severe abdominal pain,
stool floats, weight loss. Anatomy: head, neck, body of pancreas are retroperitoneal; tail is peritoneal.

Head of pancreas lies in the curve of duodenum, overlies L2 vertebra.

Body overlies L1 & L2 vertebrae, makes contact posteriorly w/: aorta, IVC, superior mesenteric vessels, left kidney.
Tail courses within the splenorenal ligament alongside splenic vessels.}