Pathophysiology Midterm

How does reperfusion injury occur? (3)

1. oxidative stress with formation of ROS
2. calcium release from SR
3. inflammation d/t release of inflammatory mediators

2 genes that govern apoptosis

BCL2 and P53

what causes fever?

endotoxin, IL-1, TNF, and prostaglandins

what secretes TL-1?

macrophage to attract Th cell

What secretes IL-2?

Th cell to stimulate maturity into Th1 and Th2 cells, which also secretes Il-2 to trigger proliferation/differentiation of B and T cells

3 functions of antibodies

neutralize
opsonize
activate complement

inactivated vaccine

virulent microbes killed
large, multiple doses often required
booster vaccines required
lose some immunogenicity

live attenuated vaccine

microbe treated to reduce infectivity and pathogenicity
may not be safe for immunocompromised
boosters required less often

toxoid vaccine

made from inactivated bacterial toxin

subunit vaccine

microbial proteins and/or polysaccharides that stimulate immune system

conjugated vaccine

microbial polysaccharides chemically coupled with proteins, so they can stimulate Th cells

synthetic vaccine

antigen formed from recombinant proteins and other molecules in lab environment

anaphylaxis s/sx

bronchospasm, bronchoconstriction
hypotension
edema
GI cramping

type II hypersensitivity methods

complement-mediated lysis
phagocytosis by macrophages
antibody-dependent cell-mediated cytotoxicity
inducing target cell malfunction

central T lymphocyte tolerance

apoptosis
T reg

central B lymphocyte tolerance

apoptosis
anergy
receptor editing

peripheral T lymphocyte tolerance

anergy
apoptosis
fewer signaling molecules by APCs
Treg

peripheral B lymphocyte tolerance

anergy
apoptosis
inhibitory receptors

clinical consequences of lupus

Skin - macular rash (butterfly); large scaly, red lesions
Joints - joint pain
Kidneys - glomerulonephritis, chronic renal failure
Heart - pericarditis, myocarditis, valve disease
Lungs - pleuritis and pleural effusions, pulmonary thrombi/emboli, pulmonary

acyclovir

DNA polymerase inhibitor�only inhibits viral (not cellular) DNA polymerase and only affects infected cells

Zidovudine (AZT)

reverse transcriptase inhibitor�blocks reverse transcriptase in retroviruses and blocks formation of viral DNA

Boceptrevir (for Hepatitis C)

a protease inhibitor; affects synthesis of protease required for virus replication

Oseltamivir (Tamiflu)

neuraminidase inhibitors; competitive inhibitor of influenza's neuraminidase enzyme, so it prevents release of virus from host, thereby decreasing flu severity

cephalosporins

interrupt peptidoglycan synthesis, can make other abx more effective

quinolones

interfere with essential enzyme activity

macrolides

bacteriostatic, target protein synthesis

mechanisms of abx resistance

Antibiotic target site on bacteria is altered
Uptake of antibiotic into bacteria is altered
Bacteria produce enzymes that inactivate or destroy the antibiotic

protein on HIV

gp120

AIDS is when

CD4+ T cells < 200 cells/mm

AIDS s/sx

Opportunistic infections
Protozoal infections (e.g., pneumocytosis or toxoplasmosis pneumonia)
Fungal infections (e.g., candidiasis, cryptococcsis, histoplasmosis)
Atypical bacterial infections (e.g., mycobacteriosis)
Viral infections (e.g., CMV, HSV, var

CrCl formula

CrCl (mL/min) = ((140-age) x Weight (kg))/(serum creatinine (mg/dL) x 72) x 0.85 (if female)