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531 Cards in this Set
- Front
- Back
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Progressive decrease in kidneys of
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Number of nephrons, and renal blood flow.
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Which leading cause of death is on the rise?
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COPD will move up to 3rd place by 2020, superceeding strokes
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Top 6 causes of death, 5 of which are related to lifestyle
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Heart disease, Cancer, Cerebrovascular diseases, COPD, Accidents, Diabetes
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Respiratory Tidal olume
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Breathing in & out, when sitting on buts in lecture
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Inspiratory reserve
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If need extra O2, have 3L reserve can fill up
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Expiratory reserve
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Can blow this out to create (with above) total capicity
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Estimated excess lung
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5X? When young
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In aged
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Reserve capacity goes to almost nothing, so pneumonia kills elderly
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Forced vital capacity
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Max amount of air you can inhale and then exhale
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FEV1
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Amount of air you can expel in 1 second. Normal is 70% of 4.8 liters.
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COPD
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Chronic bronchitis and emphysesma, 130,000 deaths per year.
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Emphysemitus changes
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Irreversible, enlargement of the airway spaces distal to the terminal bronchioles. Commonly with destruction of ___ themselves.
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Amy winehouse
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Barely 30
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Blue bloaters
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Name for these patients. Cannot move air, barrel chested (because they are using muscles) turn blue.
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Pink puffers
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can move air, respiratory rate increases, diaphragm expends so much ATP that they get skinny.
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Virus replication
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Requires host cell
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Smallest form of life
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Virus
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Virus protein making
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Requires host
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Capsid protein
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Virus envelope proteins
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Sturctural
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Non-sturctural
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HIV has protease
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2 types of viruses
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Enveloped, non-enveloped
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First step of virus
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Attachment
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Second step of virus - nonenveloped
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Either endocytosed or just inject virus
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Second step of envelpoed virus
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Viral Nucleic acid transcription
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One DNA/RNA in cell, uses cell machinery to transcribe
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Polymerase, enzymes,
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Viral assembly
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Occurs after replication
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Budding, release, exocytosis
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Types of viral infection
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Acute/lytic; chronic active; latent; may produce more than one type
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Acute viral infection
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Replicates in cell, lysis and cell death, particles released to infect other cells
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Chronic infection viral
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Like acute but host cell doesn't die
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Retroviral infection
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Viral genom integrated tino host DNA; viral genome and proteins transcrip/translated; can be latent
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Latent viral infection
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Virus is present but not replicating; ex: herpes simplex, Epstein Barr
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Type of host cell damage from virus
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Lysis, toxic viral products, effects of conscription of cell machinery
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Immune mediated response to viral
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Cytotoxic t lymphocytes
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Incubation period for virus
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Time between agent gains entry and symptoms
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Incubation time for virus dependent
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Type of infection, clinical manifestations of infection
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Viral tropism
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Propensity of virus to infect certain cell types - don't get hepatitis from flu
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This has high viral tropism for nasal mucosa
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Rhinovirus
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Hapatitis
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HSV
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Virus tropic for Erythroid precursor cells
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Parvovirus B19; may have anemia that goes unnoticed, but what if sickle cell anemia and have faster turnaround
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Indirect Virus test
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Serology
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direct
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Histology testing for virus
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Look for cellular damage in tissue, fluid
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CPE
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CMV
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Cytomegalvirus (BIG!), lung tissue
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Culture of a virus specimen
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Diff from bacteria because they require a host, ? Have to infect cell and look at cells or test for
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Antigen viral detection
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Ex: Flu testing
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Rapid virus test
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Not great reliability, back it up with other testing
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Viral Detection by Nucleic acid
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Viral therapy monitoring
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Viral serology
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IgM indicates acute; IgG indicates recont of remote.
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Difficulty of viral therapy
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Lose some targets like cell wall and ribosomes
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Viral properties that challenge therapy
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High replicationrate, high polymerase error rate (mutations), Every nucleotide mutates every _____. So give three drugs!
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Potential Antiviral Targets
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Attachment, penetration, viral polymerase (HIV)
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Proteases
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When does HIV develop
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When T-cell death exceeds what is poduced
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How is HIV diagnosed
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Serology, measuring viral load
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How is HIV therapy monitored
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Types of HIV drugs
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Nucleoside
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Mimics
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Non-nucleoside
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Use of drug combinations in HIV
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Influenza
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Antigenic shift
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Slight change in surfacde nolecules - might move to
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Antigenic drift
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Year to year
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Diagnosis
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PCR tells us if type I, III, avian, etc.
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Epidemic
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From mild shift, will have some illness
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Pandemic
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Major shift
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Amantidine, rimantidine
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Only on Flu A, currently resistent so not working now
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Oseltamivir
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Prevents release of virus
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Decompensated CHF is when
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Heart pump cannot develop sufficient CO to meet the metabolic demands of the body at rest
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Compensated CHF is when
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Normal CO because of high filling pressure adaptations
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Myocardial contractility
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The inrinsic ability of the heart to contract independent of preload and afterload
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Systolic dysfunction
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Loss of myocardial contractility
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Diastolic dysfunction
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Decrease in ventricular filling (due to hypertrophy?)
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Cor pulmonale
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enlargement of the right ventricle of the heart as a response to increased resistance or high blood pressure in the lungs.
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Clinical feature s of left sided heart failure
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Pulmonary congestion and edema, cough, dyspnea (initially with exertion and subsequently at rest), orthopnea, generalized edema, prerenal azotemia, cerebral hypoxia and encephalopathy, stupor or coma.
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Causes of left-sided heart failure
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Ischemic heart disease, hypertension, aortic and mitral valvular disease, and myocardial diseases.
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If LV is not pushing out,
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the pressure will back up to the right ventrical and you will get secondary RV hypertrophy
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Causes of right sided heart failure
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left-sided heart failure; pure right-sided failure can occur associated with cor pulmonale, pulmonary hypertension, thromboembolism, chronic hypoxia
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With right sided HHD by itself or (more commonly) left sides failure with it, the right vemtrical can't pump and
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get backup on anything proximal to the r.s. heart. Backup of blood, unstressed volume increases backing up all the way to capillary beds
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COPD - caused by
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smoking. Pulmonary hypoxia causes constriction of pulmonary arteries - right side has to work harder
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The worst thing that can happen in right side failure is pulmonary embolism (
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acute cor pulmonale) which puts so much stain on the heart that it goes into fibrilation and you will die instantly
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Ischemic heart disease
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Heart not getting enough blood for one reason or another.Cardiac myocytes aren't getting oxygen.
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IHD problems can be
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Pain, MI (ischemic death of myocytes), stop beating, or CIHD
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Over the years, the coronary blood vessels can be constricted
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Prinicipally the left anterior descending branch becomes obstructed causing angina, completely occlude, rupture and develop thrombus tha occludes
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With CAD, if not complete ischemia
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It is causing chronic ischemia to the heart, which causes CIHD generally leading to CHF and death by CFH. Not MI, heart simply is not getting enough oxygen.
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If there is acute occlusion in heart
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Necrosis of heart tissue, the surviving areas will become overworked, failure of LV, and ultimately death by CHF (if you survive the first 60 minutes)
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MI for men in what age group is no longer unusual
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Forties
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MI annually
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1.5 million
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90% of MI a result of
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Coronary artery thrombosis via atherosclerosis
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Severity of MI depends on
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Where it occurs, size of vascular bed fed by the artery, collateral blood supply,
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MI Occlusion in LAD
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Devastating, if right coronary artery will be less sever
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Collateral blood flow
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Less severe effect of infarct. Crapshoot, you don't know if you have it.
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MI complicating factors
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Other diseases - lung (hypoxic) , other cardiac disease
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LAD, LCA, RCA
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Left anterior descending, left circumflex artery, right coronary artery
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If you occlude LAD get
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Anterior MI on first part of the LV, tend to be most severe, can creep into the anterior septum
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If you occlude circumflex
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Get lateral infarction of LV
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Right coronary artery
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Get posterior infarct in posterior lead into posterior area of the septum
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Stress
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Equals catecholamines, this factor has gone out of favor in importance
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Survivability of MI
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Half die within the first 60 minutes. Success of reperfusion, size of infarct, location, wethere subendocardial or transmural, proper repair, bentricular remodeling
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Size of infarct
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Bigger means poorer prognosis
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Location of infarct
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Transmural
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Is endocard almost to epicard, very poor prognosis
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Scar tissue in MI
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Not full tensile strength for months. And diabetics don't have good repair mech
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Arrhtymias
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Persistent
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Ventricular wall
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Is damaged, can cause rupture
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Papillary muscle
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If rupture, now volve not functioning
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aneurism
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Imbalance
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One side damaged, develop CHF and can die of that
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Best strategy
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Don't have infact\\rct
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Pericardial tamponade
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Rupture of septum, reducing pressure
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Within the first day of MI, a lot of patients will die
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Chance of arrhythmias within one week of MI
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90%
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CHF
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Cardiogenic shock
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LV rupture (most within first 2 weeks)
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consequence of acute MI
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And, many patients are hypertensive to begin with.
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You're surviving, but what will this do to your lifestyle
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Sudden cardiac death
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400,000 per year, often with no prior symptoms, don't know why many occur
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HTN
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Is silent
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Cardiac hypertrophy
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Is silent
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Pulmonary HTN
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Develops in hypoxic patients because of COPD
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Most potent vasoconstrictors known
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Methamphetamine, cocaine - young people beware.
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An old slide, 5 years ago dies of heart disease
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600k dies
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One of the highest heart disease
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death rates in New York where you get what you deserve
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No to good for heard death rates in
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Louisiana
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Heart/lungs work…..
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together.in tandem
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Screwing up heart or lung
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messes up the other.
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RV pumps to lung. LV must be able to handle
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this same volume
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at all costs,
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the heart must maintain a mean arterial pressure (Pa) to insure adequate blood flow to meet the metabolic demands of the tissues, including the heart itself.
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Certain tissues need more b lood
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squash
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Eff on BP: incr ANP
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reduce blood volume, decr BP
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Eff on BP: inc kinins
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Decr BP
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Eff on BP: decr adrenergic factors
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Decrease SNS activity, decrease BP
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Eff on BP: decr blood volume
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Decrease CO, decreases BP
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Eff on BP: decr heart rate
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Decreses CO so decrease BP
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Eff on BP: decrease contractility
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Decreases CP so decrease BP
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Eff on BP: inc aldosterone
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Increases BV and CO, so increase bP
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Eff on BP: increase antiotensin II
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Constrict vessels, incr TPR; incr BP
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Eff on BP: catecholamines incr
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Constriction of vessels, increase of bp
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Eff on BP: increase thromboxane
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Increase bp
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Eff on BP: increase endothelin
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Increase b p
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Eff on BP: increase neural factors
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Increase bp
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Marathon runners don’t have huge hearts because
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They decrease total peripheral resistance with vasodilation to skeletal muscles
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CHF is progressive and affects
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5 million in US, 1mil hospitalization and over 300k deaths
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LV failure can cause LA dilation, leading to
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LA filling up with too much blood and getting atrial arrhytmias and setting self up for blood clot, then thrombotic strokes
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Ischemic HD
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#1 cause of death in both men and women.
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Clinicial presentation of IHD
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Angina, MI, Chronic IHD aka cardimyopathy
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95% of IHD caused by
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Maycardial ischemia from atherosclerosis
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IHD: Irreversible, clinicla problems show up in
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40s and fifteis,
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Don't memorize the four variants. Know the 2 kinds of angina:
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The kind that comes and goes quickly; Pre-infarction type, need immediate attention, probably coronary angiography or coronary artery bypass.
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Pandemic examples may be extra credit - behavior affects mortality
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Philadelphia had political problem with quarantines; St Louis had strong willed public health officer - closed schools and banned gatherings had half death rate (347 vs. 719 per 100k)
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St louis in 1918
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Unpopular difficult choices
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Philly in 1918
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Appeased people, didn't institute quarantine, led to 12,000 deaths in 4 months
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Eradication of Small pox in Africa
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Culture was for women to wash/prepare the dead of relative. Culture is important but led to disease
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Common conditions predisposing to ID tranmission
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Lack of clean water/poor hygiene; crowding; poor nutrition
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Poor nutrition & ID - leads to
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Leads to immunosuppressive state - malnourished low protein, remember antibodies are proteins that may be hard to make
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Lack of clean water leads to
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Fecal oral transmission
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Crowding leads to
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Respiratory or direct transmission
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After natural disasters
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Peopl living in crowded unclean facilities - respir/direct contact
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Responsibility in society and healthcare with respect to infectious disease
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We all have resp to reduce chances of passing infection to others
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How to personally reduce chance of passing disease
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Hand washing, food handling, unprotected sexual contact/shared needles, vaccination, quarantine
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What is being discussed as an employment requirement w/r/t infectious disease
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Mandatory flu vaccination in hospitals - if can't get a shot must get note from doctor
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Quarantine
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Can be voluntary or by force of law
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What not to do - TB example
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XDR TB diagnosis, flew to Europe
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What is XDR
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Multiple drug resistant TB
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Theme from XDR attorney
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Selfish, no personal responsibility
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Types of immunity
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Passive, active, herd
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Passive immunity
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Presence of antibodies in system via transfused immune globulin, maternal antibody; is short lived (6 weeks to months) - body didn't make, ex: can receive immume globulin transfusion
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Active immunity
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Exposure to organism triggers antibody production - from previous infection of vaccination. My body produces this response. Can be natural immunity or from vaccination
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Natural immunity
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Type of active immunity that develops after you have the infection
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Herd Immunity
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When a large percentage of the population is vaccinated, spread of disease is prevented. Even people who aren't vaccinated are protected. Likelihood of spreading to a non-immune personis low
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Vaccination
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Killed or weakend (shortened, altered, "attenuated") infectuous organism
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Attenuated organism protects
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Still enough or org to goose the immune system
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What does vaccination do
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Induce immunity by exposure to killed or wimpy versions of the organism so when challenged with the real org you have a defense
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Vaccination delivery routes
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Injection, inhalation, or oral
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Vaccine "life cycle"
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Frustrating to public health, people forget about how bad disease was as vaccine is successful and become focused on the (mild) adverse effects of vaccination
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Examples of vaccine lifestyle
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Rubella in CA - hippie kids; brought measles back to entire congregation
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Why people stop vaccinations
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People forget about disease, concern over adverse effects
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When a well controlled disease has caused some to not get vaccination
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Outbreaks will occur especially within the unvaccinated population - congential rubella, another
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Vaccination that left scar
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Small pox scarified the skin to activate something and left a scar
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List of vaccine preventable dieseases
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Not on exam, some required to enter school. Chick pox and Hep B becoming more common
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Viaccination for those at risk of bil warfare
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Anthrax and small pox
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Rabies vaccines
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Vets and other occupations that are expecially at risk
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Links to CDC vaccination schedules
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Polio
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Peaked in 1952 (21k cases); 1955 vaccine became available, some had iron lung, disability, death
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Poli is a
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enterovirus
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Roadblock in polio vaccination
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Nigeria(?) leader thought it was a conspiracy to sterilzed poplulation, polio spiked back up.
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Iron lung
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Pressure changing chamber for lifelong treatment of polio
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Measles
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Everyone used to get this, most deadly of the childhood illness
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Measles incidence
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From 100k to 60 (and the 60 are usually brought back from travel)
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9 reasons why you should get vaccinations (Measles)
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1991 Philadelphia 9 children died who were unvaccinated; 2005 unvaccinated 17 year old returned from Romania and started large outbreak
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Respiratory disease
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Risk of spread by droplet or airborne particle
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Large respiratory droplets
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Flu, RSV, para-influenza, pertussis, strep, mycoplasma
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Airborne transmission
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Smaller particles, <5 micron so float around for a while, TB, measles (rubiola), chickenpox (varicella); so must be in isolation w/HEPA filtration
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What requires isolation
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TB, measles, chickenpox, cuz small particles <5 micron
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How to handle prevention of respiratory disease
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Wear a mask, isolation, stay home, etiquette for cough and sneeze, wash hands
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How to cough/sneeze?
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Into sleeves: http://www.coughsafe.com/watch-videos.html
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G I disease tx mech
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Human fecal- oral contam of food or water
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GI disease typical types
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Rota, Hep A, salmonella, shigella, e.coli
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Animal-origin contamination of food for G I disease
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Salmonell campylbacter, e.coli
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Sporadic v outbreak
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Sporadic is one case here or there, Outbreak is like nunsense
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GI prevantion?
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Clean water, handwashing, don't hang with diarrhetics, proper food handling
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Salmonella
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In feces of humans, animals, birds
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Foods of salmonella
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Mostly meat esp poultry, eggs
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Salmonella: foods of animal origin practices
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Cook meat thoroughly; avoid raw eggs or use pasteurized, keep egg based foods refrigerated
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Safe raw egg cooking product
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Pasteurized raw eggs, somehow
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Salmonella contaminated fruits and vegetables
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Example of cantaloupes from Honduras - animals in fields contaminated this
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Pet reptiles and salmonella
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Gift for kids, kids get really sick, health department violation to sell these now
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Food safety
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Separate cutting boards, wash hands, clean plate after taking the raw chicken to the barbie, cook to proper temperature, bring soups or sauces to a boil for 2 minutes
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When to wash veggie/fruit
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Always Even when peeling cause you could cross contam/transfer
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Food safety prep motto
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Clean separate cook, chill
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STD
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Direct mucosal contact or fluids; genital anal or oral mucosal, behavioral not labels (homo/hetero not the issue); may be asymptomatic so don't know they're spreading
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Where STD transfer
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Genital, anal or oral mucosal surfaces
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STDs are
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Treatable and preventable
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PIC, risk to fetus
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See list
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Consequences of PIC
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Fertility interfering w/passage of egg or sperm
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Congenital risks to fetus
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Long term consequences of STD
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Chlamydia
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Infertility, ectopic, adhesions
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Syphilis
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Cardiac, neurologic, disease
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HIV
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Immunodeficiency
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HBV
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Carcinoma (hapatic_ and chronic infection
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HPV
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Cervical cancer
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HSV
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Recurrent genital ulcers, mengitis
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Transmission mechs:
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respiratory droplets/fecal-oral/STD/direct contact/vector
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Vector borne transmission
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Creatures usu insects that carry disease from one to another: Mosquitos - west nile, ticks - lyme disease. May suck blood so have infectioous disease inside of them
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Resp transmission
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Droplets in coughing/sneezing, talking kissing
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Fecal/oral trans mech
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Somehow fecal material makes it back to the mouth. Usu not washing hands or contaminated water
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STD transmission
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Direct contact or contact with bodily fluids
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Direct contact transmission
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Open cut through passage/touching
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Behavior and transmission
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Can significantly interrupt transmission, or amplify by avioidable behaviors
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Simple beh changes w/r/t transmission
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Personal hygiene, food handling, safe sex, vaccination
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Cooking
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Use therm with meat to proper temp, cook eggs, bring soups/sauces to boil when reheating
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Chilling
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Meats, eggs, dairy <40F, chill L/O within 2 hrs, don't deforst at room temp
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STD
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Diseases and treatments - din't go over
|
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Best way to prevent STD
|
Abstinence
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2nd best way to prevent STD
|
monogamy
|
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What is the chlamydia capital of Canada
|
Winipeg
|
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New partner getting tested, asking , barrier precautions, regular checkups
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Prevent of blood borne pathogens
|
Preventable, sharing needles
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To prevent trans of respiratory
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Had washing, cover cough and sneeze, wear mask
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To prevent trans of fecal-oral
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Hand washing, safe food handling, clean water supply
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To prevent trans of STD
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Safe sex practices, screening, treatment, abstinence
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To prevent trans of direct contact
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Hand washing, barrier precautions
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To prevent trans of vector-borne
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Insect repellent, clothing, nets, reduce breeding environments
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Skin/soft tissue
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Some antibiotics
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Upper resp
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Includes eye, ear, sinus, middle ear
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Lower respiratory bacterial ailments
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Bronchitis, pneumonia
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Bacterial meningitis
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CNS infection example
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CNS infections
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Mentigits, encephalitis
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Direct visualization of bacterial for diagnosis
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Gram stain off of a specimen -- I&D direct from patient and send to lab
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Direct vis is Particularly important for
|
Gram positive CNS infection - often start antibiotics before doing the LP
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Gram + in chains
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- strep
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Gram + in clusters
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= staph a
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Specimen helps know
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It's real, not just something on surface.
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Antibiotics target
|
the things that are different. In bacteria, that difference is the cell wall.
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Gram positive wall
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- thick wall
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Gram negative
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- thinner wall but extra layer
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Class by
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Respiration, shape, gram stain
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Respiration
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Aerobe,anaerobe
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shape
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Rods, cocci
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Obligate parasites
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Lost ability to live on own, life in cells - can be in amoeba, human cell
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Obligate parasite
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Chlamydia, rickettsiae, mycoplasmas
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Drug for obligate intracell
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Concentrates in cell like doxycycline
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Habitat:
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Colonization, infection, environment
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All can colonize
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Plant ones usually can't colonize in humans. Agriculturists
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Extreme einviroments
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Bacteria - like what we look for ion Mars
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Factors that influence bacterial infections
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Site of propagation, immune response (effectiveness, memory), virulence, resistence of host in innate form
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Immune response
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How effective? Memory?
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Site of prop
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Skin vs. throat
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virulence
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Can take many foms, for instance must latch on to be virulent
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Resistance in innate form
|
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Has to latch on to host to be
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virulent - one virulence factor
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E.Coli normal in GI (so in
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perineal) but if has ability to attach to host cell can cause UTI
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Intracellular survival
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Mech to survive macrophage's vacuole, then put peroxide etc in vacuole.TB is like this
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Invasion
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Infect given cell and spread - infection in GI lining then spread to lymphatics, systemic like salmonella
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Gram negative sepsis
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- can drop BP and get in trouble.
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Endotoxin
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LPS is inherent to gram negative
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Non-external pathogen
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Part of flora then becomes pathogenic
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Follow bacterial visualization for diagnosis
|
with culture - grow on various plates
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Ident culture by
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morphology, Hemolysis on blood plate?, Biochemical reactions, carb util
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Nucleic acid testing.
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Target conserved sequences and it needs to be specific.
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NA testing can
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pick up organisms that grow really slowly or organisms that are very picky what they grow on…these are the preferred tests for those organisms.
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Bordatella pertusis is detected by
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molecular methods because it’s faster and more sensitive than doing cultures.
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Antigens of surface of organism.
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This is how rapid strep tests are done with throat swab. Turns purple or doesn’t turn purple. Not sensitive but can get rapid results.
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Also how flu testing is done
|
. Antigen Can also be done from stool for Clostridium difficile testing (antibiotics associated diarrhea)
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Fungi resistance
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Develop slowly, because grow slowly, resistance is intrinsic
|
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Bacterial resistance knowledge
|
Best know of the resistance, similar to other (fungi) resistance
|
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Viral resistance
|
Replicate quickly, therefore develop resistance quickly
|
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Pencillin discovery
|
1929 discovered, Accident, contaminant that killed staph on agar plate was noticed
|
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Sulfonamide discovery
|
Found in 1930's
|
|
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When penicillin was formulated for human use
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1939
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Development of TB drugs
|
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1940's - 1950's antibiotics
|
"age of antibiotics" Streptomycin, chloramphenicol, tetracycline, TB (isoniazid)
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Resistance was noticed
|
Immediately after iscovery of AB
|
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Resistance identified
|
40's 50's, just after antibiotics, first multidrug resistant org - shigella
|
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Antibacterial agents
|
Cell wall agents, ribosomal agents, inhibitors of replication
|
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Cell wall agents
|
Beta lactams, glycopeptides
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Ribosomal agents
|
Macrolides, aminoglycosides
|
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Inhibitoors of replication
|
Fluoroquinolones - topoisomerase inhibitors
|
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Antibiotic utilization and resistance
|
|
|
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If treat organisms with pre-existing resistance
|
That subset survives and everything else dies - huge proliferation advantage
|
|
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If spontaneous mutation occurs when treating with antibiotics
|
The mutation will be selected for due to the presence of the drug.
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Non-lethal dose treatment of antibiotic
|
Like immunization, promotes exposure that slows them down and gives chance for some mutations to occur, and selection occurs.
|
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Tolerizing
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Allowing antibiotics to survive in presence of sub-lethal dose
|
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Gene mutation and steps in acquisition of resistance
|
A few bacteria will mutate, the non-resistant bacterium will die off, all of the remaining will be resistant
|
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Categories of mechanisms of resistance
|
Altered target, efflux pump, porin mutation (not allow drug to enter); inactivation (enzyme);
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Resistance gene
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Genes that allows change to take place and is selected for in presence of antibiotic
|
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Efflux pump in bacteria
|
Pumps out drug before it can act
|
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Transfer of resistance
|
Existing resistance element is acquired by bacteria as extra tool
|
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Gene coding of resistance
|
Pre-existing or develop under a/b pressure
|
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Passing of gene for effective resistance
|
Become Widespread via selection, particularly if effective
|
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Horizontal transfer
|
Gene transferred to another organism (not offspring), via conjugation, transformation or transduction
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Nucleic acid uptake
|
Bacteria take up by conjugation of just from their environment
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Vertical transfer of resistance gene
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By replication, daughter cell get gene
|
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Chromosomal transfer of resistance
|
Intrinsic; maybe inherent nature. Ex: no enterococci are susceptible to cephalosporins
|
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Plasmids - transfer of resistance
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By conjugation, sets of resistance genes passed around
|
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Transposons, plasmids
|
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Mobility of resistance carried on plasmid - common ones
|
Beta-lactamase, tet, macrolide, aminogly, SXT, other
|
|
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How to create resistance?
|
Give sub-lethal amount of drug, (that's how it's done in the lab) not finishing course of antibiotic
|
|
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Resistance develops in patients by
|
Wrong dosing, imcomplete antibiotic course, taking a few pills from someone else (sub-lethal)
|
|
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Increased use of antibiotic
|
Double edged sword - works well but frequent use increases resistence
|
|
|
When antibiotic is really good
|
It's used a lot, a lot is out there, and resistence develops. That's happening to fluoroquinolones
|
|
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Antibiotics in animal feed
|
As growth supplement, increases level of antibiotics in environment, inducing cross resistence (suspected in VRE)
|
|
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When you treat a respiratory bug , for example
|
pathogen being treated is not the only organism exposed - all orgs in the subject
|
|
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Inappropriate use of antibiotics
|
Viral, bronchitis, self-limited infections
|
|
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Antibiotic for simple bronchitis
|
Not indicated
|
|
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Broad spectrum antibiotics
|
Save for when dying in ICU, don't use inappropriately
|
|
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GI flora exposure to a/b
|
Opens ecologic space for c.difficile and others, colitis (can't pinpoint just the bronchitis remember?)
|
|
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Colitis from antibiotis
|
a. Dificile, can be fatal, best way to treat is to stop the antibiotic
|
|
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C difficile
|
Spores hard to clean, opportunistic when flora disrupted, stool transplant, stop antibiotics
|
|
|
Chronic c. difficile extreme treatment
|
Stool transplant from family - rebalance the flora
|
|
|
Candidiase
|
Thrush, vaginal; antibiotic depletes oral & vaginal flora. Fungus proliferates to fill the ecological space
|
|
|
Vast majority of staph
|
Penicillin resistant due to beta lactamase they make
|
|
|
PRP
|
Penicillinase-resistant-penicillins oxacillin, clox, diclox, nafc, methi-
|
|
|
MRSA
|
Aka ORSA, tested in vitro with oxacillin
|
|
|
|
Oxacillin used for in vitro testing
|
|
|
MRSA gene
|
Resistance due to mecA gene
|
|
|
mecA gene
|
Encodes altered target (penicillin binding protein) so prp cannot bind. Org escapes antibiotic
|
|
|
Normally oxa, methi and friends bind to
|
Bind to PBP's (penicillin binding proteins, cell wall precursors)
|
|
|
mecA gene mechanism
|
Change in target
|
|
|
Staphylococcal Cassette Chromosome (mec)
|
Is a mobile genetic element (in MRSA?) - lives on particularly small ____, which may make it more mobile
|
|
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VRE
|
a. Faecium (more likely to be VRE), e.faecalis
|
|
|
VanA
|
A gene. There is also a VanB, but VanA is the source of VRE. May have originizted with animals treated with Avoporcin
|
|
|
VRE discovery
|
Discovered in 1986 and rapidly spread - 20x increase in incidents over 5 years. Affects sick patients/immunocompromised/otherwise ill;
|
|
|
VRE conference
|
Plasmid borne VanA gene
|
|
|
VRE effects what kind of patients
|
Debilitated ones because enterobacter is not very virulent
|
|
|
d-ala-dlac
|
vanA gene causes cell wall precursors that vancomycin can't bind to, so cell wall synthesis process
|
|
|
VRE
|
Associated with previous use, other abx, entorocci in GI,
|
|
|
Control of VRe
|
Surveillance, contact precautions for colonized patients, handwashing
|
|
|
Concern of VRE
|
Pass gene to staph aureus leading to more virulent esp. S aureus; "VRSA"
|
|
|
VRSA story
|
Fortunately rare, 12-13 patients. One of which was inappropriately given vanc for 15 months and had staph infection in foot.
|
|
|
MIC creep
|
Vancomycin levels needed to kill are getting higher, maybe being watched
|
|
|
ESBL first describe
|
1983
|
|
|
Beta lactamases (>200, incl TEM,SHV, CTX-M)
|
|
|
|
ESBL found in what patients
|
Nosocomial, long term hospitalzation
|
|
|
Emergence of ESBLs tied to
|
Overuse, mususe of 3g ceph, other drugs
|
|
|
Hosp formulary changes
|
Change resistance rates - can watch it happen!
|
|
|
Other nosocomial - pseudomonal
|
Ubiquitous, biofilm, can become MDR
|
|
|
No drugs left
|
Colistin (polymixin E - toxic), pharmacodynamics become important - tweak dose to get any effect.
|
|
|
Acinetobacter
|
Very suscept or very resist; seen from returning military and have nothing left, MDR or pan resistant,
|
|
|
Colistin
|
Last line, nephrotoxic, neurotoxic, ploymyxin E
|
|
|
HIV concern
|
High mutation rate, rapid turnover error pron polymerase
|
|
|
Hiv strategy
|
Multidrug to reduce likelihood of resistence
|
|
|
Removal of HIV drug
|
Re-emergence of wild type, with resistent one still hiding and will re-emerge
|
|
|
% of new HIV-1 transmission that is resistent
|
3-5% for greater than one class, 6-16% for 1 class
|
|
|
HIV-1 drug resistance testing
|
Genotyping, phenotyping
|
|
|
Genotyping drug resistence
|
Sequence HIV RT and protease
|
|
|
Phenotyping HIV drug resistance
|
Patient derived RT and pretease genes into laboratory HIV clone, very expensive
|
|
|
Antimicrobial resistance
|
Integrated map of factors
|
|
|
Access
|
Affordability may affect whether fulll course of abx is taken
|
|
|
Doctors understanding of drug costs
|
Not always known
|
|
|
Side effects
|
Can induce a patient to stop taking it.
|
|
|
Narrow spectrum
|
Not use broad abx to reduce opportunity for resistance
|
|
|
Microbial response to AB
|
New weapon, new way to avoid weapon
|
|
|
If non-resistant bacteria is treated
|
Bacteria dies
|
|
|
If resistant bacteria is treated with a drug
|
Bacteria proliferates
|
|
|
MRSA common in
|
Skin and soft tissue in otherwise healthy persons
|
|
|
Vancomycin binds to
|
d-ala-d-ala precursors
|
|
|
ESBL
|
Extended spectrum beta lactamases - active against 3rd generation
|
|
|
How many beta lactamases are the
|
Over 200
|
|
|
ESBL sensitivities
|
Cephamycins (cefoxitin, cefotetan) and carbenems
|
|
|
ESBL seen in
|
Klebsiella, e.coli, some in salmonella
|
|
|
ESBL transference
|
Plsamid-mediated, horizontal, plasmid may contain other resistance genes
|
|
|
|
|
|
|
2000 BC - Here eat this root
|
2000 AD here eat this root
|
|
|
Winkessel vessels do what
|
have very low compliance and deliver blood
|
|
|
The energy required to stretch the vessel wall
|
is contained in vessel walls and contracts back to further push the blood forward
|
|
|
Low compliance in a vessel
|
They can stretch, but it takes a lot of energy to stretch them
|
|
|
Even smaller arteries are
|
windkessels
|
|
|
Pre Capillary arterioles
|
Less muscle, but some
|
|
|
Veinsare very compliant,
|
easily stretched under low pressure.
|
|
|
Veins helps
|
maintain a good blood volume due to their high compliance. Blood volume maint is impt for cardiac function
|
|
|
Most of blood in our bidies is
|
In the veins, they can take fluctatution in volume due to compliacne and teherefor regulate blood coming back to heart
|
|
|
Energy is stored in the vessel wall of arteries pushes the blood along
|
|
|
|
Aging
|
|
|
|
Know the top 6 killer (Behavior!!)
|
Heart disease, cancer, CV (stroke) COPD+, Accidents, diabetes
|
|
|
What is normotensive, BP hyper, and pre-hyper
|
120/80
|
|
|
What is hypertensive
|
>130/90
|
|
|
What is prehypertensive
|
>120/80 up to 130/90
|
|
|
Lamina w/r/t
|
difference
|
|
|
Sudden cardiac death
|
Usually due to prolonged systemic hypertension (chronic 140/90)
|
|
|
|
|
|
|
Behavioral changes to reduce hypertension
|
Increase K+, reduce stress, d/c tobacco, reduce alcohol
|
|
|
Arteriosclerosis
|
2 kinds
|
|
|
Atherosclerosis
|
Inflammatory repair process withiin the artery wall
|
|
|
Arteriolosclerosis
|
Occurs in small arteries, not induced by tahte___ process but by high bp. can blow out arteries in eye (hypertensive retinopathy), kidney
|
|
|
3 layers of muscular artery
|
|
|
|
Intima
|
Endothelial on basement membrane
|
|
|
Media
|
|
|
|
|
Gives the artery compliance
|
|
|
Adventitia
|
|
|
|
Athero
|
Intima & media
|
|
|
Endo
|
Produces anti____
|
|
|
Endothelial produce antithrombotic, pro
|
Like protacyclin, NO
|
|
|
|
If damaged
|
|
|
Endo - synth/release growth factors
|
|
|
|
Better have happy endothelium
|
|
|
|
role of endethelial cells in inflammation
|
Expressing cell adhesion molecules
|
|
|
What can injure intima
|
HBP, Smoking, viral infection, Type III immune complex, vasculitis, blood pressure, anything that makes it unhappy.
|
|
|
Intima injury
|
If prolonged, endo cells or plateles produce growth factors as they adhere to endo, chemotaxins attract immigration of smooth muscle cells into the intima, then replicate; Intefere with laminal blood flow
|
|
|
Smooth muscle immigration
|
Intimal thickening,
|
|
|
Accumulation of lipid and thickened intima
|
Fatty streak - the first leasion in the development of atherosclerosis. Reversible if you behave.
|
|
|
x
|
|
|
|
Heart disease exploided over the last 100 years. Genes didn't change over the last 100 years, but what did?
|
Behavior. look what happened to cholesterol
|
|
|
What do we need to change?
|
Our "decadent, disgusting behavior"
|
|
|
Heart and lung partnership
|
a problem with one affects the other.
|
|
|
CV disease cost
|
$433 billion plus lost productivity of $226 billion for just CV disease.
|
|
|
If we don't do something quickly about healthcare costs
|
They will flush us down the toilet.
|
|
|
Stressed volume
|
keeps the blood flowing
|
|
|
Unstressed volume
|
GIVES COMPliance and regulates total blood volume and blood flowing back to the heart
|
|
|
Stressed/unstressed volume quantities
|
300 + 400 mL; 300 + 2300 + 900 mL
|
|
|
Under even low pressure, the veins can
|
sequester large volumes of blood, whereas the arteries store energy.
|
|
|
The energy stored in the vessel walls moves blood along during
|
diastole
|
|
|
As we age, larger arteries
|
get less compliant. We need more energy to fill them up. More energy is pressure, meaning HTN. HTN is involved in
|
|
|
HTN is involved in
|
Accelerating atherosclerosis, hemoragic storkes, thrombotic storkes
|
|
|
Heart and lungs - jobs is to
|
supply enough blood to all the various tissues.
|
|
|
SNS and PNS give blood regulation
|
change re-distribution of where blood goes. (except squash and heart/lungs can't be shut down)
|
|
|
At all costs..
|
The heart needs blood, meaning adequate BP
|
|
|
Veins are more compliant because of the structure
|
more smooth muscle, int/ext elastic lamina
|
|
|
Large areteries: distribtuion and regulation
|
of BF esp in diastole
|
|
|
Pre-cap arterioles:
|
resitance - can shunt blood somewhere else, regulate BP
|
|
|
Many drugs regulate
|
the tone for the precapillary resistance vessels
|
|
|
Mean arterial BP -
|
a constant pressure involved in the delivery of blood to the tissues.
|
|
|
Mean Arterial Pressure
|
CO x TPR CO is amount of B in mL that the heart can pump in a minute; TPR is the amount of pressure it takes to pum a certain vol of blood throught the vessel.
|
|
|
If we knew PRE-HYPERTENSIOn as you creep up to HTN
|
, could intervene and stop a lot of disease
|
|
|
Type II diabetics that are hypertensive?
|
75% "even under control?"
|
|
|
If we knew pre-HTN, could know they're maybe
|
pre-diabetic,developing metabolic syndrome, accelerates atherosclerosis
|
|
|
Our class didn't know its BP, so societn
|
Doesn't know
|
|
|
Whati fi no health insurance?
|
No charge to go into HEB and check BP on your way to buy beer
|
|
|
If CO increases and TPR stays the same,
|
--> HTN
|
|
|
If CO increases and TPR increase
|
Gonzo HTN
|
|
|
If CO drops
|
BP can go lower, can go into shock
|
|
|
f you increase the bv to your body,
|
more blood will be going to the heart. Heart only has certain volume capacity per beat, heart rate increasesbecause of the incr in volume, CO increases,>>HTN
|
|
|
Humoral factors for BP
|
Constrictors (Angiotensin II, catechols, endothelin, etc) or Dilators (prostaglandin, kinins, NO)
|
|
|
Balance between humoral factors
|
Helps maintain even keeled BP
|
|
|
90% to 95% of HTN is
|
"essential" (don't know what causes it) can't define patho situation
|
|
|
19 year old male showing coronary lesions
|
|
|
|
Also used if you find out after the fact.
|
|
|
|
Altered target: common with the ribosomal or cell wall type.
|
|
|
|
Aorta - had
|
|
|
|
Bacterial meningitis kills quickly.
|
|
|
|
Biggies for Strep are skin and soft tissues and pharyngitis. Emperic therapy for skin and soft tissue would be for staph and strep. That’s what you’re covering.
|
|
|
|
BP damages small blood vessels (arteroloscleroisi blows kidneys)
|
|
|
|
Can foster infarct to heart
|
|
|
|
Can treat it, but don't know cause. Being overweight is one of the worst. Just lose weight to get BMI below 25. Half of overweight people would become normotensive.
|
|
|
|
Chlamydia trachomatis (most common) can lead to sterility and pelvic inflammatory disease. Usually asymptomatic and mildly symptomatic. People don’t often seek treatment. That’s why it’s recommended that all women are screened so they can be treated if they are positive. Culture has poor sensitivity so nucleic acid testing is the way to go.
|
|
|
|
CO is dependent upon total blood volume. I
|
|
|
|
Contact precautions in CSF
|
|
|
|
Disks on plate are soaked in antibiotic
|
|
|
|
Do identification of resistance mutations sometimes by molecular methods especially for MRSA (most common) also vancoresistant ___ (neuro?)cocci.
|
|
|
|
E. Coli can be in the environment as well. E.g. E. coli. Contaminated spinach comes from E. coli on the cows. Number one cause of the UTI (99%). Some E. coli can acquire virulence factors such as the hemorrhagic E. coli (GI tract) . So you can have outbreaks of that.
|
|
|
|
Efflux pump: pump in surface of cell that pumps drug out.
|
|
|
|
For a couple of the characteristic resistance factors that are epidemiologically persistent like MRSA, this is the way to look for them.
|
|
|
|
Fungi are mostly plant pathogens - immunocompromised & gardening?
|
|
|
|
Gene transfer
|
|
|
|
Genotyping is not as commonly done in bacterial infections, but occasionally is if there is epidemiological reason.
|
|
|
|
Group A streptococcus is cause of strep throat and also skin and soft tissue infections…staph infections. Strep and staph are the biggies for skin and soft tissue infection.
|
|
|
|
HIV viral load
|
|
|
|
HTN accelerate athero
|
|
|
|
HTN involved in hem and thr strokeF
|
|
|
|
HTN: Aneurisms blow in dissections
|
|
|
|
HTNYou don't know you have it!
|
|
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I don’t want you to know a lot of details of these examples. You should know the highlights,, gram stains and some of the clinical things for the biggies but I’m not going to ask detailed questions.
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If type II Diabetic HTN potentiates hyperglycemia
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Inactivation like beta lactamase that chews up the antibiotic.
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Inflamation results in accumulation of macrophages, _____ = fibrosis 9scarring) , eventually.
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Inhibitors of replication also include DNA gyrase inhibitors like your fluoroquinolones.
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Likewise for TB, although it is more sensitive to do cultures.
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Molecular epidemiology…did they eat the same green onions from the salad bar? How they figured out various contaminated items.
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Molecular epidemiology…is this organism in this patient the same as the patient in the next bed. Did the nurse not wash her hands or did they both eat the same food. Investigate source of infection (if the infection come from the same source)
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Neisseria meningitis. A type of bacterial meningitis. It’s very contagious and very virulent. You would give antibiotics immediately in ER before you do a lumbar puncture because they might die in hours. When you do spinal tap, you might have killed enough of organisms that you can’t grow anything (Might have to do molecular testing if that is the case)
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Not looking at organism itself, or find out after the fact.
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Numbers are the milliseconds it takes to transmit the signal
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Porin mutation that keeps drug from coming in.
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Post infectious complications: Rheumatic fever after Group A strep infections.
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Pseudomonas: kind of an environmental water bug. Has numerous ways to be resistant
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Resistance develops under the pressure of antibiotics. Can be passed between bacteria.
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Resistance genes are detected by molecular methods. It is these genes (pass around or inherited) that produce the changed cell wall feature or changed ribosome or that pump that allow organism to be resistant. Resistance is developed under the pressure of antibiotics.
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Resistance mechanisms. Methicillin resistance. The MecA gene for MRSA. For VRE (Vancomycin resistant enterococci. That doesn’t work for a lot of because organisms have all kinds of ways to be resistant to antibiotics.
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For a couple of the characteristic resistance factors that are epidemiologically persistent like MRSA, this is the way to look for them.
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See the textbook
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Skin and soft tissue infections are the biggies for staph aureus. Can be resistant to all classes beta lactams, particularly MRSA. Culture is typical diagnosis.
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Target cell wall - because we don't have one
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The major differ in gram pos/neg is why the drugs are so different
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The remainder could use less drugs, and these drugs have side effects.
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Tray (each well has a different concentration of the antibiotics) MIC is concentration where you can’t see growth anymore. It’s clear, not turbid.
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You can do rapid diagnosis using nucleic acid amplification from a direct specimen. Often done for TB. Otherwise it could take weeks to diagnose. You need to trace contacts of patient and put patient in isolation.
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You can use molecular methods to identify and characterize culture isolates. Sometimes something weird will grow. Send off to lab for sequencing. Lab will identify the organism.
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You’re looking for the response mounted against the organism. You’re not looking for the organism itself (ideal way).
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Zone is clear area where antibiotic has diffused away from the disk and is inhibiting the growth of the organism.
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