CP week 3 notes

coronary atherosclerosisusually no symptoms, but canangina/ acute coronary symptoms

Management: goal is to improve survival and improve symptoms (2˚ prevention)

1˚ prevention: prevent disease (reduce modifiable risks i.e HTN, diabetes, smoking
2˚ prevention: prevent disease progression (i.e. prevent MI/angina, same methods)

Stress Test: 1st stepfunctional impairments

Cardiac cath: @wristradial guide wire  cath.- JR JL rings r/l), orthoganol view˚stenosis

Treatment Options:

Medical: least expensive least invasive,

Anti-platelet drugs: aspirin (limited evidence for clopidogrel, and IIB/IIIa inhibitors)
Anti-Thrombin drugs: i.e. heparin
Anti-schemic therapy: nitrates, and Beta blockers
**angina relief better managed with PCI, but questional evidence about mortality

Percutaneus ballon angioplastoy (PCI): catheter procedurestent (drug stents less restenosis)
Indications: myocardial risk, unadaptable lifestyle,>class II angina, 2-3 large epicardials (focal)
Vulnerable plaques: PCI of @risk plaques, no supporting evidence

CABG: high risk invasive, venous (saphenous) < arterial grafts (internal mammary),
Indications: >50% Left main stenosis, 3 vessel, proximal LAD+ other, diabetes, LV dysfunction
Risk: high risk patients can benefit the most from CABG

By Patient Class
Asymptomatic/ low risk: PCI/CABG iff large area @risk, >50% left main stenosis, high risk job
CCS II-IV angia: PCI/CABG iff refractory or large area of ischmia
Unstable angina: catherize-->PCI/CABG

DVT/PE
presentation: immobility, low O2 sat, unilateral LE edema (DVT), pleuritic pain, hypotension,
tachycardia, syncope, shortness of breath

Cardiac exam: may be associated with loud S2/ parasternal lift, tricuspid regurg. murmur
intervention: IV heparin (PTT target of 60-80), CXR, EKG, contrast CT for PE/ DVT (LE), VQ scan
CXR: may be normal
EKG: non-specific ST-T changes
CT: segmental filling defects in lungs, and or DVT
VQ lung scan: ventilation will be normal perfusion will be impaired
Non-invasive scans: high sensitivity, used with renal insufficiency/ contrast allergy
Risk Factors: venous stasis, endothelial damage, hypercoagulability

Upper extremetiy thrombosis: >occurance 2˚ to devices

Pelvic/ proximal leg DVT: very high risk of PE
Isolated calf vein thrombi: not necessarily PE, but risk of paradoxical embolism

Pathophysiology of PE
Embolization: thrombus dislodgespulmonary artery (limits perfusion)
PEconstriction in Pulmonary arterymore resistance (less compliance)> breathing work
PEimpaired perfusionincreased alveolar dead spacehyperventilation
Paradoxical embolism: PFO or ASDemboli in arterial circulationstrokes

Right Ventricular dysfunction: common death cause (2˚ to dilation 2˚ to PA pressure),

intact RV function: associated with good outcomes with heparin alone

Clinical Syndromes:
Pulmonary infarction: 2˚ to small PE, hemoptysis (red infarcts), and pleuritic chest pain
Small to moderate PE: no increase in troponin, or BNP, usually anti-coagulats alone sufficent
Moderate to large PE: BNP elevated with RV hypo kinesis
Massive PE: hypotension

D-Dimer: used when PE is unlikely (used to rule out PE, not rule it in), sensitive not specific

Peripheral Artery disease

Association with atherosclerosis: marker of coronary atherosclerosis progression
Symptoms: exertional pain (claudication) or critical limb ischemia (unstable angina parallel)
Stenosis: symptoms usually only manifest after 60-75% stenosis
Atypical leg pain: on DDX w/any LE pain not associated with joints

Risk for PAD: atypical, >50 with risk factors, everybody >70/ cardiology, diabetes/ smoking
History: intermittent claudication/pain brought on by exercise, rest relieves, stable consistent
Symptoms: patients may think symptoms are a product of aging, so specifically ask
Occlusions: 2 levels of occlusions must be present (unless end artery) for symptoms to develop

Muscle affected: muscles below lesion level

Aorta/ iliacbutt, hip thigh, and erectile dysfunction (lerich syndrome, atrophy of LE muscle)
Femoral thigh/ calf (**most common)
Popliteal calf, ankle, foot
Critical Limb ischemia: combination of ischemic rest pain, arterial ulcers, and gangrene
Ischemic rest pain:
Cause: ischemic neuritis,
Begins: distal foot/ ischemic ulcer
Exacerbated by: elevation, relieved by use interferes with sleep

Evaluation of PAD BP both arms, hyperlipidemia, nails, hair, bruits (@carotid bifurcation)
Pulses: lack of DP pulse is not conclusive for PAD, but absent DT pulse is abnormal
Bounding pulse: buzz word for aortic insufficiency
Subclavian steal: transient subclavian ischemia, ASCflow to contralateral vertebrals
Frank sign: ear changes sing of PAD
Xanthomas: physical manifestations of high serum lipids
Bueger’s test: pallor associated with elevation
Dependent Rubor: redness associated with use

Ulcers:
Arterial: painful and on foot, no granulation tissue/ bleeding (no nutrient transport), PAD
Venous ulcer: Perilamelolar, painless, granulation tissue builds up, CVI (may be on ankle)
Neuropathic ulcers: (mostly) diabetesno sensation Pressure point infections (foot bottom)

ABI: ankle systolic pressure/ brachial artery systolic pressure using Doppler in supine position
Change: should be less than 15%, >.9
Unreliability: diabetes vessel calcifications (use toe pressures instead)

DDX
Neurogenic Claudication: very variable (location, timing, activity, etc), 2˚ to lumbar stenosis
Drugs: statins

Mortality: with claudication (25% (7% risk of amputation), but with critical limb ischemia (50%)
Treatment: exercise, risk modifications (stop smoking), antiplatelet drugs, statins, procedures

Revascularization: usually not for claudication (unless limits lifestyle), based on HP not #s
Modalities: angioplasty, stents, etc.
Aorto-illiac occlusive disease: aorto-bitemporal bypass graft (5 year patency)

Evidence
Class I>IIa >IIb no class III (risk),i.e. strength of recommendation
Level of evidence: A (metanalysis), B: clinical trials C. expert consensus (no data)
IA: exercise, antiplatelet therapies with sympatomic PAD
Chronic Venous Insufficiency (CVI): incompetent valves (many causes)/ obstructionvein HTN
Manifestations: Varicose veins, Lipodermatoscerlosis, Stasis dermatitis, venous ulcerations

Venous Anatomy: all veins have valves

Deep Veins: deep in surface (accompany arteries)
Superficial Veins: superficial, questionable need
Perforator Veins: connect both Cockett’s: ankle, Paratibial: midcalf, Boyd’s @knee

Calf Muscle pump:

muscle contractions increased DV pressure, and perforator valve closure
muscle relaxation low DVP, perforator valve opens (superficial venous blood flows into DV)

Ambulatory Venous HTN: incompetent valves elevated VP during exercisecapillary leak

Symptoms: spider veins, varicose veins, ulcers, and aching pain

Physical exam: look at the stuff, deduce limb circumference @tibial tubercle

Varicose Veins: large superficial vein dilation vs. spider veins (small superficial veins)
Treatment: removal of veins

Lipodermatoscelosis: cuteanous replacement with fibrous tissue

Acute phase: stasis dermatitis (painful, thick, hot, tender skin)
**although venous ulcers are painless stasis dermatitis is painful***
Chronic phase: scar

DUS: used to localize venous insufficiency, retrograde flow longer than 2s is bad

Prevention: recognition that DVT @ high riskDVT prophylaxis and treatment when necessary

Treatment:

mechanical therapies (compression, and elevations),

graduated compressive stokcings:, high pressure drives blood into deep system, compliance?
Multi-layer compression therapy: treat active ulcers severe edema,
Sclerotherapy: aseptic agents in cutaneous veins block (shunts blood to deep circulation)
Laser treatment: ablations of small spider veins

Surgeries: when refractory to non-surgical interventions

Options: saphenous vein stripping ligation, stab avulsion phlbectomy (varicose vein removal)

Pulmonary Medicine:
Coughing: nonspecific 2˚ to mechanical/chemical irritation airway, GERD
Dyspnea: “subjective awarenss” of increased breathing difficult, @rest: think anxiety
Hemoptosis: bronchoitis, extensive workup eliminates serious, quant. values >600 =massive
Pleuertic pain: sharp pain inspiration worsens, from parietal pleura, reproducible by palpation

Physical Exam: inspection, RR 16-18, and Inspiratory/expiratory ratio 1:2, (longer= obstruction)
Palapation; even expansion, tactile fremitus > with consolidated pneumonia < with effusion

Percussion:
resonant= normal,
dull= consolidation/ effusion
hyperressonant= air (i.e COPD)
interface lines between resonant and dull regionsdiaphragm excursions

Ascultation:
Bronchial breath sounds: = in inspiration/expiration, heard over trachea or consolidated areas
Vesicular breath sounds: inspiration>> expiration, normal noise
Bronchovesular sounds: combination of two sounds heard @apicies
Wheezes: musical sounds heard in expiration, result of COPD and asthma (problem with air out)
Crackles: short discontinuous sounds, indicative of interstitial lung disease /pulmonary edema
Ronchi: coarse, heard during inspiration and expiration, indicative of airway narrowing
Friction rubs: creaking sounds, in sisnpiration and expiration rubbing of pleuarls

Pulmonary function Test

Volumes: isolated measurement vs. capacity: ≥2 volumes

IC: Inspiratory Capacity: TV+IRV

TV: normal breath in and out
IRV: air that lungs can accept beyond tidal breath

FRC: air in lungs after a normal expiration ERV+RV, chest expansion=lung collapse, rest pt.
ERV: expiratory reserve volume total air blown out beyond TV (only air left in lungs is RV)
RV: air that remains in lungs no matter what (cannot be measured with spirometry)

Total Lung Capacity: all air in lungs

Vital Capacity: all “functional” air in lungs all lung volumes except RV

Spirometry: FVC: about 5L and FEV1: about 4 L the ratio should be >.7
Bronchodilator testing: 12% and .2L increase in FEV/FVC is +

Curves:
Restrictive: slope is equal (FEV1/FVC=.7), since all volumes decrease
Obstructive: slope is not equal (FEV/FVC <.7), air gets in but doesn’t get out

Flow loops: same principles

Restrictive: curve will be smaller (all volumes are lower)
Obstructive: curve will have a longer “tail” indicative of longer time to get rid of air
Diffusion capacity: CO exchange in lungs (tests basement membrane)
Values: asthma, bronchitis= airway probs.= normal diffusion intrinsic problems= low diffusion

6 minute walk test: determines O2 sat. @rest and exercise (should be >95% both times)
**shouldn’t fall with excercise

Gas Exchange
Ventilation: lung air flow RR*TV, pCO2 monitors, <35= hyperventilation, >45= hypoventilation
Oxygenation: O2lungstissues

Hypoxemia: low PaO2, 2˚ to hypoventilation, V/Q mismatch, shunt, diffusion problems

Hypoxia: low O2 in tissues cyanideno O2 utilization by cells (histologic), anemia, circulatory

FiO2: fraction of oxygen in air normally .21 (masks= .5),

Po2: partial pressure of oxygen normal pO2= 80-95 torr, or 160 mmg Hg, dissolved O2 in blood
** should be proportional to FiO2 (lungs oxygenation ability), not affected by RBC amount,

A-a difference: normal is 5-10

PAO2= FiO2*(Pb-47)-PaCO2/.8
FiO2*(Pb-47)=150 (on normal air)
** hypoxemia 2˚ to hypoventilation A-a is normal (lungs ability to oxygenate is intact)
**large gradient = intrinsic pulmonary problem i.e. shunt, VQ mismatch, or poor diffusion
**shunts respond to increased oxygen (hypoxia without hypoxemia would not)

P/F ratio= pO2/FiO2, normally about 450 (95/.21)

ARDS: <300

Saturation pressure curve: (is the Hb-o2 binding curve)

Small differences in partial pressure large differences in %saturation
Shift right: hyperthermia, hypercarbia, and acidosis (less O2 affinityO2 in tissue)
Shift left: hypotherlmia, hyocarbia, alkalosis, (more O2 affinity less O2 in tissue)

Oxygen Content: bound O2+ dissolved O2

Bound O2: Hb*1.34*SaO2 (saturation)
Dissolved O2: PaO2**.003
Changes in Oxygen content: high FIo2≠effective, but hyperbaric O2 more O2 content

O2 to tissue: CO*aO
O2 uptake: VO2= CO* (CaO2-CvO2)
Pulmonary emboli
Emboli vs. thrombi (when thrombi detachemboli)
Risk factor: prior PE high liklehood of recurrance

Saddle Embolims: @pulmonary artery bifurcationimpinged outflow tract

Sudden Death: ≥60% arterial obstruction
Pulmonary infarct: occur in periphery (small artery occlusion 2˚ to small emboli)
lower lobe affected, wedge shaped hemorrhagic infarctcoagulative necrosis

Morphology:
Layers: granular outer layer (alternating dark and light areas= lines of zahn), twisted on itself

Pulmonary HTN: pulmonary arterial pressure >25 mm

Cause: usually 2˚ to anything that increases pulmonary pressure
Reversible: medial hypertrophy, and intimal hyperplasia

Pulmonary Edema: transudate in alveolar spaces (low protein infiltrate)

chronic congestionhemosiderin intra-alveolar macrophages (iron stain)

Diffuse Alveolar hemorrhage:

Goodpasture syndrome: linear IgG to BM (lungs and glomeruli involvement)
Presentation: young men with hemoptysis with renal failure

SLE: immune complexes granular fluorescence pattern

Wegner’s: -flourescence, ANCA, bilateral lung nodules and cavities,

Necrosis: large ares with serpingous borders
Vasculitis: focal, eccentric, transmural, with destruction of inner outer elastic laminae

Pneumonia

Lobar (1 single lobe with consolidation): vs. lobular: (diffuse involvement of both lobes)
Lobar: caused by S. pneumonia
Stage 1: congestion: exudate, with bacteria
Stage 2: red hepatization: polyps, RBCs, fibrin
Stage 3: Gray hepatization: stuff dies
Stage 4: resolution, architecture is predominantly intact
Lobular pneumonia: starts @ broncus goes down, hyperplasia of perihilar lymph nodes
Causes: stpah, Haemophiliu,s klebsiella
Complications
Abscess: necrosis with lots of PMNcavity
Empyema: purulent exudate buildup within pleural cavity/ thorax (complication of abscess)
Plevritis visceral pleura inflamed fibrinous exudate cavitation lobar pneumonia complication

Abscess
CXR: upper portion: radiolucent, lower portion: radio-opaque
Composition: generally, includes anaerobes
Pathogenies: aspiration of infectious agents into lung, bronchial obstruction, infectious cause
Aspiration: location usually right lung in posterior upper lobe and apical lower lobe

Community acquired atypical pneumonia

Presentation: no alveolar exudate, less sputum production
Causes: Mycoplasma, viruses, and chlamydia
Pathology: intestinal lymphocyte rxn confined to alveoli wall-septa (alveolar space ≠ exudate)

Aspiration Pneumonia
Presentation: debilitated patients (like stroke patients) with gag/swallowing problems
Etiology: mixed GI/oral (anaerobes) with some aerobes
Pathology: necrotizing pneumonia, likely to form abscesses

Noscomial Pneumonia
Presentation: >48 hours in hospital, immunosuppressed, long Ab use, invasive devices, ICU
Causes: enterobacteriacae (klebsiella, Serratia, E.Coli) Pseudomonas, and MRSA

Tuberculosis: rare in US, unless immigrant, TB most of time, but AIDS/HIV think M. Avium
1˚ TB: new TB case,
Pathology:
inhalation of organism
 distal upper lung/upper lower lung infection (Ghon Focus)
Caseous granuloma formation
 peribronchial lymph node drainage
 nodal caseous granulomas (gohn complex)
Histology: granulomatisu inflamtion with caseous necrosis with multinucleated giant cells
2˚ TB: reactivation @apex of upper lobe (2˚ to high O2 tension in apex)

Fungi
Candidia: immunocompromised, yeast with pseudo and true hyphae

C. Neoformans: immunocompromised, systemic infection (brain)

Morphology; budding yeast, with thick polysaccharide capsule, fills alveolar space
Stain used: india ink
Opportunistic Moulds
Phycomycoses: nonseptated hyphase that branch @right angles
Aspergilus: septated hyphage that branch @ acute angles
**angioinvasivetissue infarcts and cavitations

Viral pulmonary infections

CMV: AIDs, transplant, and neonates, intranuclear owls eye + intracytoplasmic inclusions

Pneumocystis Jiroveci: only in immunocompromised

Morphology: intralveolar exudate, fomany, pink, septa edema minimal monoculear infilitrate
CXR: bilateral interstitial infiltrate
Stain: silver stain

Upper Respiratory tract infections

Rhinosinuisitis:
Cause: mostly viral, sometimes S. pneuomniae, or H. influenza

Acute bacterial rhinosinuisitis: post viral (≥1 week), T >39˚C, purulent discharge, and facial pain
Symptoms: minor, or major: major= facial pain, fever (acute cases), or nasal discharge
Diagnosis: 2 major symptoms, or 1 major symptom and 1 minor symptom
Diagnosis: paransal sinus culture (invasive test, usually treatment is empiric)
Treatment: Amoxicillin-Clauvanate (lactamse inhibitor), doxyclcine,
**kids: levoflxoaxcin (respiratory floroquinolones), topoisomerase inhibitor (Doxyclcyline CI)

S. Pneumoniae:
Shape: g+ lancet shaped diplococci
Virulence factor: capsuleantiphagycotic, antigenserotype,
MOA: native Nasopharyngeal flora, kids= short eustachin tubes > risk otitis media/ sinusitis
Infections: MOPS, most common: meningitis, otitis media, pneumonia (community), sinusitis
Vaccines: PCV13 >PPSV23, given to kids <2, and adults >65, or normal age with conditions

H. Influenzae
Morphology: usually coccobacilli, may be pleomorphic
Media: chocolate agar, fastidious organism that requires factor X (hemin), and V (NAD)
Virulence factor: capsuleantiphagocytic, and IgA protease
Cause of disease: currently predominantly nontypable strains, because of universal vaccine
Infections: nasopharynxotitis media, sinusitis, epiglottitis, and meningitis
Presentation: obscured ear landmarks,
Otoscopic exam: bulging erhtymetous tympanic membrane, with effusions
Why kids: short straight eaustachian tube> chance of ear infections (otitis) media)
Otitis media: 3 causes S. Pneumoniae, H. Infulenzae, or Moraxella Catarrhalis
Treatment: most resolve, >2 days Augmentin (Ampicllin/ Clauvanate)
Otitis Externa: outer ear infection, associated with ear discharge (otorrhea)
Treatment (adults): neomycin (aminogycloside)-polymixinB-hydrocortisone
Treatment (kids): Flouroquinolone combination (Cipro+ dexamthesone)
Cause: usually pseudomonas (sometimes staph)

Pseudomonas:
Presentation: grape like odor, blue green pretty color, oxidase+
Virulence factors: pilli, capsule, LPSCFTR binding, exotoxin, elastaseecthyma gangrenosum

S. Aurueus
Blood agar: gold pigment with zones of B-hemolysis
Alternative to culture: coagulase+ (you know it’s staph)
Protein A: binds to Ig prevents opsonization
Virulence factors:
Enterotoxins: SEA rapid food poisioning, SEB (non-tampon related TSS)
Exfoliative toxin: scalded skin syndrome
TSST: superantigenmenstrual related TSS

Group A strep: “strep Pyogens”

Pharyngitis: Viral vs. strep: viral= cough, strep≠cough, but + petichaal spots/ lymphadenopathy
Diagnosis: rapid antigen detection not sensitive, children and adolescen – antigenculture
Treatment: penicliin, amoxicillin, 1st generation cephalopsorings,
Gram stain: G+ cocci in chains
Virulence factors:
M protein,
Streptococcal pyrogenic exotoxins (Spe)shock (≥30% mortality vs. staph 3%)
RF: post pharyngitis infection, with both a type II and type IV hypersensititivy reaction
Acute glomerulonprheitis: post impetigo/ post pharyngitistype III HS
Lab tests: bacitracin sensitive (dog in sketchy)

Epiglottitis:
Causes: MRSA + H. infulenzae, rare in US (H.Flu vaccine)
Presentation: child leaning forwardmore air in lungs, muffled “hot potato” speech,
Physical exam: very red eplitlottis
CXR: associatd with thumb sign on X-ray (the epliglottis is bigger)
Treatment: establish airway treat with ceftriaxone (crosses BBB) and Vanco. (MRSA activity)

Diphtheria
Pathogeneis: no invasion, Dipheteria toxin mediated
Membrane: pseudomembrane bleeds when scraped off, Bulls neck
Systemic diphtheria: cardiomyopathy+polyneuropathy
General characteristics: G+, nonmotile, metachromatic X,V shaped or chinese characters
Daignosis: verification of diphtheria toxin presence,
Toxin: AB toxinADP ribosylation of E2Fno protein synthesis
Treatment: erythromycin

Pertusis
Pathogeneisis: no invasion, pertussis toxin mediates symptoms
Pertusis toxin:Gi inhibitionexcess cAMPmucus secretionlymphocytosis
Stages:
1. CattarhaL: nonspecific incubation period
2. Paroxysomal stage: inspiratory cough, double cough
3. Convalescent stage: symptom resolution over time
Stain: G-, coccobaclli, encapsulated
Culture: fastidious organism requires special stain (regan Lowe-stain)
Treatment: erythromycin, and DaPT vaccine

Community Pneumonia

Defense Mechanisms
Cilia: prevent things >10 microns from reaching alveoli, inhibited by cilia
Surface liquid: epithelial cells, glands, alveoli secrete lysosome, lactoferin, alpha 1-anti-tryp
Alveolar lining fluid: fibronectinIL-IbPMN migration
Surfactant: from club cellsopsonization of pathogens
Phagoycts: alveolar macrophages eliminate organism vs. interstitial macs= APCs

Causes of CAP: many causes, candidia only causes CAP in severe prolonged neutropenia

Diagnostic tools:
Gram stain
History physical
Urine antigen: best for legionella and pneuomoccocla antigens
Pulse oximetry: PCP

CAP by age
<2: think RSV
10-16: mostly bacterial

typical vs. atypical: not used often, atypical includes: chylamdia, legionella, and Mycoplasma
Strep Pneumoniae: 10% mortality rate fastidious organism that is difficult to culture
S. Pyogens: very virulent organism, >20% mortality

Winter time: Influenzae like illness

RSV:
Metapneumovirus: virulent in elderly
Influenzae: rarely causes pneumonia, when it does it is fulmiant
I say you says
HIV: P. Jiroveci
Travel: Histoplasmosis, blastomycosis, coccidomycosi (Arizonia, South California)
Bird exposures: histoplasmosis, or psittacosis (Chylamidia)
Barnyards: C. burneti

PCP pneumonia
Presentation: HIV+ CD4 <100 and low O2 Sat >5% (drops with exertion)
CXR: diffuse “interstitial infiltrate” **looks interstitial but is alveolar
Pathogneies: alveolar infilitratethickneingig of BMimpaired oxygen sat.
Treatment: Bactrim corticosteroids added in more severe cases to prevent intubation

Virulence Factors
S. Pneumoniae: capsule, neuroamidase (RT colonization), pneuomylsiin (pores), hyalurinodase
C. Pneumoniae: cilostatic
M. Pneumoniae: cillliocidial
Legionella: resist microbicidial activity of phagocytes

Pneumococcal pneumonia risk factors

Multuple myeloma and hypogammaglobemia
Splenectomy

Spleen: produces opsoninscomplement fixation, and properidin (alt pathway activation)

Risks: PIM infection, Strep Pneumonia, H. Infulenxa, and N. Meningitidits
Overwhelming Postsplenectomy Infection: OPSI, high mortality rate

H. Infleunzae: not in kids anymore, associated with COPD and smokers (no cilia)
Presentation: Gram variable cocco bacillus

Mycoplasma:
Demographics: military recruits, college dorms
Onset: slow
Cough: non-productive
Associated symptoms: weakness, risk of GBS
CXR: disappropriate phyxical and CXR findings
Diagnosis: PCR better, cold agglutinins

Legionella: high fever, male smokers, non-productive cough, nothing on gram,

Presentation: high fever in smoker, nothing on gram stain with exposure to bad water
Staph
aspiration type: high rate post infulenzae associated with bronchopneumonia with abcess
Hematogenous type: associated with IV drugs,
Symptoms: high fever, productive cough, G+ in clusters “grapes of staph”

Treatment: 8 hour windowhigh rate of empiric AB uses (problematic in other areas)

Outpatient: changes a lot but may be omadyacycline+ b lactams
Inpatient: Ceftriaxone+ Azithrymycin
Aspiration: possibly add metronidazole for anaerobic coverage
Empymea: pus in pleural space, add metronidazole (may require drainage)
New agents:
baloxavir marboxil (used for flu A and B) inhibits acidic endonuclease
Omadacycline: better tetracycline

Blood cultures: only useful for Pneumococall pneumonia (2˚ to fastidious organism), before AB
Gram stain: specimen should have >25 PMN, <10 epithelial cells, not spit but deeper

PCR: obviorusly used for viruses, but also used for Bordatella, chylmadiphila, and Mycoplasma

HAP vs. VAP: just @hospital vs. on ventilar, >time=>risk of pneumonia

VAP: pneumonia ≥48 hour intubation, mortality ≥30%, most common ICU nosocomial infection
VAP risk factors: male, emergency surgery, burn victims, organ dysfunction, CNS dysnfuycntion
Hospital risksL tracheotomy, NG tubes, supine position (prevent BP changes) transfusions
HCAP: health care associated pneumonia, types of pneumonia associated with outpatient

VAP organisms: ESKAPE, less common: legionella (thermophile), aspergillus, RSV (other viruses)
Enterococus
Staph Aeruesu
Klebseilla
Acinobacter: g- diplococci, look like Neisseria, treat with carbapenem, high mortality
Psuedomona: exoU phospholipase and needle like apparatusdestruction of PMN membrane
Enterobacter: may produce beta lactamasestreatment difficulty (use carbapenems)
Source of organisms: patients GI tract, and poor healthcare worker sanitation practices
**candidia may show up but it’s treated rarely a cause of pneumonia

Pathogenesis: biofilm production on tubeentry into airways

Fibronectin: increased salivary proteaselow fibronectinno mucus coveringg- rods invade

CXR: may be normal, get a CT scan

Microbiolgoy Studies: gram stain is god, if gram stain is empty (VAP unlikely)
Treatments: 8 days if getting better
g- anti-pseudoal drug PipTaz + aminoglycosides (increased coverage), penem, gentamycin
g+: vancomycin linezolid may switch to methicillin if MSSA

prevention:
hand washing
thin cuffed ventiliation
not supine posture (semi-recumbent posturing)