Glossary of Block 6 PBL lectures
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- non-bacterial thrombotic endocarditis
- infectious endocarditis pathogenesis
Interaction between the two
- Infectious endocarditis: random facts
- Continuous bacteremia
Embolic phenomenon (petechiae, strokes, TIA etc), abscesses, microscropic hematuria
CHF due to valve damage most common cause of death.
- Osler's node vs
Janeway lesion vs
- Finger/toe pad
- Duke's criteria
- Positive blood cultures
Positive vegs on echo
Valvular or endocardium involved.
- Bacterial causes of SBE
- Strept viridans group
HAECK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) Yikes.
- Bacterial causes of ABE
- Staph aureus
- Infectious endocarditis: treatment
- Must be bacteriaCIDAL
Treat 4-6 weeks
If indicated, surgery NOW, don't wait. (CHF, PVE IE, abscess, large vegs).
Prophylaxis (amoxacillin) before dental procedures.
- Arterial flow is directly proportional to:
Indirectly proportional to:
- Pressure (diastolic pressure, most coronary flow during diastole)
Square of the radius (lumen size)
Length of the stenosis
- Angina: pharacological treatment
- One ASA, 80mg min
Reduce O2 consumption: B-blocker, Ca-channel blocker, Nitrates
Increase O2 supply: nitrates
- Nitrates in angina: random facts
- Nitric oxide donor -> activate cGMP -> VENULAR ONLY (nitroglycerin) smooth muscle dilatation -> reduced LV EDP (preload) -> reduced O2 consumption
TOLERANCE: must have nitrate free intervals (at night)
SubLing(give to all pts), Oral, topical available.
- Beta blockers: examples
Toprol XL (metoprolol) -- 2x more expensive
- In order: 4 determinants of MVO2
- Myocardial oxygen consumption!
- Calcium channel blocker names and relative effects on AV node, inotropy, BP?
- L-Type Ca channel blocker
Contra: 2nd, 3rd AV block, hypotension,
Caution: CHF, MG, bradycardia
Adverse: AV block, CHF, hypotension, CONSTIPATION
- L-type Ca channel blocker
Contra: 2nd, 3rd AV block, WPW, acute MI
Caution: CHF, LVSD, liver/renal impairment
Adverse: brady, AV block, CHF, erythema multiforme.. but these are uncommon. Well tolerated.
- 1st generation dihydro.
NO LONGER ANY ROLE FOR USE IN ANGINA! SERIOUS COMPLICATIONS.
- 2nd generation dihydro
Contra: hypersensitivity to this drug
Caution: severe CAD, CHF, liver disease, aortic stenosis
Adverse: arrhythmia, syncope, EM, etc.
- Ranexa. Na channel inhibitor -> lower sodium decreases Ca overload via Na/Ca exchanger -> reduces stiffness of diastolic wall, relieving pressure on vessels. Cyclical. Basically the anti-digoxin.
- ACE inhibitors in angina
- No effect. May help lower high BP, reducing afterload.
- Nonpharmacologic therapy in angina
And follow up.
SMOKING CESSATION (-25% risk in 1yr)
Monitor lipids, drug compliance, side effects, smoking cessation.
- Characteristics of normal EKG
+P wave axis in I,II,III, aVF
QRS 90 to -30
PR .12-.21, QRS < .10
QTc < .46 (QT/root(RR interval))
Precordial R wave progression (V3-V4 transition)
Baseline ST seg
T wave dir same as chest QRSs
- Difference between ectopic atrial rhythm and wandering pacemaker?
- Both have variable waves but wandering has 3+ P wave morphologies, with none of them appearing consistently sinus.
- Early afterdepolarizations
- Occur in Phase2/Phase3 of AP
Occur under conditions that prolong the action potential duration
May require concomitant “dispersion of refractoriness”
(eg, prolonged QT syndromes where disparity between epi-, mid- and endomycardial APD)
- Stroke prevention in A.Fib
- ASA 81 – 325 mg: age < 75 and < 1 risk factor
Warfarin INR 2-3: >1 risk factor, age > 75.
Warfarin INR 2.5-3.5: RHD, prosthetic valves etc.
- Class Ib, Na+ channel blocker
Treatment of ventricular arrhythmias in acute setting (V.Tach!!!!)
- Class III (and I,II,IV effects)
K+ channel blocker, blocks repolarization prolonging APD.
Great for A.fib and V.Tach.
Pulmonary toxicity, thyroid metabolism
- Class Ia, Blocks Na (slow automaticity) and K (longer APD)
Great for WPW when presents with A.Fib. Slows accessory conduction.
Can cause lupus syndrome, long QT.
- Opens outwards K+ channels, hyperpolarizing pacemakers. Slows sinus rate, depresses AV conduction.
Acute treatment (HL<8s) of SVT! NOT FOR WPW.
- Beta blockers in arrhythmias
- Slows HR, decreases DAD (triggered automaticity), decreases myocardial demand.
For long term SVT.
Can cause broncospasm.
- Diltiazem and verapamil in arrhythmias
- Ca channel blockers
Slows AV nodal conduction
NOT for WPW!!!
For long term SVT.
Can cause hypotension.
- Vagotonic effect on AV node... slows HR. (in addition to use in CHF)
A.fib, especially in LV dysfunction when you cant use a Ca channel blocker!!
Narrow therapeutic range.
- Phamacologic treatment of SVT: acute and preventive
- Acute: adenosine, Ca channel blockers, B blockers, Digoxin
Prevention: B blockers, Digoxin, Type Ia, Ic, III.
- Stages of HF
- A: high risk
B: + structural
C: + symptoms
D: + refractory
- NYHA functional class of HF
- Symptoms with:
1: major exertion
2: normal exertion
3: minor exertion
4: at rest
- Six general causes of heart failure:
- Systemic HT
High output state
- 5 causes of high output HF:
Paget's disease of bone
- Pulsus paradoxus
- Normally pulse weaker on inhalation and stronger on exhalation... exaggeration of this causes more beats on auscultation than periphreal pulses felt.
- Pulsus alternans
- Amplitude of normal pulse alternates between strong and weak.
Indicates severe left ventricular dysfunction.
- Framinghman criteria for CHF:
- 2/0 or 1/2
Major: PND or orthopnea, JVP, rales, cardiomegaly, S3, +HJR
Minor: ankle edema, night cough, DOE, hepatomegaly, pleural effusion, HR > 120/min
- ANP & BNP: random facts
- ANP: response to volume expansion... used to dx asymptomatic HF
BNP: response to increased ventricular filling pressures... used to dx acute decompensation
- BNP values:
- No HF: <100pg/mL
Non-cardiac dyspnea: 350pg/mL
Acute HF: 700pg/mL
Correlates with NYSA class:
FC I 244 to FC IV 817 pg/mL
- Kussmaul's sign
- JVP going up with inspiration rather than down as is normal. Due to impaired filling of RV.
- Normal right sided pressures on Swan-Ganz:
- RA: 5
- Normal LV, aorta pressures
- LV: 120/8
- Equations for SVR and PVR:
- SVR: (MAP-RAP)/CO * 80
PVR: (MPAP-PCWP)/CO * 80
- Normal and abnormal O2 sats:
- Arterial 95-100%
70% (CI = 3L/min) normal
50% (CI = 2L/min)
30% (CI = 1L/min)
- 3 hemodynamic pathologic states and pressures/resistance seen in them:
- Volume loss: low pressures, high SVR
Septic shock: low pressures, low SVR
Cardiac shock: low pressures, high filling pressure (PCWP, LVEDP)
- Murmurs heard during systole vs diastole?
- Systole: AS, PS, MR, TR
Diastole: AR, PR, MS, TS
- Causes of AS, AR, MS, MR, TR, PS
- AS: bicuspid valve, calcific valve
AR: collagen disorder, degenerative, Marfan's, syphilis, dissection
MR: Cardiomyopathy, prolapse, ischemia
TR: left heart disease
- Auscultory signs of AS, AR, MS, MR, TR, PS
- AS: systolic click, systolic murmur
AR: Early diastolic decresendo murmur
MS: Loud S1, opening snap, mid-diastolic murmur
MR: Holosystolic murmur in mitral area
TR: Holosystolic murmur, increases with inspiration
PS: Systolic ejection murmur
- Balloon valvuloplasty effective in? not effective in?
- effective in mitral stenosis, pulmonic stenosis
NOT for aortic stenosis in adults.
- Spectrum of ischemic heart disease (4)
- Chest discomfort on exertion: Angina
Increase in frequency/ at rest: Cardiac enzymes negative: Unstable angina
Chest discomfort at rest plus elevated enzymes: Non-ST elevation MI
Chest discomfort at rest plus ST elevation: ST elevation MI
- WHO definition of MI
- 2 of 3
Q waves on EKG
Positive enzymes (troponin)
- 7 steps to take for acute STEMI:
- Cardiac monitor
Reperfusion (cath or chem)
- Thrombolytic agents:
- Alteplase (rTPA)
- Indications for PTCA (percutaneous coronary angioplasty)
- Cardiogenic shock
Pt. recieved CPR (bleeding risk)
Contraindication to thrombolytic therapy (stroke?)
- 3 acute MI mechanical complications:
Myocardial rupture (tamponade)
- NSTEMI: treatment
- Thrombolytic therapy NOT indicated
Immediate Revascularization (CABG, PTCA)
Size of infarct smaller
Future events higher
- Unstable angina: treatment
Thrombolytic therapy NOT indicated
- Chronic stable angina: treatment
- Identification and treatment of associated diseases
Reduction of risk factors
Revascularization (PTCA, CABG)
Aspirin, B-blocker, cholesterol/cigs, diet/diabetes, education/exercise
- Blood pressure levels and classifications
- Normal: <120 / <80
PreHTN: 120-139 / 80-89
Stage 1: 140-159 / 90-99
Stage 2: >160 / >100
- Older pts have thick, hard arteries. More cuff pressure required to occlude vessel, hence higher BP readings.
Final diagnosis made by intra-aterial pressure measurement.
Suspect if antiHT therapy results in hypotensive symptoms (dizziness, syncope etc)
- White coat hypertension
- Hypotensive symptoms (weakness, dizziness) on a variety of different antihypertensive medications.
May develop sustained HT, higher risk of strokes!
Have patient take pressure outside of office.
- Relationship between CVD and HTN:
- Each inrease of 20/10 doubles risk of CVD, starting at 115/75.
Lower BP can reduce risk of stroke ~40%, MI 25%, HF 50%
Even pre-hypertension has these risks (minus stroke)!
- Good prognostic indicators for HTN:
- microalbuminuria (Bad)
reduced GFR (bad)
- HTN therapy goals:
or <130/80 if DM, chronic kidney disease
- Lifestyle steps to reduce HTN
- Weight reduction
Reduce sodium intake
Moderation of alcohol
DASH eating plan (low sat fat/cholesterol)
- Combined alpha/beta blockers in HTN, drug names and benefits:L
- Carvedilol, labetalol
Alpha 1 blockade reduces SVR by vasodilation.
- Benefits of ARBs over ACEi
- No cough, reduces aldosterone output, can be used in pts with a history of angioedema.
- HTN in African americans
- More prevalent, severe.
Resistant to BBs, ACEi, ARBs
Use CCBs, diuretics.
- General principles of HTN therapy
- Goal – BP < 140/90
Most drugs are equally effective
Start with low doses, slowly titrating BP down
Use formulations that provide 24-hour efficacy... one dose increases compliance
Fewer side effects – combination of drugs with low dose – excellent control
Gradual reduction of BP except in people with severe target organ damage
Start with thiazide, if +20/10 over normal with thiazide, add 2nd agent.
- Light's criteria + albumin addon
- Total protein < .5 serum
LDH < .6 serum
LDH < 2/3 max serum LDH (200)
NOTE: if unsure, add albumin gradient, if serum > 1.2g over pleural fluid, transudate.
- Criteria and 3 underlying causes for hemothorax
- Pleural fluid Hct > 50%
Malignancy, Trauma, pulmonary embolism
- Neutrophilic pleural fluid suggests:
- Eosinophilic (>10%) pleural fluid suggests:
Blood 2ndary to trauma
Drug rx (nitrofurantoin!)
- Basophilic pleural fluid suggests:
- Leukemic involvement of pleural space
- Lymphocytosis (>50%)pleural fluid suggests:
Get a biopsy!
- Low glucose in pleural fluid suggests:
and other rare causes
- High amylase in pleural fluid suggests:
- Pancreatic disease
- Low pH in pleural fluid suggests:
<7 vs 7-7.2 vs >7.2 ?
- Esophageal rupture
Complicated parapneumonic effusion
Tube thoracostomy vs repeat eval looking for falling pH vs no tube necessary.
- Top 6 causes of pleural effusion in order:
Cirrhosis with ascites
- CHF and pleural effusion treatment:
- If no chest pain, fever etc, diuresis and observe. Should go away within 3 days. If not, thoracentesis.
- 4 types of acute respiratory failure
- Type 1: acute hypoxemic (normocapnic)
Type 2: ventilatory (hypercapnic)
Type 3: perioperative
Type 4: shock
- Acute Hypoxemic Respiratory Failure
- Due to airspace filling
Pneumonia, ARDS, puledema
See dyspnea, anxiety
- Ventilatory Respiratory failure
- Alveolar hypoventilation, high dead space
COPD, CVA, ALS
- Perioperative respiratory failure
- Atelectasis due to reduction in FRC with increased closing volume.
- pCO2 formula, normal values of VCO2, alveolar ventilation, pC02
- CO2 production * .863
200ml/min, 4.2L/min, 40mmHg
- A-a gradient calculation, normal value
- AaDO2 = 150 - PaCO2/.8 - PaO2
Normal Age/4 + 4 or less.
- Change in A-a gradient with increase in Fi02
- Increases 5-7mmHg for each 10%.
- Expected PCO2 equation, in terms of bicarbonate:
- 1.5(HCO3) + 8 +-2
If PCO2 is higher than expected, consider SIRS, Sepsis, anxiety, pain etc.
- Overall 5 year mortality of HF:
- Life prolonging medications in HF and who should be on them?
- Ace inhibitors: all patients
B-blockers: all patients
Aldosterone antagonists: all patients with class HF 3-4 in the last 2 months.
Hydralazine-Isosorbide dinitrate: not specified
All of these imply no contraindications or intolerance!
- ACE inhibitors in HF: treatment guidelines
- All patients with asymptomatic LV dysfunction, HF class 1-4, or LVEF < 40%.
Contra: hyperkalemia, angioedema, pregnancy
Use ARB if ACEi not tolerated.
- B-blockers in HF: treatment guidelines
- All patients with asymptomatic LV dysfunction, HF class 1-4, or LVEF < 40%.
Contra: cardiogenic shock, severe reactive airway disease, 2/3rd degree HB
Monitor HR, BP
- Aldosterone antagonists in HF: treatment guidelines
- All patients with Class II to IV HF due to LV dysfunction (LVEF < 0.40).
Contra: hyperkalemia, Cr>2.5/2.0 men/women
MUST MONITOR POTASSIUM AND RENAL FUNCTIONS!
- Role of ICD in heart failure?
- Reduces mortality in patients with LVEF < 35, Class II or III symptoms.
- Role of Resynchronization + ICD in heart failure?
- Reduces mortality in patients with LVEF < 35, QRS > 120 ms, Class III or IV.
- Treatment of stage A HF
- Control risk: treat HT, DM, lipids, CAD, smoking, alcohol
- Treatment of stage B HF
- All stage A methods and...
ACEi + Beta blocker, valve replacement if necessary
- Treatment of stage C HF
- All stage A&B methods and...
hydralazine + isosorbide dinitrite
AICD, pacing if LBBB, valve repair, home oxygen, salt restriction.
- Treatment of stage D HF
- All stage A&B&C methods and...
hBNP infusions for acute decompensation
Mechanical assist devices
- Drugs to avoid in HF
- CCBs, NSAIDS, alcohol, thiazolidinediones
- Two most important things to get if suspect ILD:
Other critical points:
- HISTORY!!! Detail is critical!
OLD CXR!!! Also critical!
Speed of onset, duration of symptoms.
- Traction bronchiecstasis:
- Dilation of the bronchi due to fibrosis. Fibrotic alveoli contract and pull on the walls of the bronchi, dilating them.
- Drugs associated with ILD
- Conditions associated with UIP:
- IPF, CVD, drug toxicity, asbestosis, hypersensitivity pneumonitis
- Chronic fibrosing interstitial pneumonia
UIP histological pattern
NO MEDICAL THERAPY PROVEN TO WORK though cautiously try steroids + azathioprine.
- NSIP. Fibrotic stage
- NSIP cellular stage
- UIP, normal elements to lowerleft.
- Most common rheumatoid arthritis associated ILD?
Others do occur though! UIP, etc.
- Loose granulomas in hypersensitivity pneumonitis
- Loose granulomas in hypersensitivity pneumonitis
- Well formed NCGs in Sarcoidosis.
- 7 causes of lung cancer
Radon exposure -- 10%!
- Pan coast's syndrome
- Usually due to NSLC compressing brachial plexus.
Pain in shoulder, scapula, fingers
Atrophy of hand muscles
- Superior vena cava syndrome
- Lung cancer causes 60-80% of cases, compression of SVC.
Patients commonly experience fullness in the head and dyspnea. Vein distention for collateral to IVC. Resolves with chemo/radiation.
- Paraneoplastic syndromes in lung cancer:
Clubbing and Osteoarthropathy
Deep Vein Thrombosis
Nonbacterial Thrombotic Endocarditis
SIADH (small cell – antidiuretic hormone)
Hypercalcemia (squamous cell - parathyroid)
Cushing’s Syndrome (ACTH)
Neurologic Syndromes (Eaton-Lambert syndrome, retinal blindness, polymyositis, periph. neuropathy)
- Frequent sites of mets in lung cancer?
- Brain, Bone, Liver, Adrenals
- Staging of lunc cancer, NSCLC vs SCLC?
>3cm, nodal involvement
Limited(one hemothorax--30%) or extensive (anything else 70%)
- Palliative measures for stage IV NSCLC
- Photodynamic therapy
Placement of airway stents
- Screening for lung cancer?
- Not recommended. False elevation of 5-yr survival. No real mortality benefits.
- Carcinoid Tumor
- ~1-4% of 1º lung neoplasms
From neuroendocrine cells
Low grade malignancy invade locally, mets uncommon
Mostly 4th decade of life
Commonly in major bronchi
Present with no symptoms, pneumonia, hemoptysis, or focal wheezing
Carcinoid syndrome is rare
Surgical removal gives 5-yr survival of >90%
- Mucoepidermoid Carcinoma
- Rare tumor
Derived from minor salivary gland tissue from proximal tracheobronchial tree
50% of patients aged <30 years
Generally central in location
Patients present with cough, pneumonia, or hemoptysis
Diagnosis by bronchoscopy
Treatment – surgical resection
- Malignant Fibrous Histiocytoma
- Most common sarcoma
Relatively slow growing
If surgically resectable, prognosis is good
Present with symptoms of bronchial obstruction
If surgically resectable, prognosis is good
- Rarely benign.
Latent period 20-40 yrs
No assoc. with smoking!!!!!!
Present with dyspnea or chest pain
Pleural effusion or mass on CXR
Local invasion can occur
Diagnosis –pleural bx
Treatment – surgery, chemo, XRT
- Clinical definition of chronic bronchitis:
- After ruling out all other causes of productive cough...
Presence of productive cough for at least 3 consecutive months in two consecutive years.
- Pathological definition of emphysema:
- enlargement of airspaces distal to terminal bronchioles and destruction of their walls without obvious fibrosis.
- Genetic risk factor to develop COPD?
- alpha-1 antitrypsin deficency... not present to break down elastases that destroy alveoli.
- Natural history of COPD via FEV1:
- Pathogenesis of asthma vs COPD
noxious agent (cigs)
Not completely reversible
- Pathology of chronic bronchitis?
- Mucus and inflammation of large airways.
Repeated cycles of injury of small airways, remodeling, scar, and narrowing.
Destruction of bronchioles, pulmonary capillaries and loss of elastic recoil in parenchyma.
- Smoking history necessary to get COPD symptoms?
- ~20 pack years or longer
- Physical exam findings in COPD:
- Prolonged expiration
Distant breath and heart sounds
Accessory muscle use
Pursed lip breathing
Cor pulmonale signs (edema etc).
- Radiographic signs of COPD
- hyperinflation, flattened diaphragms.
- Role of spirometery in COPD?
- If normal rules out COPD.
Expect decreased FVC and FEV1, with decreased FEV1/FVC ratio.S
- GOLD criteria for staging COPD by FVC and FEV1?
- All require FEV1/FVC < 70%
I: FEV1 > 80% predicted
II: FEV1 50-80% predicted
III: FEV1 30-50% predicted
IV: FEV1 < 30% predicted
- Treatment of COPD by stage?
- Classes of bronchodilators used in COPD
- Short B2 agonists (alburerol)
Long B2 agonists (salmeterol)
- Long term corticosteroids in COPD?
- NOT indicated. No benefits, possible harm.
- Vaccines in COPD?
- Influenza every Fall, lowers mortality by 50%.
Pneumococcal every 5 years. Less benefit than flu.
- Oxygen therapy in COPD?
- Long term administration increases survival! > 15hrs/day
- Indications for O2 therapy
- PaO2 < 55mmHg
SaO2 < 88%
55-60 or 89% if signs of pulmonary HTN, right HF, or PCV.
- Goal of pulmonary rehab? Time length?
- Dealing with non-pulmonary problems
Muscle wasting and weight loss
MUST be 2 months or longer... the longer the better.
- Surgical treatments and requirements for transplantion in COPD?
- Bullectomy, Lung volume reduction surgery, transplantation.
FEV1 < 35% predicted
PaO2 < 55-60 mm Hg
PaCO2 > 50 mm Hg
Secondary pulmonary hypertension
- Only COPD treatment that improves survival?
- Oxygen therapy.
Drugs and surgery merely relieve symptoms.
H1 blocker, competes with histamine.
Hay fever, allergic rhinitus.
Use with caution in asthma... may increase secretions (!cholinergic activity)
- Purpose of COHB (HBCO) on PFts?
- CO poisoning OR smoking!
- Which two pulmonary diseases have increasing prevalence?
- COPD, Asthma
- Atopic vs nonatopic asthma
- Genetic vs ???
Young vs old
IgE vs no IgE
Antigen exposure vs other triggers
positive vs negative skin prick
- Genetically determined state of hypersensitivity to environmental allergens.
Includes rhinitis, asthma, hay fever and eczema.
- Top 4 trigger factors for asthma
- The big 3 in asthma pathophysiology
- Airway inflammation
Smooth muscle dysfunction
- Asthma management A to F
- A - Allergen avoidance & Environmental Control
B - Beta agonists
C - Corticosteroids
D - Other Drugs
E - Education
F - Functional Assessment
- Asthma classification system?
- Step up and Step down in asthma?
- Find the minimum possible drug regimen needed. Step up if not enough, step down by removing the most toxic drug if controlled for several weeks to find threshold.
- Benefits of inhaled corticosteroids in asthma?
- Fewer symptoms
Improved pulmonary function
Decreased airway hyperresponsiveness
Reduced exacerbation frequency and severity
Reduced airway remodeling
- Drugs used in asthma?
- Short and long acting B agonists
Mast cell stabilizers (Cromolyn)
Leukotriene modifying agents (Zafirlukast)
- Recombinant anti-IgE antibody
May help to control symptoms and reduce exacerbations in patients with elevated serum IgE levels
- Immunotherapy in asthma
- S.Q. injection of allergen extracts
Induce immunologic tolerance
related to exposure to an unavoidable allergen to which the patient is sensitive
occur all year or during a major portion of the year
are difficult to control with medication
Treatment requires regular injections for ≥3years
Symptoms improve in most patients
Risk of anaphylaxis
- Peak flow color zone system
- Top 4 causitive organisms for community acquired pneumonia?
- S. pneumoniae (45%)
H. influenzae (10%)
Aspiration pneumonia (10%)
- Aspiration pneumonia: % of CAP, risks, 3 syndromes
- 5-10% of CAP
Risks: Altered consciousness, seizures, dysphagia,age
1. Acid- chemical pneumonitis, sick quick
2.Neutral fluids or solids- mechanical obstruction
3.Infected secretions- pneumonia in 2-5 days
Bugs- oral flora, anaerobes and others
Chest X-rays- dependent segments
- Legionella pneumonia: organism, reservoir, pathogenesis?
- Gram negative rod, aerobic, fastidious
L. pneumophila and others
Water- aerosols, hot water systems, cooling towers
Alveolar macs ingest but can’t kill
Cell mediated immunity key
HIGH mortality 5-25%
Treat with macrolide, quinolone
- Mycoplasma Pneumonia: % of CAP, signs & symptoms, treatment
- 2-30% of hospitalized CAP
Common in children and young adults
Incubation 2-4 weeks, only 3% get pneumonia
“Atypical”- prodrome, dry, persistent cough
Chest X-ray- looks worse than patient does
Complications- hemolysis, CNS, rash
Diagnosis- cold agglutinins, serology, culture
Treatment- macrolide, tetracycline, quinolone
- Chlamydophilia Pneumoniae: % of CAP, signs & symptoms, treatment
- 5-15% of CAP
Mild in young healthy
Worse with reinfection, older, co-morbidity
Coinfection with pneumococcus
Viral URI prodrome, sore throat, then pneumonia
Treatment- macrolide, tetracycline, quinolone
- Inhalational anthrax: epidemiology, diagnostic studies, microbiology, pathology
- Sudden, multiple cases flulike illness, high mortality
Widended mediastinum, gram+ bacilli on smear
Cultures out with large gram +bacilli
Hemorrhagic mediastinitis, meningitis
- Nosocomial Pneumonia: usual organisms, risk factor.
- Gram negatives, staph.
Being on a respirator.
- 3 endemic fungal infections
- Viral Bronchitis
- Most respiratory viruses
Very common- Please hold the antibiotics
- Viral pneumonia
- lung parenchyma
Adults- influenza, Adenovirus types 4, 7
Kids- RSV, parainfluenza, influenza
Elderly, immunocompromised- all of the above
- Influenza virus
- Orthomyxovirus, ss-RNA, types A, B
Type A- H and N antigens- H3N2, H1N1, Bs
Avian H5, H7, H9, horse/dog-H3N8
Antigenic drift, shift(pandemic)
Yearly winter epidemics, varying severity
Affects all ages; M+M in elderly, illnesses
- Influenza clinical presentation
- Incubation 1-2 days, abrupt onset of symptoms
Fever, malaise, myalgia, headache, eye ache
Dry cough, rhinitis, sore throat
Pneumonia- primary viral, secondary bacterial
COPD, Asthma, CHF exacerbation
Myositis/rhabdo, TSS, Reyes (ASA)
DX- clinical, antigens (respiratory), cultures
- Influenza Vaccination
- Prevents illness in ~70-90% of healthy persons <65yo
Elderly persons and persons with certain chronic diseases my develop lower post-vaccination antibody titers
In nursing homes, vaccination can be 60% effective in preventing hospitalization and pneumonia, and 80% in preventing death
Protection against influenza take 2 weeks to develop
Indications: >50 yo,< 2yo, high risk underlying illness, health care workers, household contacts of high risk
Give yearly in fall or before flu season
- Respiratory Syncytial Virus
- Paramyxovirus, ssRNA
Infects all ages, repeated infections
Pneumonia and tracheobronchitis in 6-24 month old
URI and tracheobronchitis in older kids, adults
LRI in elderly and immunocompromised adults
Can treat with Ribavirin...
- Hantavirus Pulmonary Syndrome
- Hantavirus- Bunyaviridae, RNA
Hemorrhagic fever with renal syndrome
Pulmonary- Sin nombre et al, rodent hosts
Zoonosis- inhaled rodent excreta
Since 1993- 234 US cases, 40-60% mortality
Febrile viral prodrome- then pulmonary capillary leak
Rapid hypoxemia, respiratory failure, hypotension
Increased WBC, Hct, atypical lymphs, LFTs
- Severe Acute Respiratory Syndrome-SARS
- Discovered 3/03 Hong Kong, Guangdong 11/02
Novel coronavirus-animal related- palm civets, et al
8437 cases, 813 deaths, adults, HCWs (65% in Canada)
Transmission-?droplets,aerosols,GI; “hyper spreader”
Viral prodrome, progressive pulmonary disease
Neutropenia, lymphopenia,thrombocytopenia,high LDH
Diagnosis- clinical, epidemiologic
Treatment-? Ribavirin, corticosteroids?, ?interferons
- Predominantly infants- 2-10 months, seasonal
RSV- winter, parainfluenza- fall, spring
Viral infection of small bronchi, bronchioles
Epithelial damage, cuboidal non-ciliated cells
Viral URI prodrome, then cough dyspnea
Respiratory distress, wheezes, rales
Predisposes to asthma?
- Affects segmental or subsegmental bronchi
Damaged walls, permanent dilated, plugged
Results from infectious or toxic insult, immune
Ciliary problems- (Kartagener's)
Signs, symptoms, X-rays
- Criteria to diagnosis ACUTE vs CHRONIC leukemia
- FAB: >30% blasts
WHO: >20% blasts
- Acute leukemias vs chronic leukemias
- immature vs mature cells
present vs absent nucleoli
rapidly vs slowly progressive
potentially curable vs incurable
- ALL: WHO classification
- Precursor B-lymphoblastic leukemia/lymphoma (85%)
Precursor T-lymphoblastic leukemia/lymphoma (15%)
Choice between leukemia/lymphoma depends if marrow has > 25% malignant cells = leukemia
3 types: L1, L2, L3
- ALL: T-cell CD patterns
- CD2, CD5, CD7 positive
NOT yet CD3 usually.
Usually CD4/CD8 too...
- ALL: FAB classification
- ALL-L1: small uniform cells
ALL-L2: large varied cells
ALL-L3: large varied basophilic cells with vacuoles (Burkitt's type leukemia... t(8;14) effecting c-myc)
- 4 components of ALL therapy
- remission induction, consolidation, continuation, and treatment of subclinical CNS leukemia
- ALL: drug therapy
- 3-4 drugs, which may include a glucocorticoid, a vincristine, an asparaginase, and an anthracycline
- M0, undifferentiated AML
myeloblasts, little cytoplasm, CD13, CD33. Negative cytochemistries.
- M1, myeloblastic, without maturation.
Small blasts with high N/C ratio
MPO, NASD, Sudan Black Pos.
- M2. Myeloblastic, with maturation.
More mature leukemic cell
Auer rods present
Good prognosis with t(8;21)
t(8;21) is 15% of AML
Cytochemisties strong positive
- M3. Promyelocytic.
Moderate N/C ratio
Prominent cytoplasmic granules
- Treatment of AML M3.
- All Trans Retinoic Acid (ATRA)
Vitamin A analog
Induces cell differentiation
Improved with demethylation
- M4, Myelomonocytic
Contains granulocytic and monocytic cells
7-10% of AML.
- M4eo. Myelomonocytic together with bone marrow eosinophilia.
Inv(16) or t(16;16).
Breakpoint at 16q22.
Involves the CBFb gene (normally bound to AML1, the gene involved in M2 AML).
Subtype of AML
- M5, Acute Monoblastic
Moderate amount of cytoplasm
Very prominent nucleoli
Faint or no granules
M5a monoblastic, M5b promonocytic
- M6 Acute Erythroblastic
5% of AML.
Often associated with deletions in chromosomes 5 and 7.
Poorer prognosis, often preceded by myelodysplastic syndrome.
Seen in older patients.
- M7 Megakaryoblastic
Variably faint granules
Trisomy 21, inversions or translocations of chromosome 3, t(9;22); t(1;22) in infants.
Also seen in Klinefelter’s syndrome XXY.
- WHO AML classifications?
- Acute Myeloid Leukemia with Recurrent Genetic Abnormalities
Acute Myeloid Leukemia with Multilineage Dysplasia
Acute Myeloid Leukemia and MDS, Therapy-Related
Acute Myeloid Leukemia, NOS
- Rituxan® was the first monoclonal antibody found to be effective and safe for the treatment of lymphomas in the US. While it was aimed more at indolent lymphomas, it is now being used to treat aggressive CD20+ lymphomas and leukemias.
- monoclonal antibody that targets the CD20 antigen and is linked to the radioisotope 90Yttrium
- Survivorship issues in cancer and specifically leukemias.
- fatigue; cognitive changes; body image; sexual health and functioning; infertility; fear of recurrence; PTSD and stress syndromes; family/caregiver distress; socioeconomic issues; and distress, anxiety, and depression
- Composition of hemoglobins:
% of each in an adult
- alpha2, beta2 95%
alpha2, delta2 3.5%
alpha2, gamma2 1%
- Macrocytic anemias?
- MCV < 80: iron def, chronic blood loss, sideroblastic, thalassemias
MCV > 100: folate, B12, alcohol, hepatic disease
Norm: Chronic disease, hemolytic, hemoglobinopathies, early iron def, red cell membrane disorders
- Retic Production Index:
- retic count x (HCT/45)
times .5 if polychromatic??
Normally 2-3... < 2 suggests insufficent response to anemia
- Warm vs cold hemolytic anemias
- Warm (IgG): idiopathic (primary), drug-associated, systemic lupus erythematosus, malignant neoplasms
Cold (IgM): mycoplasmal infection, EBV infection
- Total body iron amount and distribution:
Functional pool: 60% Hg, 10%myoglobin
Storage pool: 29% ferritin, hemosiderin
Plasma: 1% bound to transferrin for transport
- Red tongue, glossitis?
- One amoung many symptoms of B12 or folate deficiency
B12/folate def leads to impaired DNA synthesis in RBC precursors. Due to lack of cofactors in converting dTMP to dUMP
- Schilling test, 2 parts
- part 1: oral radiolabeled B12, large B12 dose IM. Looking for excretion in urine to check absorption... (5-35% excreted)
Part 2: Same exact thing but give IF with oral dose. If urine B12 output corrects was pernicious anemia.
- Sideroblastic anemia
- Although adequate iron is present, a mitochondrial defect (decreased activity of D-ALA or ferrochelatase) prevents the incorporation of iron into hemoglobin.
Iron accumulates in mitochondria ringing the red cell nucleus forming "ringed sideroblasts".
Seen in myelodysplasia, alcohol, lead, drug ingestion.
How's the marrow look?
How's the marrow look?
- Pathology of WAIHA
- Most common form of AIHA, active at 37 C
Half are idiopathic, half are secondary:
Often IgG, rarely IgA that coats the RBC surfaces
Antibody Fc fragment get caught by monocytes/macrophages in spleen and liver
Partial phagocytosis leading to spherocyte formation
The spleen then clears the spherocytes
Presented as extravascular hemolysis
- Pathology of CAIHA
- IgM antibody, do not react at 37 C, most active at 0-4 C,
Not typically cause clinically significant hemolysis, but chronic low-grade hemolysis
RBC destruction by activating complement on the RBC surface (lysis); the C3b fragments on the surface lead to phagocytosis by monocytes/macrophages.
Positive DAT or agglutination on peripheral blood
Seen in mycoplasma pneumonia or infectious mononucleosis
Idiopathic condition or in association with lymphoproliferative disorders
Increase reticulocytes, RBC agglutinates
What's going on here?
- WAIHA. Sphereocytes due to macrophates in spleen.
What's going on here?
- CAIHA. RBC agglutination due to C3 and IgM
- Direct and indirect Coombs test?
(ALSO CALLED DAT/IAT for direct antiglobulin test)
- Direct: patients RBCs + anti-IgG. If it agglutinates, IgG must have been on the RBCs.
Indirect: patients serum + clean RBCs + anti-IgG. If it agglutinates, IgG must have been in patient's serum.
- Different labs seen in intravascular vs extravascular hemolysis:
- Intravascular has positive urine hemosiderin and hemoglobin, and a negative DAT. Extravascular is the opposite.
Findings and disease?
- Bite cells, Heinz bodies.
- Alpha and beta thalassemias: genotypes
- B-Thal major: B0/B0 or B+/B+
B-Thal inter: B0/B or B+/B+
B-Thal minor: B0/B or B+/B
Hydrops fetalis: -/- -/-
Hb H disease: A/- -/-
Silent carrier: A/A/A/-
- Lipid disorders:
- Familial hypertriglyceridemia: triGs
Familial combined hyperlipidemia: triGs, LDL, premature CAD
Familial hypercholesterolemia: LDLs, premature CAD
Low HDL: HDL duh. Diabetes and metabolic syndrome often present.
- LDL response to diet?
What is a good diet for hyperlipidemia?
- Drop by ~8%
Avoid trans-fatty acids -- increases LDL decrease HDL.
Add fiber, sterol ester margerines.
Add fish and omega 3 fatty acids.
No evidence to support vitE or beta carotene as helping!!
- Benefit of weight loss and exercise in hyperlipidemia:
- Lowers TG, raises HDL-C, reduces risk of diabetes.
- Diagnostic criteria for metabolic syndrome
TriGlyc > 150 mg/dL
HDL-C < 40mg/dL
BP > 130/85
Fasting glucose > 110 mg/dL
- ATP risk categories, LDL treatment goals and when to use drugs?
- HIGH RISK CHD history or risk: <100mg/dL >130mg/dL
MODERATE RISK 2+ risk factors: <130mg/dL, 160mg/dL
LOW RISK <2 risk factors: <160mg/dL, >190mg/dL
- MOA of statins?
- Reduce hepatic cholesterol synthesis by blocking HMG-CoA reductase, lowering intracellular cholesterol, which stimulates upregulation of LDL receptor and increases the uptake of non-HDL particles from the systemic circulation.
- Adverse effects of statins?
- Headache, GI intolerance
Elevated liver enzymes
Myopathy-- requires discontinuation in 0.4% of pts.
- MOA of bile acid resins?
- Bind bile acids in the intestine, which reduces the enterohepatic recirculation of bile acids. This promotes the upregulation of 7-alpha hydroxylase and the conversion of more cholesterol in the hepatocyte into bile acids. This decreases the cholesterol content in the hepatocyte, which enhances LDL-receptor expression, which in turn increases the removal of LDL and VLDL remnant particles from the circulation
- Adverse effects of bile acid resins?
- GI intolerance
Drug interactions: binds other negatively charged drugs... must give other drugs at least 1 hr before or 6 hrs after BARs.
- MOA of nicotinic acid?
- Niacin appears to exert its effects by inhibiting lipoprotein synthesis and decreasing the production of VLDL particles by the liver. It inhibits the peripheral mobilization of free fatty acids, thus reducing hepatic synthesis of triglycerides and the secretion of VLDL. LDL is made from VLDL so it is also decreased.
- Adverse effects of nicotinic acid?
- Flushing, itching, headache (immediate-release)
Hepatotoxicity, GI (sustained-release)
Activation of peptic ulcer
Hyperglycemia and reduced insulin sensitivity
DO NOT GIVE IN LIVER OR PEPTIC ULCER DISEASE.
- Benefits of fish oils?
- Lowers triGs 30-40%
BUT may increase LDLs.
Best in hypertriglyceridemia!
- Churg-Strauss Syndrome
- Allergic angiitis and granulomatosis
Infiltration of tissues by eosinophils
Lung involvement is predominant with a strong association with asthma
Severe asthma attacks and pulmonary infiltrates
- Virchow's triad and other risk factors for PE?
- Trauma, stasis and hypercoagulopathy.
Hormone replacement therapy.
Age, smoking, genetics, surgery.
NOT DIABETES, NOT hyperlipidemia!
- EKG sign of PE (not always present!!)
Large S wave in lead I
Large Q wave in lead III
Inverted T wave in lead III
- D-dimer in pulmonary embolism?
- NEGATIVE test rules out PE.
Positive test requires MORE testing (V/Q scan or contrast CT, venous ultrasound, pulmonary angiograhy -- gold standard but .5% mortality so use only other tests don't rule in/out)
- Therapy for pulmonary embolism?
- Heparin: get PTT to 2 times normal within 24 hours
LMWH: as good as heparin, safer
Warfarin: !pregnancy, INR 2-3, overlap with heparin for 3 days.
Therapy for 3-6 months if first PE. 12 months if hypercoagulopathy. Lifelong if any recurrance of PE.
- Role of thrombolytic therapy in PE?
- Very little: does not change mortality.
Indicated only in MASSIVE PE with hemodynamic instability and hypoxemia.
- IVC filters used when?
- PE with contraindication to anticoag therapy. Patients with recurrant PE. Other recurrent thromboembolic problems.
- Numerical definition of pulmonary hypertension
- Mean PAP at rest > 25.
Mean PAP exercise > 30.
Normal is 10-20.
- Conditions associated with primary pulmonary HTN?
- Connective tissue disease (SLE, mixed connective tissue, Scl)
Portal hypertension & liver disease
Toxins (L-tryptophan, rapeseed oil)
- Treatment of PPH?
- Chronic anticoagulation
Vasodilators: calcium channel blockers, Epoprostenol infusion
Endothelin receptor antagonist (Bosentan)
- Proteins in the blood?
- MGUS criteria?
- Monoclonal gammopathy:
IgG < 35 g/L; IgA < 20 g/L
BJ Protein <1.0 g/L
<10% plasma cells in marrow.
No bone lesions, no anemia, renal failure, hypercalcemia. NO SYMPTOMS. But may develop into malignancies.
- Risk factors for MGUS developing into malignancy?
- Higher initial concentrations of Ig.
IgM or IgA riskier than IgG
Kappa MAY be riskier than lambda.
- Polyclonal gammopathy... causes?
- Liver, Lymphomas, Cancer, Infection, connective tissue diseases...
- Smoldering Multiple Myeloma (SMM) criteria?
- Monoclonal gammopathy:
IgG > 35 g/L; IgA >20 g/L
BJ Protein >1.0 g/L
10-20% plasma cells in marrow
No lytic lesions, no renal/anemia/hypercalcemia. Track, no treatment.
- Solitary plasmacytoma of bone criteria?
- Solitary bone lesion
Histologically proven plasmacytoma
Bone Marrow: normal <5%
No anemia, renal failure or hypercalcemia
M-Protein IgG < 35 g/L IgA <20 g/L*
BJP < 1g/24h*
Give RADIOTHERAPY to single lesion! Must MRI spine!
- Extra-Medullary Plasmacytoma (EMP) criteria?
- Solitary biopsy proven lesion
Bone Marrow (distant site) normal <5%
M-Protein same as SPB (normal or slightly elevated)
No anemia, renal failure or hypercalcemia
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