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An acute lower respiratory tract illness (inflammation of lung parenchyma) associated with fever, symptoms and signs in the chest and abnormalities on the chest x-ray.

1. Increased risk of exposure


Crowded places like Prisons


3. Defective complement function

Defective bacterial clearance

a. Congenital asplenia, hyposplenia

b. Splenectomy

c. Sickle cell disease

2. Respiratory infection, inflammation

4. Multifactorial conditions

a.   Influenza, other viral respiratory infections
b.   Air pollution
c.   Allergies
d.   Cigarette smoking
e.   COPD
f.    Defective antibody formation
g.   Common variable hypogammaglobulinemia
h.   Selective IgG subclass deficiency
i.    Multiple myeloma
j.     CLL
k.   Lymphoma

a.   Infancy & Aging
b.   Alcoholism
c.   Malnutrition
d.   HIV infection
e.   Glucocorticoid treatment
f.    Cirrhosis of liver
g.   Renal insufficiency
h.   Diabetes mellitus
i.    Anemia



Important Points:


Classification and causes of pneumonia

  1. Community-acquired pneumonia (CAP) may be primary or secondary to underlying disease.
    1. Streptococcus pneumoniae is the commonest cause Q, followed by Haemophilus influenzae Q and Mycoplasma pneumoniae Q. Moraxella catarrhalis.
    2. Staphylococcus aureus, Legionella species, and Chlamydia
    3. Gram negative bacilli, Coxiella burnetii and anaerobes are rare.
    4. Virus account for up to 15%.
  2. Hospital acquired (nosocomial) (>48hrs (MCQ) after hospital admission). Most common Gram negative Q enterobacteria or Staph aureus. Pseudomonas Q, Klebsiella Q, Bacteroides Q, Clostridia Q.
  3. Aspiration Those with stroke, myasthenia, bulbar palsies, consciousness (postictal or drunk), oesophageal disease (achalasia, reflux), or with poor dental hygiene, risk aspirating oropharyngeal anaerobes Q.
  4. Immunocompromised patient: Strep. pneumoniae Q, H. influenzae Q, Staph. aureus Q, M. catarrhalis Q, M. pneumoniae Q, Gram -ve bacilli Q and Pneumocystis jiroveci (formerly named P. carinii,). Other causes are fungi, viruses (CMV, HSV), and mycobacteria. 

Clinical features Symptoms: Fever, rigors, dyspnoea, purulent sputum, hemoptysis, and pleuritic pain.

: Fever, cyanosis, confusion (may be the only sign in the elderly), tachypnoea, tachycardia, hypotension


Signs of consolidation

  1. Diminished chest expansion,    
  2. Trachea is central
  3. Dull percussion note,                
  4. Increase vocal fremitus/vocal resonance      
  5. Bronchial breathing

Core adverse features: 'CURB - 65' score:

  1. Confusion:                       
  2. Urea >7mmoI/L (7 x 2.8 = 19.6 mg%)
  3. Respiratory rate > 30/min       
  4. BP <90 systolic and/or <60mmHg diastolic)      
  5. Age > 65.


0-1 = home treatment possible           
2 = Hospital Therapy    
3 = Indicates severe pneumonia.

Important Points:


Other features increasing the risk of death are:

  1. Co-existing disease (DM)                 
  2. Bilateral multi lobar involvement
  3. PaO2 <60 mmHg                             
  4. Oxygen saturation <92%.  


  1. Antibiotics
  2. Oxygen keep PaO2 >8.0 and/or saturation 0.92%.
  3. IV fluids (anorexia, dehydration, shock).

Causes of recurrent pneumoniae in the same segment

  1. Foreign body            
  2. Sequestration of lung           
  3. Neoplasm       
  4. Bronchiectasis 

Specific Pneumonias

  1. Staphylococcal pneumonia
    1. It may complicate influenza Q infection or occur in the children Q, elderly Q, intravenous drug users Q or patients with underlying disease (eg leukemia Q, lymphoma Q, cystic fibrosis Q, (CF).
    2. It causes a bilateral CXR pneumatocele cavitation Q bronchopneumonia & pneumothorax.
    3. Treatment: flucloxacillin Q. MRSA: vancomycin Q.
  2. Pneumococcal pneumonia  
    1. It is the commonest Q cause of community acquired bacterial pneumonia.
    2. It affects all ages, but is commoner in the elderly Q, alcoholics Q, post-splenectomy Q, immuno­suppressed Q, and patients with chronic heart failure Q or pre-existing lung disease Q.
    3. Clinical features: fever, pleurisy, herpes labialis Q. Rusty sputum & features of consolidation on clinical examination.
    4. CXR shows lobar consolidation
    5. Treatment: amoxicillin Q, benzylpenicillin Q, or cephalosporin Q.
Extra Edge  Clinical features of consolidation
  1. Trachea is central
  2. Reduce chest expansion on same side
  3. Dull on percussion
  4. Increase vocal fremitus and vocal resonance
  5. Bronchial breathing (Tubular breathing) (LQ 2012).


Extra Edge  Types of bronchial breathing:
  1. Tubular – Low pitch, heard in consolidation. (LQ 2012)
  2. Cavernous – High pitch heard in cavity.  (LQ 2012)
  3. Amphoric – Metallic quality, heard in tension pneumothorax
  4. Klebsiella pneumonia (Frielander’s pneumonia).
    1. Occurs in elderly Q, diabetics and alcoholics Q
    2. Causes a cavitation pneumonia Q, particularly of the upper lobes, chocolate colour sputum.
    3. Treatment: cefuroxime Q. Aminoglycoside
  5. Pseudomonas pneumonia
    1. It is a common pathogen in bronchiectasis Q and Cystic Fibrosis Q.
    2. It also causes hospital acquired infections Q.
    3. Treatment: anti pseudomonal penicillin, ceftazidime, meropenem, or ciprofloxacin.


Table 257-4 Empirical Antibiotic Treatment of Community-Acquired Pneumonia (Ref. Hari. 18th ed., Pg-  2135) 

  1. Outpatients
    1. Previously healthy and no antibiotics in past 3 months
      1. A macrolide [clarithromycin or azithromycin
      2. Doxycycline
    2. Comorbidities or antibiotics in past 3 months: select an alternative from a different class
      1. Respiratory fluoroquinolone [moxifloxacin, gemifloxacin, levofloxacin
      2. β-lactam – ceftriaxone,  cefpodoxime, cefuroxime plus a macrolide
  2. Inpatients, Non-ICU
    1. A respiratory fluoroquinolone [moxifloxacin,  gemifloxacin, levofloxacin.
    2. β-lactam [cefotaxime, ceftriaxone, ampicillin, ertapenem] plus a macrolide [oral clarithromycin or azithromycin.
  3. Inpatients, ICU
    1. β -lactam [cefotaxime, ceftriaxone, ampicillin-sulbactam] plus
    2. Azithromycin or a fluoroquinolone
  4. Special Concerns
    1. If Pseudomonas is a consideration
      1. [Piperacillin/tazobactam, cefepime, imipenem, meropenem] plus either ciprofloxacin or levofloxacin
      2. The above β-lactam plus an aminoglycoside [amikacin or tobramycin and azithromycin]
      3. The above β-lactam plus an aminoglycoside plus an antipneumococcal fluoroquinolone
    2. If CA-MRSA is a consideration
      1. Add linezolid or vancomycin.

Atypical Pneumonia

Causes of Atypical pneumonias

  1. Mycoplasma pneumonias
  2. Viral pneumoniasa.
    1. Influenza
    2. RSV
    3. Adenovirus
    4. Rhinovirus
    5. Rubeola
    6. Varicella
    7. Corona virus
  3. Chlamydia pneumonia     
  4. Coxiella burnetii   
  5. Pneumocystis               
  6. Legionella 
  1. Legionella pneumophila
    1. Colonizes water tanks Q kept at <60°C (eg air cooling system Q) causing outbreaks of Legionnaire's disease.
    2. It is type of interstitial pneumonia.
    3. 'Flu-like symptoms (fever, malaise, myalgia) precede a dry cough Q and dyspnoea
    4. Extra-pulmonary features include anorexia, Diarrhea & Vomiting, hepatitis Q, renal failure Q, confusion and coma Q.
    5. IP: 2 – 10 day
    6. CXR shows bi-basal opacity.
    7. Blood tests may show lymphopenia Q hyponatremia, and deranged LFTs Q.
    8. Urinalysis may show hematuria.
    9. Diagnosis: Legionella serology/urine antigen.
    10. Treatment: clarithromycin rifampicin Q, fluoroquinolone Q.
Extra Edge:
  1. In legionella infection, commonest organ system involved is GIT & NOT respiratory!!!) (FAQ)
  2. Legionella micdadei is another species in this group. It is AFB positive organismQ. It is also known as Pittsburg pneumonia agent Q.
  1. Mycoplasma pneumoniae:
    1. It can occurs in epidemics Q.  
    2. It presents insidiously with 'flu-like symptoms (headache, myalgia, arthralgia) followed by a dry cough Q.
    3. Patient may not Q have any clinical finding on auscultation because its type of interstitial pneumonia Q
    4. CXR shows bilateral patchy consolidation.
    5. Diagnosis: mycoplasma serology.
Extra Edge : 

Cold agglutinins may cause an Coombs positive autoimmune haemolytic anaemia Q (LQ 2012)


  1. Skin rash: erythema multiforme, Stevens-Johnson syndrome        
  2. Meningoencephalitis or myelitis
  3. Guillain-Barre syndrome.

Treatment Erythromycin Q /clarithromycin or Doxycycline.

  1. Chlamydia pneumoniae
    1. Person to person spread occurs causing a biphasic illness Q: pharyngitis, hoarseness, otitis followed by pneumonia. Horder’s spots on the term Q.
    2. Diagnosis: Chlamydia serology (non-specific).
    3. Treatment: doxycycline
      1. Alternative agent      
      2. Erythromycin               
      3. Clarithromycin   
      4. Azithromycin   
      5. Fluoroquinolone
  2. Chlamydia psittaci
    1. It causes psittacosis, an ornithosis acquired from infected birds Q (typically parrots).
    2. Symptoms include headache, fever, dry cough, lethargy, arthralgia, anorexia, and D&V.
    3. Extra-pulmonary features are rare
      Meningoencephalitis Q, infective endocarditis Q, hepatitis Q, nephritis Q, rash Q, splenomegaly Q
    4. CXR shows patchy consolidation.
    5. Diagnosis: Chlamydia serology.
    6. Treatment tetracycline.
  3. Viral pneumonia The commonest cause is influenza Q. Other viruses that can affect the lung are: measles, CMV, and varicella zoster.
  4. Pneumocystis pneumonia (PCP)
    1. It causes pneumonia in the immunosuppressed Q (HIV). ) as well as in COPD cases (Harrison, 18th edition, Page 1671).
    2. The organism responsible was previously called pneumocystis carinii Q, and now called pneumocystis jiroveci
    3. It presents with a fever, dry cough & exertional dyspnoea (LQ 2012)
    4. CXR may be normal or show bilateral perihilar interstitial shadowing.
    5. Persons at risk for Pneumocystic disease (Pneumocystosis)
      1. AIDS
      2. Patients Receiving immunosuppressive therapy.
      3. Children with primary immunodeficiency diseases
      4. Premature malnourished infants (immunodeficient)
      5. Pneumocystic Pneumonia: Diagnosis
      6. COPD 

Clinical features of pneumocystis Carinii pneumonia 
  1. 2-3 week history
  2. Fever with dry cough
  3. Disproportionate breathlessness
  4. No response to standard antibiotics
  5. Few signs on auscultation
  6. Exercise – related desaturation

Pneumocystic Pneumonia: Diagnosis


Diagnosis Pneumocystic Pneumonia is based on specific identification of organism in respiratory specimen with appropriate histological staining

  1. Usually diagnosed by sputum examination
  2. Sputum samples should always be obtained by induction (with hypertonic saline)
  3. Routine sputum specimen is often inadequate
  4. BAL forms the mainstay of diagnosis for Pneumocystic Pneumonia

Important Points:

  1. If organisms are not seen on induced sputum examination a Bronchoalveolar lavage specimen should be obtained. BAL forms the mainstay of diagnosis for Pneumocystic Pneumonia
  2. Sputum <BAL<Biopsy

Pathogenesis and Pathology (Ref. Hari. 18th ed., pg - 1671)

  1. Pneumocystis commonly colonizes patients who are immunosuppressed or who have chronic obstructive pulmonary disease.
  2. Pneumocystic carinii pneumonia is characterized by a prominent eosinophilic Alveolar exudates and mild interstitial pneumonitis.
  3. These is damage to type I pneumocytes and associated compensatory hypertrophy of type II pneumocytes.
  4. The host factors that predispose to the development of PcP include defects in cellular and humoral immunity. The risk of PcP among HIV-infected patients rises markedly when circulating CD4+ T cell counts fall below 200/µL.
  5. The principal host effector cells against Pneumocystis are alveolar macrophages, which ingest and kill the organism, releasing a variety of inflammatory mediators. Proliferating organisms remain extracellular within the alveolus, attaching tightly to type I cells. Alveolar damage results in increased alveolar-capillary permeability and surfactant abnormalities, including a fall in phospholipids and an increase in surfactant proteins A and D.
  6. The alveoli are filled with a typical foamy, vacuolated exudate. Severe disease may include interstitial edema, fibrosis, and hyaline membrane formation. The host inflammatory changes usually consist of hypertrophy of alveolar type II cells, a typical reparative response, and a mild mononuclear cell interstitial infiltrate.
  7. Malnourished infants display an intense plasma cell infiltrate that gave the disease its early name: interstitial plasma cell pneumonia.

Differences between PCP infection in adult & infant

Pneumocystic pneumonia in Adults

Pneumocystis pneumonia in malnourished infants

In adults the disease appears to be predominantly alveolar


Air spaces (alveoli) are filled with a foamy, eosinophilic exudate and appear honey coombed The intra-alveolar exudate consists of organisms, surface glycoprotein exudate and debris of macrophages and inflammatory cells.

In infants the disease has a predominant interstitial component


The interstitium is filled with fluid plasma cells and lymphocytes.


These formed elements seem to overflow into air spaces which are filled with a frothy eosinophilic exudates.


Drugs used for treatment of pneumocystic carinii infection include:




First choice drug

Second choice

Third choice


Pneumocystis carinii

Mild to moderate pneumonia

Trimethoprim sulfamethoxazole

Trimethoprim – Dapsone

Clindamycin – Primaquine


Sever pneumonia

Trimethoprim sulfamethoxazole


Clindamycin – Primaquine



Indications for prophylaxis against Pneumocystic carinii

  1. An absolute CD4 count <200/μL (CD4 percentage <20%) (Primary prophylaxis)
  2. Oropharyngeal candidiasis (Primary prophylaxis)
  3. Prior Pneumocystic carinii pneumonia (Secondary prophylaxis)
  4. Children born to mothers with HIV infection should receive prophylaxis with trimethoprim-sulfamethoxazole (TMP-SMX) beginning at age 4-6 weeks.
  5. Children who are determined to be HIV positive through the first year of life, then as determined by age-specific CD4 levels, should receive prophylaxis.
  6. Prophylaxis may be discontinued in patients with HIV infection whose CD4 count > 200/µL for 3 consecutive months while on highly active antiretroviral therapy (HAART). Prophylaxis should be restarted if the CD4 count drops below 200/µL.
  7. Prophylaxis should be continued for life in patients who developed PCP while their CD4 level exceeded 200/µL. 
Chemoprophylaxis regimens
  1. TMP-SMX is the agent of choice for PCP prophylaxis.
  2. Dapsone is given with pyrimethamine
  3. Atovaquone
  1. Avian influenza
    Avian-to-human transmission the H5N1 strain of influenza A causes serious infection in humans with a 50% mortality.

Treatment: Oseltamivir Q (Tamiflu).



Recent advances

Zanamivir, Oseltamivir, and Peramivir

  1. These are inhibitors of the influenza viral neuraminidase enzyme, which is essential for release of the virus from infected cells and for its subsequent spread throughout the respiratory tract of the infected host.
  2. Zanamivir and oseltamivir are used for PROPHYLAXIS and treatment of influenza.

Differences between typical & atypical pneumonia


AIR space pneumonia (Typical pneumonia)

Interstitial pneumonia (Atypical pneumonia)

Exudate in alveoli i.e. consolidation

No exudate, alveoli are air filled i.e. no consolidation (infiltrate in interstitium)

Infiltrate is primarily of neutrophils (PMN)

Infiltrate is primarily lymphocytic

Agents responsible are extracellular

Agents responsible are intracellular

Cough is productive of purulent sputum

Cough is dry

Chest X-ray shows alveolar pattern

Chest X-ray shows interstitial pattern

  1. Aspiration pneumonitis is characterized by an acute onset of dyspnea, tachypnea (M/C feature), bronchospasm and cyanosis with a chest radiograph often showing diffuse opaciti

Treatment of Sepsis

Table : Initial Antimicrobial Therapy for Severe Sepsis with No Obvious Source in Adults with Normal Renal Function (Ref. Hari. 18th ed., Table 271.3 Pg- 2229)

Clinical Condition

Antimicrobial Regimens (Intravenous Therapy)

Immunocompetent adult

1. ceftriaxone or ticarcillin-clavulanate or piperacillin-tazobactam
2. imipenem-cilastatin or meropenem or cefepime.
3. Gentamicin or tobramycin may be added to either regimen.
4. ciprofloxacin or levofloxacin plus clindamycin. 


Neutropenia (<500 neutrophils/mL)

1. imipenem-cilastatin or meropenem or cefepime
2. ticarcillin-clavulanate or piperacillin-tazobactam plus tobramycin.
3. vancomycin should be added

a. if the patient has an infected vascular catheter,
b. if staphylococci are suspected,
c. if the patient has received intensive chemotherapy that produces mucosal damage,
d. if the institution has a high incidence of MRSA infections, 


a. Cefotaxime or ceftriaxone b. vancomycin plus ciprofloxacin c. levofloxacin or aztreonam

IV drug user

a. Nafcillin or oxacillin plus gentamicin. If the local prevalence of MRSA is high or if the patient is allergic to beta-lactam drugs, vancomycin with gentamicin should be used.


a. Cefepime, ticarcillin-clavulanate, or piperacillin-tazobactam plus tobramycin

b. Ciprofloxacin or levofloxacin plus vancomycin plus tobramycin.

Table 152-2 Antibiotic Treatment of Infections Due to Pseudomonas Aeruginosa
  1. Bacteremia
    1. Non-neutropenic host –
      1. Ceftazidime
      2. Cefepime
      3. Piperacillin / tazobactam  
      4. imipenem
      5. meropenem
      6. doripenem
      7. Amikacin.
    2. Neutropenic host –  Cefepime or all other agents (except doripenem) as mention above.
    3. UTI – Ciprofloxacin or levofloxacin.
    4. Multidrug – resistant P. aeruginosa infection – Colistin for the shortest possible period to obtain a clinical response.
Recent Advances
  1. Ceftaroline is a 5th Generation cephalosporin. It is being used in the treatment of Skin and soft tissue infections; MRSA, community acquired bacterial pneumonia. (It is not given in 18th edition of Harrison!!!) 
  2. Doripenem / Faropenem / Ertapenem are the new carbapenems, they are being used in Serious infections
Extra Edge:

Severe acute respiratory syndrome (SARS) is caused by SARS-COV virus-a coronavirus Q. (AIIMS Nov 2012)

  1. Major features are persistent fever >38°centigrade, chills, rigors, myalgia, dry cough Q, headache, diarrhea, and dyspnea-with an abnormal CXR and leukopenia Q.
  2. Respiratory failure Q is the big complication.
  3. The mechanism of transmission of SARS-COV is only by close contact Q with other patients.
  4. Management is supportive.

Complications of pneumonia
  1. Respiratory failure : Type 1 respiratory failure is relatively common.
  2. Hypotension may be due to a combination of dehydration and vasodilatation due to sepsis.
  3. Atrial fibrillation is quite common, particularly in the elderly.
  4. Pleural effusion
  5. Empyema is pus in the pleural space.
    Bacterial pneumonia are the most common cause of empyema.
  6. Lung abscess is a cavitation area of localized, suppurative infection within lung.
  7. Pericarditis and myocarditis may also complicate pneumonia.
  8. Jaundice: This is usually cholestatic, and may be due to sepsis or secondary to antibiotic therapy (particularly flucloxacillin and co-amoxiclav).
  9. Meningitis
  10. Septicemia and septic shock.


Table: Definitions used to describe the condition of septic patients


Presence of bacteria in blood, as evidenced by positive blood cultures


Presence of microbes or their toxins in blood

Systemic inflammatory response syndrome (SIRS)

(May be infectious or non -infectious etiology) (MCQ, AIPG 09)

Two or more of the following conditions (LQ 2012)

1. Fever (oral temperature >38oC) or hypothermia (<36oC)

2. Tachypnea (>24 breaths/min)

3. Tachycardia (heart rate >90 beats/min)

4. Leukocytosis (>12,000/mL), leukopenia (<4000/mL), or >10% bands; may have a noninfectious etiology.


SIRS that has a proven or suspected microbial etiology

Severe sepsis (similar to *sepsis syndrome)

Sepsis with one or more signs of organ dysfunction – for example:

1. Cardiovascular: BP 90 mmHg or mean arterial pressure 70 mmHg that responds to administration of intravenous fluid.

2. Renal: Urine output <0.5 mL/kg per hour for 1h despite adequate fluid resuscitation

3. Respiratory: Pao2/FlO2 250 or, if the lung is the only dysfunctional organ, 200.

4. Hematologic: Platelet count <80,000/mL

5. Unexplained metabolic acidosis:

6. Adequate fluid resuscitation: Pulmonary artery wedge pressure 12 mmHg or central venous pressure 8 mmHg.

Septic shock

Sepsis with hypotension BP <90 mmHg systolic or 40 mmHg less than patients normal blood pressure) for at least 1 h despite adequate fluid resuscitation; or Need for vasopressors to maintain systolic blood pressure 90 mmHg or mean arterial pressure 70 mmHg

Refractory septic sock

Septic shock that lasts for >1 h and does not respond to fluid or pressor administration.

Multiple-organ dysfunction syndrome (MODS)

Dysfunction of more than one organ, requiring intervention to maintain hemostasis.


Recent Advances:

  1. Procalcitonin (PCT) is a  precursor of the hormone calcitonin. It is produced by parafollicular cells (C cells) of the thyroid and by the neuroendocrine cells of the lung and the intestine.
  2. The level of procalcitonin in the blood stream of healthy individuals is below (10 pg/mL). 
  3. The level of procalcitonin rises up to 100 ng/ml in a response to a proinflammatory stimulus, especially of bacterial origin.
  4. It does not rise significantly with viral or non-infectious inflammations.  

USE for Diagnosis and prognosis of sepsis

  1. Measurement of procalcitonin can be used as a marker of severe sepsis caused by bacteria and generally grades well with the degree of sepsis.
  2. PCT has the greatest sensitivity (85%) and specificity (91%) for differentiating patients with  SIRS from those with bacterial sepsis, when compared with non bacterial sepsis. 

Pathophysiology of Septicemia 

  1. Endothelial injury (Ref. Hari. 18th ed.,  Pg - 2224)  
    1. Vascular endothelial injury as the major mechanism for multiorgan dysfunction.
    2. Leukocyte-derived mediators and platelet-leukocyte-fibrin thrombi may contribute to vascular injury.
    3. TNF-alpha induce vascular endothelial cells to produce and release cytokines, procoagulant molecules, platelet-activating factor (PAF), nitric oxide, and other mediators.
    4. In addition, regulated cell-adhesion molecules promote the adherence of neutrophils to endothelial cells.
    5. Endothelial cell activation can also promote increased vascular permeability, microvascular thrombosis, DIC, and hypotension.
    6. Tissue oxygenation may decrease as the number of functional capillaries is reduced by luminal obstruction due to swollen endothelial cells, decreased deformability of circulating erythrocytes, leukocyte-platelet-fibrin thrombi, or compression by edema fluid.
  2. Septic Shock
    1. The hallmark of septic shock is a decrease in peripheral vascular resistance that occurs despite increased levels of vasopressor catecholamines. Systolic BP <90 mmHg.
    2. Before this vasodilatory phase, many patients experience a period during which oxygen delivery to tissues is compromised by myocardial depression, hypovolemia, and other factors.
    3. During this "hypodynamic" period, the blood lactate concentration is elevated, and central venous oxygen saturation is low.
    4. Fluid administration is usually followed by the hyperdynamic, vasodilatory phase during which cardiac output is normal (or even high) and oxygen consumption is independent of oxygen delivery.
    5. The blood lactate level may be normal or increased, and normalization of the central venous oxygen saturation (SvO2) may reflect either improved oxygen delivery or left-to-right shunting.
    6. Prominent hypotensive molecules include nitric oxide, beta-endorphin, bradykinin, PAF, and prostacyclin.
Extra Edge  Antimicrobial pharmacodynamics
  1. Antimicrobial pharmacodynamics is the relationship between concentration of antibiotic and its ability to inhibit vital processes of endo- or ectoparasites and microbial organisms. 
  2. Concentration-dependent effects
    The minimum inhibitory concentration and minimum bactericidal concentration are used to measure in vitro activity antimicrobial and is an excellent indicator of antimicrobial potency. They don't give any information relating to time-dependent antimicrobial killing the so called post antibiotic effect
  3. Post Antibiotic Effect (LQ 2012)
    a. The post antibiotic effect (PAE) is defined as persistent suppression of bacterial growth after a brief exposure (1 or 2 h) of bacteria to an antibiotic even in the absence of host defense mechanisms
    b. Aminoglycosides, fluoroquinolones, tetracyclines, clindamycin, and rifampicin and rifabutin induce long-term PAE against susceptible bacteria.


Extra Edge: Table 270–4. Physiologic Characteristics of the Various Forms of Shock (Ref. Hari. 18th ed., Pg- 2219)

Type of Shock


Cardiac Output

Systemic Vascular Resistance

Venous O2 Saturation

1. Hypovolemic

2. Cardiogenic

3. Septic (Hyperdynamic)

4. Neurogenic

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