___1_____ is anything that causes an immune response and it reacts with preformed components of the immune system, like ___2____ & ___3_____.  There are 3 types:

a)  ____4_____ : induces formation of immune system responses

b) ___5______: reside on the surface of RBCs.

c) ___6_____: disease causing

An antigen is anything that causes an immune response and it reacts with preformed components of the immune system, like lymphocytes & antibodies.  There are 2 types:

a) Immunogen : induces formation of immune system responses

b) Blood group antigens : reside on the surface of RBCs.

c) pathogen: disease causing antigen

What are the 3 lines of defense?

1)Line 1: provide examples. how are pathogens cleared?

2)Line 2: what are the 3 plasma protein systems?

3) Line 3: Name some characteristics and the associated cells and their specific responses.

1) Innate Immunity: epithelial cells in skin, GI, GU, Respiratory systems.  Mechanical clearance prevents pathogenic entry into body: cough, sneeze, vomit, urination, sloughing, mucous, cilia.  Biochemical secretions: mucous, saliva, tears, sweat, cerumen, flora.

2) Inflammatory Response

a) complement system

b) clotting system

c) kinin system

3) Adaptive Immunity

Specificity and Memory

Lymphocytes: B cells (humoral response) and T cells (cell mediated response)

Adaptive Immune System:

1) What cells are involved? 

a) When do they develop

b) What do they recognize

c) where do they differentiate

d) during antigen presenting, what is their function?

2)  Describe the two components of the adaptive  immune response?

1) Lymphocytes (B and T cells) which are a type of WBC.

a) Lymphs Develop before birth

b) recognize only 1 foreign antigen

c) differentiate into B (in bone marrow) or T lymphocytes (in thymus).

d) The function of T cells and B cells is to recognize specific “non-self” antigens, during a process known as antigen presentation.

2) Adaptive Immune Response Components:

a) Humoral: B Cells transform into plasma cells which secrete antibodies. Antibodies bind to antigens on the surfaces of invading microbes, which flags them for destruction.  humours=body fluids.

b) Cell-mediated Immunity:T cells differentiate into cytotoxic T cells during an infection.  They induce apoptosis in cells displaying foreign antigen or activate other leukocytes: macrophages & NKs.  Also secrete cytokines (play a role in inflammation)

Lymphoid Tissue:

1) Function...

2) composition

3) Primary Tissue

4) Secondary Tissue

1) defending the body against the infections and spread of tumors.

2) It consists of connective tissue with various types of white blood cells enmeshed in it, most numerous being the lymphocytes.

3) Thymus and bone marrow: production of lymphocytes

4)lymph nodes, tonsild, Peyer's patches (sm bowel), spleen, adenoids, skin, etc. that are associated with the mucosa-associated lymphoid tissue (MALT): environment antigens to interact with the lymphocytes.

Immune System Key Players

1) RBC: aka...; O2 transport; part in immune response

2) WBC: aka; normal values/L.  Increase/decr in # called...

a) granulocytes and 3 types.

b) agranulocytes and types

1) Erythrocytes:  composed of hemoglobin whose heme temporarily bind to O2 in lungs and transport through body and exchanges for CO2.

When lysed by pathogens such as bacteria, their hemoglobin releases free radicals that break down the pathogen's cell wall and membrane, killing it.

2) Leukocytes:

4500 to 10,000 cells/mL.

Leukocytosis vs. Leukopenia.

a) Granulocytes: polymorphonuclear leukocytes (PMN) most numerous - enzymes that kill microbes and phagocytize.

• Neutrophil granulocytes - 50-60%, phagocytize IgG coated bacteria
  
• Eosinophil granulocytes - kill parasites (IgE), phago, APCs, destroy tumors, promote repair
  
• Basophil granulocytes - <2%, IgE, IgG, complement, histamine.  Inflamm response
• Mast cell - inflamm process.  IgE
  

b) Agranulocytes:

a) lymphocytes: b cell (make antibodies), t cell (coordinate immune response), NK cells (kill virus infected cells)

b) monocytes: aka macrophages once migrate to tissue.  Present pathogens to T cells to be recognized and killed.

What are Proteins that function a chemical signals btwn cells?

a) play a role in...

b) list the key types (4):

Cytokines

a) play a role in acquired/adaptive immune response and inflammation

b) Interleukins (required for immune system functioning.  Mostly secreted by CD4), interferons (interfere w/ viral replication), tumor necrosis factor (TNF), transforming growth factor (upregulated in CA to stim normal cell growth)

Immunity: Active Vs Passive

1) Active (2)

2) Passive (3)

1) Active: produced in response to natural exposure to antigen (natural) or after immunization (Induced)

2) Passive: no host immune response.  Antibodies transferred:

-mama to fetus (vertical, natural)

-immunotherapy (induced)

-immune globulins after disease exposure (rabies, induced)

1) ______ label surface proteins on WBCs, and contribute to immune response.  What are the markers for helper and cytotoxic T cells?  What infection can they monitor?

2) _____ is a cell that displays a foreign antigen complex. 

-What is on this complex's surface and in what cells is it found?

3) CD1

1) CD (cluster of differentiation) cells.  Helper T (CD4) and cytotoxic T (CD8).  Monitor HIV.

2) Antigen Presenting Cell (APC).

Major Histocompatibility Complex (MHC)/HLA on surface (found in all cells except RBC).

3) Myocobacterium tuberculosis relation??

Antibody

1) aka

2) produced by

3) recognize

4) describe the 5 classes (¨GAMED¨)

1) immunoglobulin, proteins in blood serum

2) plasma cells (B cells)

3) recognize specific antigen

4) 5 classes:

• IgG - Most abundant, passively/maternally acquired fetal immunity.  2º exposure, rises quickly (memory).
• IgA - in secretions, common mild genetic immunodeficiency (asymptomatic) resulting in lack of protection of mucous membranes of mouth, airways, GI tract (chronic sinus, lung, GI candida, URI infections)
• IgM - large, on 1st exposure, 1st produced
• IgE - least conc, rises in allergic and parasitic infections
• IgD - ??? b-cell activator.

1º and 2º immune response.

(Visualize the graph)

1st exposure: 1-7 d IgM high.  Followed by IgG.

2nd exposure: Amnestic reponse - rapid and large production of IgG (memory cells).

[image]

Hypersensitivity Rxns: definition and requirement.

Classes I-IV: description, examples, mediators

Hypersensitivity rxns :undesirable (damaging, discomfort-producing and sometimes fatal) reactions produced by the normal immune system; require a pre-sensitized host.

I) Allergy - histamine release -Anaphylaxis, Asthma, Urticaria, Rhinitis, Mucus, Edems - IgE

II) Specific target activates complement cascade and lysis - RBCs destroyed in hemolytic anemics or mismatched blood transfusion - IgM, IgG, Complement

III) Immune Complex - antigen-antibody complexes in tissues,bld vessesl, joint, kidney that are attacked by complement & destroy tissues.  Sx: pain, inflammation.  IV Dx rxns, SLE, Raynaud's - IgG, Complement

IV) delayed rxn/cell-mediated - Cytotoxic/Helper T cells, no antibody, direct attack on cells - MS - T cells

1) Lack of immune tolerance to self antigens

2) immune rxn to another person's tissue (graft rxn, transfusion)

1) Autoimmunity

2) Alloimmunity

State the Class of Hypersensitivity Rxn and the Mediators

1) Autoimmune hemolytic Anemia

2) Vomitting Diarrhea Cramps after eating shellfish

3) RA

4) Hashimoto Thyroiditis

5) DM type 1

6) Raynaud's (why?)

7)PPD (TB)

8) MS

9) Urticaria

10) IV Drug  Rxn

11) Graft Rejection

1) Autoimmune hemolytic Anemia: Class II, cytotoxic, antibody dependent: IgG, IgM, Complement

2) Vomitting Diarrhea Cramps after eating shellfish: Class I Allergy, IgE

3) RA: CLass IV

4)Hashimotos Thyroiditis: IV

5) DM type I: Class IV

6) Raynaud's (why?): Class III Immune Complex, IgG, Complement.  Cryoglobulins precipitate at lower temps.

7) PPD: IV

8) MS: Class IV delayed/cell mediated, antibody independent: T cells

9) Urticaria: Class I Allergy, IgE

10) IV drug rxns: Class III Immune Complex, IgG, Complement.

11) Graft Rej: IV

Rheumatic Fever

(GABHS: group A beta hemolytic streptococcus)...let strep throat go untreated.

Production of autoantibodies against nucleic acids (DNA; RNA), RBCs, coagulation proteins, lipids, lymphocytes (B, T, NK cells), platelets. Immune complexes with antibody host DNA are deposited and produce tissue damage.

What disease and what hypersensitivity rxn?

SLE

Class III rxn: immune complex - IgG, complement systems.

1) Virus

2) Bacteria - prokaryotes (no nucleus)

3) Fungi

4) Parasite

Bacteria

1) Nucleic acid, growth and reproduction

2) Gram stain & Cell wall (2).  Majority of bacteria?  Effect of PCN? Which bacteria produces an endotoxin and why?.

3) Common gram +/- bacteria.  (6+, 2-)

4) What bacteria requires acid-fast staining and why?

5) 4 shapes

6) Classify the following as: aerobe, anaerobes, obligate intracellular parasites (no ATP), lack cell wall.  State morphology, staining, and disease.

• Clostridium
• Legionella
• Mycobacteria
• Rickettsia
• Bacteroides
• Chlamydia
• Neisseria
• Mycoplasma

1) Contain DNA & RNA, independent growth, reproduce asexually (binary fission)

2) Gram +(purple): thick cell wall with layers of peptidoglycan and techoic acids.

Gram -(red/pink): thin cell wall with few layers of peptidoglycan surrounded by lipid membrane with LPS (acts as endotoxin and elicits immune response when gram - bacteria lysed).  MAJORITY OF BACTERIA gram neg.

PCN: beta-lactam inhibits peptidoglycan cross-links - has an effect on gram + cells.

3) +: Streptococcus, Staphylococcus, Corinebacterium, Listeria, Bacillus, Clostridium

-: Neisseria (gonorrhea), and the REST.

4) Mycobacteria (tuberculosis), lacks cell wall.

5) Cocci, bacilli (rods), spirochete (syphilis, lyme), branching

6)

• Clostridium: gram+, anaerobe, bacilli
  • C. botulinum: botulism
  • C. difficile: overgrowth in gut during antibiotic therapy=pseudomembranous colitis
  • C. perfringens: food poisoning
  • C. tetani: tetanus
• Legionella: gram-, aerobe, pleomorphic, flagella
  • L. pneumophila: Legionairre's Disease
• Mycobacteria: acid-fast bacteria, aerobe, waxy cell wall.
  • M. tuberculosis: 
• Rickettsia: gram-, obligate intracellular parasite
  
  • R. rickettsii: RMSF
  • Typhus
• Bacteroides: gram-, anearobes, bacilli, normal GI flora
• Chlamydia: gram indeterminate (or neg), obligate intracellular pathogen.  C. trachomatis.
• Neisseria: gram-, aerobe, diplococci
  • N. gonorrhoeae
  • N. meningitidis: 10% mortality rate
• Mycoplamsa: no cell wall (no PCN effect), polymorphic
  • M. pneumoniae: atypical/walking pneumonia.

Explain the role of these physical structures in virulence.  What bacteria do they appear on?

1) Flagella

2) Pili

3) Capsule

4) Spores

1. Flagella: motility.
   • Vibrio: gram-, curved rod shaped anaerobes: Cholera transmitted in contaminated H20.
   • Escherichia coli: gram-, rod shaped anaerobes: normal flora; virulent strains cause gastroenteritis, UTI, peritonitis
2. Pili: adherence
   • Neisseria: gram- diplococci
   • Bordatella: gram-, coccobaccili, aerobe: pertussis,
3. Capsule: surround cell wall, prevents phagocytosis, mostly gram-. Macrophage can eat it ONLY after opsonization (binding of IgG, IgA).
   
   • Pathogens: ¨Some Killers Have Pretty Nice Capsules¨: S. pneumoniae, K. pneumoniae, H. influenzae, P.aeruginosa, N. meningitis, C. neoformans (yeast).
4. Spores: survival in unfavorable conditions for long periods of time.  Dormant= Clostridium & Bacteroides.

Exotoxin vs. Endotoxin

-release by....

-produced by which bacteria (gram stain)?

-immunogenic (can it produce immune response)?

-host fever?

-conversion

-overall effects: systemic or localized?

Exotoxin                                 Endotoxin

excreted by living cells            in cell wall,released with lysed bacteria

 gram pos & neg               mostly gram neg

 very immunogenic           weak immunogenicity

 no fever                          high fever 

 toxoid (weakened toxin)   TNF-->IL-1-->septic shock

 localized                          systemic

Streptococcus pyogenes

1) gram stain and morpholgy

2) aka

3) name 3 immediate local infections.  They are due to what enzymes and what toxins?

4) Latent complications later on due to...

Name 2.

1) gram + chains of cocci

2) GAS: group A (beta-hemolytic) strep

3) pharyngitis, cellulitis, scarlet fever (produced by extoxin release).

Produce hemolysis (an exotoxin that causes localized lysis of RBCs.)

4) latent, chronic complications are the result of immune induced processes, NOT the effect of the bacteria.

• Rheumatic Fever: inflammatory disease 2-3 wks after GAS-->possibility of antibody mediated myocarditis (manifesting as CHF)
• PSGN (post-strep glomerulnephritis)--->antigen-antibody complex induced RENAL FAILURE.
  

Bacterial- Host relationships

Define.

1) symbiosis.  where are these groups of microbes found?

a) H. pylori, E.coli, Bacteroides

c) Ureaplasma, Candida, Strep agalactiae

b) (Strep viridans, Actinomyces, Candida

2) parasitism

a) give an example and where is it seen?

1) Mutualism (both gain something) or commensalism (other is not harmed nor helped)

a) GI Flora: H. pylori, E.coli, Bacteroides

c) GU FLORA: Ureaplasma, Candida, Strep agalactiae

b) Oral flora: Strep viridans, Actinomyces, Candida

2) one benifits, another is harmed

a) chlamydia: GU, eye, lungs

What causes normal flora to become pathogens?

Bacteria that colonize are always ________.

In immunocompromised pts (HIV, DM, antibiotic tx), normal flora can become opportunistic infections (candida, MAC**).

**MAC: Mycobacterium avium complex common in HIV pts with decreasing CD4 counts.

Bacteria that colonize are always pathogens.

Routes of Bacterial Infection: list the bacterial

1) Aerosols

2) Direct contact (verticle)

3) ingestion

4) vectors

Aerosols: Neisseria meningitidis, strep pyogenes, Legionella, Haemophilus influenzae, Mycobacteria tuberculosis.

Direct contact: STDs – Treponema, N. gonorrhea, Chlamydia, Herpes.
¨Vertical: mother-fetus
Ingestion of contaminated food and water: toxin (staph), bacteria (Salmonella).
Vectors: ticks (Lyme disease –Borellia), chiggers (RM spotted fever –Ricketsia)

Stages of Bacterial-Host relationship....define

FYI:

Diagram: overview of Bacterial Infections

[image]

general bacterial infection

**leukocytosis (high WBC count)

Viruses

1) size

2) nucleic acid

3) classification

4) structure

5) DNA viruses

6) 4 pathogenitic features

1) smallest

2) DNA or RNA

3) obligate intracellular parasite dependent on host for replication

4) nucleic acid, capsid, possible envelope

5) HHAPPP:

6) Ubiquity, Antigenic Enzymes (HA, NA), Antigenic drift (small mutation during replication), antigenic shift (can jump species)

1) What is the only DNA virus that causes hepatitis?

2) What virus is involved in Kaposi sarcoma in HIV pts?

3) If you see a roseola rash in a ped pt, what is the cause?

4) Pt presents with viral URI and gastroenteritis, what is your Dx?

1) HBV: hepatitis B virus in hepadenaviridae family

2) HHV 8

3) HHV 6 - roseolovirus

4) adenovirus

**ALL OF THESE ARE DNA viruses

HA (hemagglutinin) -  causes RBC to agglutinate.  Allows attachment of virus to cell surface during reproduction.

NA (neuraminidase) - on surface of virus that enable virus to be released from host cells.  NA inhibitors [zanamivir (Relenza) and oseltamivir (Tamiflu)] limits the severity and spread of the flu.

1) Which virus kills T helper cells?

2) Which virus inhibits complement?

3) which virus has a latency pd of 5-65mnths?

4) Which virus is responsible for cervical cancer?

5) Which virus causes Burkitt lymphoma?

1) Which virus kills T helper cells? HIV

2) Which virus inhibits complement? CMV (HHV5)

3) which virus has a latency pd of 5-65mnths? HIV

4) Which virus is responsible for cervical cancer? HPV 16 & 18

5) Which virus causes Burkitt lymphoma? EBV (HHV4)

State the route of viral infection:

1) Measles

2) HSV 1,2

3) Hep A

4) West Nile encephalitis

5) HIV

6) Hep B

7)VZV

8) Influenza

9) Which viruses have vertical transmission (4)?

1) Measles - Airborne inhalation of droplets

2) HSV 1,2 - direct contact

3) Hep A - fecal-oral/ingestion

4) West Nile encephalitis - vector

5) HIV - blood/body fluid

6) Hep B - blood/body fluid

7)VZV - airborne and direct contact

8) Influenza - Airborne inhalation of droplets

9) Which viruses have vertical transmission (4)?

-Rubella, HHV, Hep B, HIV-

Capacity of microorganism to produce disease.  What is this term?

MIT VIP

1) MOA: direct infection of host cell

2) Infectivity: ability to invade and multiply in host: enzymes break barriers, adhesion, plasmid, capsule, spores

3) Toxigenicity: generate endotoxins (gram - , septic shock)/exotoxins

4) Virulence: potency (# of microbes/ug of toxin required to kill host: rabies is high, measles is low) & latency

5) Immunogenicity: ability to induce immune response aka antigenicity.  ALL VIRAL ENZYMES ARE IMMUNOGENIC.  Bacterial cell, toxins, enzymes.

6) Pathogenicity: reproduction spd, tissue damage, toxin production)

18 y/o with general edema, LBP, brown urine.

PMH: multiple strep throat infections, casually treated.

Lab: urinalysis: hematuria, RBC casts.  CBC: incr IgG

Renal disease from PSGN (post-strep glomerulonephritis).  Inflammation of glomeruli of kidneys. 

Sx: general edema, HTN, hematuria.  IgG raised because of secondary exposure.

The result of immune response to GAS that was left untreated.

33y/o male with myalgia, fatigue, loss of apetite.

Lab: moderate lymphocytosis.

F/u visit: jaundice.  Lab: anti HBc IgM present.

HBV - hep B virus.

Key risk factors include perinatal exposure, multiple sexual partners, men who have sex with men, injection drug users.

Serum HBcAb (IgM) : Appears within weeks of acute infection and remains detectable for 4 to 8 months. During the window period (several weeks to months) after the disappearance of HBsAg and before appearance of HBsAb, detection of IgM HBcAb, may be the only way to make the diagnosis of acute HBV infection. Some patients with chronic HBV or inactive HBV carriers become positive for IgM antibody during acute flares or acute reactivation, making positive IgM HBcAb not an absolutely reliable marker for acute infection

e coli

strep b

listeria

Sickle cell pts...do not have opsonization complement system working.  Very important to vaccinate against capsuled bacterium...strep pneumoniae, n meningitis, h influenzae.

Infections that cause congenital/neonatal complications: ToRCHeS -- all of these organisms can cross the blood-placenta barrier.

a. Toxoplasma gondii -- can cause chorioretinitis, blindness, seizures, mental retardation, microcephaly, encephalitis, and stillbirth if infections is acquired early in gestation.

b. Rubella (Rubivirus) -- risk is greatest with infection early in fetal development. Heart: PDA,VSD and pulmonary artery stenosis. Eye: cataracts, chorioretinitis. CNS: mental retardation, microcephaly, deafness.

c. CMV -- most common viral cause of mental retardation. Also cause microcephaly, deafness, seizures.

d. Herpes -- neonate is often infected during delivery. Manifestations vary -- vesicular lesions or CNS involvement.

HIV

e. Syphilis -- Treponema pallidum high rate of mortality (still-birth, spontaneous abortion, and neonatal death). Survivors will go on to develop Early of Late congenital syphilis.

1. Early: occurs w/in 2 years and is like severe adult secondary syphilis -- widespread rash and condyloma latum. "Snuffles" -- mucous membrane involvement with runny nose.

2. Late: similar to adult tertiary syphilis except cardiovascular involvement rarely occurs.

What types of lung disease are the following?

[image]

a) Normal fas exchanges (O2-->CO2)

b)Consolidation (pneumonia): aveoli fill with blood, pus, edema

c)Restrictive Lung Disease (resistance to inspiration): stiff lungs with thick aveolar walls, stiff chest wall, resp muscle weakness.

d)Obstructive Lung disease (resistance to expiration): decreased aveolar elastic recoil: ephysema, chronic bronchitis, asthma, cystic fibrosis

e) Pulmonary blood supply issues: PE, pulm HTN

Stiff lungs with thick aveolar walls, stiff chest wall, and/or resp muscle weakness are all examples of what lung pathology?

They all make it difficult to inspire or expire?

Restrictive Lung Disese

Resistance to inspiration

1) What is: Decreased aveolar elastic recoil.

2) This lung pathology makes it difficult to inspire or expire?

3) Give 4 diseases/examples.

Obstructive Lung Disease

Resistance to expiration.

Emphysema, Chronic Brochitis, Asthma, CF

Compare Obstructive Vs. Restictive Lung Disease

1) disease of the...

2) aveoli consistency

3) FEV1/FVC incr/decr/norm? (define these and give normal values).

4) difficulty breath in/out

Obstructive                                      Restrictive

disease of the airway                     disease of the parenchyma (lung tissue)

alveoli floppy                                  alveoli stiff

decreased FEV1/FVC *                  increased/normal FEV1/FVC*

pt unable to get air OUT               pt unable to get air IN

FEV1: max volume of air that can be forcibly blown out in 1st second during the FVC maneuver (nml value: 70% of FVC).

FVC: forced vital capacity:  volume of air that can be forcibly blown out after full inspiration (nml value: 80% of TLC).

Asthma

1) What type of Lung Disease?

2) pt present with....

3) On auscultation, what is heard?

4) if left untreated....

1) Obstructive

2) dyspnea

3) wheezing

4) respiratory failure

Allergens, cold air, exercise, stress...cause

IgE and irritant mast cell degranulation causes the release of inflammatory mediators( histamine, leukotrienes etc) which causes bronchospasm,vascular congestion, edema, mucus secretion,thickening of airway wall, and acute airway hyperresponsiveness.

Asthma:

An Obstructive Lung Disease

that causes

Chronic Airway Inflammation and Brochial hyperreactivity

Progressive destruction of aveolar walls, decr in aveoli elastic recoil, collapse of brochioles.

Toxins in cigarette smoke (#1 cause) lead to inflammation of airway epithelium with neutrophils,macrophages and lymphocytes arriving on the scene which leads tp cytokine release which inhibits antiproteases which leads to an imbalance of protease/antiprotease which leads to breakdown of elastin in alveoli which leads to decrease in elastic recoil.

Emphysema:

An Obstructive Lung Disease

Cigarette Smoke

Toxins in cigarette smoke (#1 cause) lead to inflammation of airway epithelium with neutrophils,macrophages and lymphocytes arriving on the scene which leads tp cytokine release which inhibits antiproteases which leads to an imbalance of protease/antiprotease which leads to breakdown of elastin in alveoli which leads to decrease in elastic recoil.

Brochial edema, hypersecretion of mucus, bacterial colonization of airways.

What disease is this?  Is it obstructive or restrictive?  what is required for Dx?

Chronic Bronchitis:

An Obstructive Lung Disease

Dx: chronic, productive cough x 3 months

Size and # of mucus glands and goblet cell in the airway lining increase because of inspired irritants (smoke, pollution) which causes more secretions. This mucus is thicker and stickier than normal and attracts bacteria (strep) which embed in the lining…chronic bronchitis is one infection after the other. Infection occurs as ciliary fxn is decreased. Becomes a vicious cycle.

Chronic Bronchitis:

An Obstructive Pulmonary Disease

Obstructive Lung Disease

1) Name the big 3

2) Characterized by _______ of the airway, increased

         __________ in the airways and increased tendency for __________.

        Pt presents with ______.

        On auscultation, ________ is heard.

Asthma, Chronic Brochitis, Emphysema

Characterized by obstruction of the airway, incr resistance in the airways, and incr tendency for airway closure.

Pt presents with dyspnea.

On ausculatation, wheezing  heard.

Restrictive Lung Disease

1) Difficulty on inhale/exhale?

2-a,b,c) 3 causes and some associated disorders.

3) Pt present with...

4) What heard on auscultation

5) 2 scenarios for FEV1/FVC ratio

1) Difficulty inspiring

2a) Weak resp muscles: ALS*, MS, Myastinia Gravis*, muscular dystrophy, Guillain-Barre*, spinal cord injury

2b) Stiff chest wall: obese, kyphoscoliosis, ankylosing spondylitis*.

2c) Lung stiffness: insterstitial lung disease caused by drugs, connective tissue diseases (RA, SLE, scleroderma), pneumoconiosis* (asbestosis, coal miners...fibrosis), idiopathic pulm fibrosis.

3) dyspnea

4) crackles

5) FEV1/FVC remains constant because they decr at same rate.  OR, FEV1/FVC increases b/c FVC decr more than FEV1.

*Helpful FYIs:

-ALS: Amyotrophic lateral sclerosis (Lou Gehring's Disease)is a disease of the nerve cells in the brain and spinal cord that control voluntary muscle movement.

-Myasthenia gravis is a neuromuscular disorder characterized by variable weakness of voluntary muscles, which often improves with rest and worsens with activity.

-Guillain–Barré syndrome (GBS)  is an acute inflammatory demyelinating polyneuropathy (AIDP), an autoimmune disorder affecting the peripheral nervous system, usually triggered by an acute infectious process.

-Ankylosing spondylitis is a long-term disease that causes inflammation of the joints between the spinal bones and the joints between the spine and the pelvis. It eventually causes the affected spinal bones to join together.

-Coal worker's pneumoconiosis is a lung disease that results from breathing in dust from coal, graphite, or man-made carbon over a long period of time.

Acute infection of Lung Parenchyma

1) What disorder is this?

3) define parenchyma

4) ranking in cause of US deaths

5) risk factors

6) 3 classifications

7) 3 routes of contraction

1) Pneumonia

3) parenchyma: aveolar space + interstitial space

4) #6 leading cause of death in US

5) Elderly, immunocompromised, chronic disease, alcoholics, bedridden, smoker, ET (endotracheal) tube

6) typical/atyp, community/nosocomial acquired, causative mechanism (bacteria, virus, parasite, protozoa, funghi)

7)

-direct inhalation of droplets

-aspiration of oropharyngeal contents

-hematongenous spread (think immunocompromised or IV drug users)

Typical Pneumonia

1) causative agent and visualization of microbe

2) CXR reveals....

3) Sx (3)

Atypical

1) causative agents (3)

2) CXR

3) Sx (2)

4) aka

Typical Pneumonia

1) Strep pneumoniae: gram + cocci anaerobe in long chains

2) CXR reveals lobar/segmental consolidation due to inflammatory fluid in aveolar space.

[image].

3) Sx: productive cough, fever, chills

Atypical Pneumonia

1) causative agents: Viral, Mycoplasma, Chlamydia

2) CXR shows instersitial/diffuse/fine opacities w/o lobar consolidation.

[image]

3) Sx: dry cough, myalgias

4) aka ¨walking pneumonia¨

CAP

What is the most common viral CAP?

What is the most common bacterial CAP?

What is the most common CAP in young adults?

CAP= community acquired pneumonia

Most common CAPs...

viral: influenza virus

bacterial: strep pneumoniae

young adults: Mycoplasma Pneumonia

Tell if the folling Pneumonias are CAP, Nosocomial, or seen in immunocompromised host (HIV).

*Also state any defining characteristics (most common in...) if applicable.

1. H. influenza
2. E. coli
3. Moracella catarrhalis
4. protozoa
5. Klebsiella pneumoniae
6. Strep pneumoniae
7. Staph aureus
8. Influenza virus
9. Funghi
10. Mycobacterium tuberculosis
11. P. aeruginosa
12. Chlamydia pneumoniae
13. Pneumocystis jeroveci
14. Mycoplasmic pneumoniae
15. Legionella pneumophila
16. Parasites

1. H. influenza - CAP
2. E. coli - Noso
3. Moracella catarrhalis - CAP
4. protozoa - immunocomp
5. Klebsiella pneumoniae - Noso
6. Strep pneumoniae - CAP (*most common)
7. Staph aureus - Noso
8. Influenza virus - CAP (*most common viral CAP)
9. Funghi - immunocomp
10. Mycobacterium tuberculosis - immunocomp
11. P. aeruginosa - noso
12. Chlamydia pneumoniae - CAP
13. Pneumocystis jeroveci - immunocomp
14. Mycoplasmic pneumoniae - CAP (*common in young adults)
15. Legionella pneumophila - CAP
16. Parasites - immunocomp

Excessive accumulation of extra-vascular fluid in aveoli

1) What pulm disorder is this?

2) causes (3).  *most common?

3) Pt c/o... (2)

4) Ausculation, Percussion, Heart Sounds, CXR

1) Pulm Edema

2)

-heart disease (*most common): LV failure=backup in lungs=incr pressure=incr capillary permeability.

-capillary injury: surfactant prodution disrupted.  acute resp distress syndrome, toxic gas inhalation

-lymph obstruction (edema, tumor, fibrosis): can't drain excess interstitial fluid

3)dyspnea, othopnea

4) Insp crackles, percussion dullness @bases, S3 gallop, cardiomegaly

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Collapse of Lung Tissue

1) Name

2) 2 types and causes (3,1)

3) Pt presents with....(4)

4) ausculatation

5) common in what pts?

6) Prevention

1) Atelectasis

2)

-compression (tumor, foreign body, fluid/air in pleural space)

-absorption (inhale conc O2 or anesthetic agents)

3) dyspnea, cough, fever, tachycardia

4) crackles

5) common in post-op pts

6) prevention: early ambulation, deep breathing, change positions, handheld sparometer

Air/gas in pleural space.

1) Name

2) 4 types and causes (*which is medical emergency?)

3) pt presents with... (2)

4) Tracheal Shift?

5) How do you fix it?

1) Pneumothorax

2)¨TASS¨

a) Spontaneous: bleb rupture (air-filled blister-like growth in visceral pleura)

b) secondary: usual cause is chest trauma

c) iatrogenic: unintentional medical mistake (central line placement, mech ventilation)

d) Tension: *med emergency*.  Air enters pleural space, collapses lung, compress mediastinum (heart and great vessel compression!!!!)

3) dyspnea, chest pain (symptoms vary depending on size of pneumothorax)

4) contralateral

5) Spontaneous resolvment or tube to equalize pressure

Persistant, abnormal dilation of bronchi

1) Name

2) Occurs in conjuction with what 2 conditions (give examples of each)

3) pt presents with (5)...

4) Lung and Heart PE findings.

5) 50% of cases are in pts with....

6) 3 types

1) Brochiectasis

2) Respiratory (actelectasis, aspiration, chronic LRIs, CF, TB)

Systemic (rheuma diseases)

3) cough, purulent mucus, hemoptysis, clubbing, halitosis

4) abnl breath sounds, crackles, wheezes, rhonci, tachypnea, tachycardia

5) Cystic Fibrosis

6) Cylindrical, saccular, varicose

Obstruction in pulmonary circulation due to clot.

1) Name

2) Virchow triad

3) where does the clot usually come from?

4) Pt presentation....

5) causes (3)

1) Pulm Embolism (PE)

2) venous stasis, hypercoagulability, & injury to endothelial lining of vessels (causes thrombuli)

3) lower extremities

4) tachypnea, tachycardia, dyspnea....also, pt may just feel vaguely anxious

5) venous stasis: sluggish blud with immobile pts, post-op, >60yrs, long trips.

Hypercalcemia.

Hypercoag: genetic, birth control pills (estrogen), malignancies.

Increased Pressure in Pulmonary vasculature

1) Name

2) most common cause?  Due to...(4)

3)PPH: %, cause

4) If the condition not corrected...

1) Pulm HTN

2) Incr in LA pressure due to...

a) LV failure, valvular disorders

b) Obstrction of pulm vascular bed (vasculitis)

c) vasocontriction of pulm vasc bed (hypoxia, acidosis)

d) Damaged interstitium and aveoli

3)PPH - primary pulm HTN: rare (5%), idiosyncratic.

4)Not corrected? Develops into Cor Pulmonale=RHF due to chronic/acute lung disease and backup into IVC and SVC systems (COPD)

RHF due to chronic/acute lung disease and backup into IVC and SVC systems.

What is this disease and 2 possible causes

Cor Pulmonale

Causes: COPD, PPH (prim pulm HTN)

condition in which the level of oxygen in the blood becomes dangerously low or the level of carbon dioxide becomes dangerously high.

Name and O2 or Co2 values

1) What condition causes episodes

2) Etiology

3) Pt presents with...(2)

4) PE findings: breathing, HR, BP

5) Symtoms and official name for low O2 (5) & high CO2 (4) in blood.

6) What happens if left untreated?

Acute Respiratory Failure (ARF)

Hypoxemia: PaO2<50mmHg

Hypercapnia: PaCO2>50mmHg

1) chronic pulmonary diseases are the cause of ARF

2) direct trauma to lung, airway, chest wall or another body system

3) dyspnea and/or headache

4) tachypnea, tachycardia, incr BP

5)

hypoxemia: cyanosis, confusion, restless, tremor, anxiety

hypercapnia: impaired consciousness, papilledema, asterixis*, hyperemia*

6) ARDS

*FYI:

-Asterixis is a tremor of the wrist when the wrist is extended (dorsiflexion)

-Hyperemia describes the increase of blood flow to different tissues in the body.

Severe, massive injury of the alveolo-capillary membrane-->non-cardiogenic severe pulmonary edema-->sever diffusion damage-->hypoxemia

1) Name

2) Caused by untreated case of...

3) why is there ¨non-cardiogenic severe pulmonary edema¨?

4) what causes even more hypoxemia?

5) Causes (2)

6) Mortality rates

7) Survivor lung capacity after illness?

1) ARDS (acute resp distress syndrome)

2) If ARF left untreated

3) due to sudden, massive inflamm response b/c of unjury to alveolo-capillary membrane

4) decr surfactant synthesis=collapse of aveoli=more hypoxemia=fucked pt.

5)toxic, septic (multple trauma, burn, pneumonia, aspiration, CABG*, pancreatitis)

6) 30-40%, up to 90% if ARDS+sepsis

7) survivors experience nearly norm lung capacity 1 yr after acute illness.

*FYI:

CABG: coronary artery bypass surgery. For pts with significant narrowings and blockages of the heart arteries (CAD).  Creates new routes around narrowed and blocked arteries, allowing sufficient blood flow to deliver oxygen and nutrients to the myocardia.

3 unrelated Pts present with dyspnea, on three different months.  Wheezes heard on exhale.  Use of accessory muscles noted.

1) What is your differential dx?

Pt 1: Acute onset. PMH of similar occurences.  Was excercising before he came in.

Pt 2: Pt<40yrs and non smoker. Symptom onset occured gradually over years.  Productive cough and SOB on exertion.  SH: works in dry cleaning business.

Pt 3: chronic productive cough for 3 months.  Smoker.

**If pts 2 & 3 where the same person, what would your dx be?

1) Obstructive Lung Diseases: Asthma, Chronic Brochitis, Emphysema

Also: foreign body, CF

Pt 1: Asthma

Pt 2: Emphysema (not COPD origin) but genetic caused: alpha-1-antitrypsin deficiency...autosomal recessive trait causes ineffective activity of the specific protease inhibitor alpha-1 antitrypsin, which is the enzyme responsible for neutralizing neutrophil elastase and preventing inflammatory tissue damage in the lungs

Pt 3: chronic bronchitis.

** COPD: chronic bronchitis + emphysema.

After becoming immunocompetent, both types of lymphocytes undergo and differentiation...

1) T lymphocyte subpopulations...

2) B lymphocyte subpopulation...

3) all differentiated (specialized) lymphocytes, T or B, can develop ___3____.

1) T regulatory (previously called suppressor), T helper, T cytotoxic

2) B lymphocytes subpopulation -  plasma cells (B able to produce antibody)

3) memory

T helper group, consider 2 main lymphocytes:

1)group..-->activates...-->mech of...

2) group...-->activates...-->secretes...-->mech of....

1) T helper 1-->activates T cytotoxic-->mech of cellular immunity

2) T helper 2-->activates B lymphocyte-->plasma cell secreting antibody-->mech of humoral immunity

Antigen presented by molecules

1) MHC II

2) MCH I

are recognized by what antibody on what cell?

1) MHC II recognized by CD4 on T helper

2) MHC I recognized by CD8 on T cytotoxic

Fluid in the pleural space:

1) name

2) pathophysiology:

a) increased...(3)

b) decreased...(1)

c) disruption of...(1)

3)  The 2 classes and Light's criteria.

4) Etiology: name 7 causes and classification.

5) pt presents with... (4) 

6) PE: Breathing, HR, BP, percussion, egophony, others...

7) Definitive Dx & Tx

1) Pleural Effusion

2)

a) Incr: capillary permeability, hydrostatic pressure, negative intrapleural pressure

b) Decr: oncotic pressure

c) Disruption of pulmonary lymphatics

3) Transudative (watery) or Exudative (less watery b/c more WBC and proteins).

Light's Criteria for EXUDATIVE effusions (meet 1):

1. Pleural fluid protein: serum protein > 0.5
2. pleural fluid LDH: serum LDH > 0.6
3. Pleural fluid LDH > 2/3 normal upper limit for serum LDH

4)

-Common Transudative Effusions: HF, Cirrhosis w/ ascites, PE, nephrotic syndrome caused by incr neg intrapl pres, incr hydrostatic pres, OR decr oncotic pres

-Common Exudative Effusions:Malignancy, Pneumonia, PE, Viral infections, CABG caused by incr capillary permeability OR disrupted pulm lymph vessels.

5) pleuretic chest pain (pain on inhale), cough, dyspnea, fever(?)

6)   pt has tachypnea, tachycardia, decreased BS and dullness to percussion and egophony over pleural effusion, possible friction rub heard.

7) Thoracentesis for Dx.  Tx: get rid of underlying cause and drain (if large effusion).

Plasma Cascade/Protein System of the Inflammatory Response:

1) Complement System

2) Kinin System

3) Clotting System

1) Complement System -Kills bacteria by punching holes in it.  Also marks it for destruction

2) Kinin System- plays a role in inflammation, Its important mediators bradykinin and kallidin are vasodilators

3) Clotting System - Platelets form a plug at the site of injury. Simultaneously, proteins in the blood plasma (coagulation factors)form fibrin strands, which strengthen the platelet plug