352 EXAM 1 Study Questions

Does Inflammation cause infection?

No

If there is an infection, is there inflammation?

yes

What does the inflammatory response involve?

* Vascular Response
* Cellular Response
* Cell Mediators

T/F? The inflammatory response depends on the reactive capacity of the individual.

true

What is innate immunity?

The physical and biochemical barriers of the individual

* Normal Microbiome
* External Barriers
* Secreted Substances

T/F? Inflammation is NOT part of immunity.

False! Inflammation is part of innate immunity.

What is adaptive immunity?

A more specific immune response that our body develops over time.

It includes lymphocytes:

* T Cells
* B Cells
* Macrophages
* Dendritic Cells

Inflammation Definition

Complex non-specific response to ANY tissue injury.

What does inflammation intend to do?

* Minimize the effects of injury or infection.
* Remove the damaged tissue
* Generate new tissue and facilitate healing

Infection Definition

The invasion of host tissues by **disease causing agents**

T/F? Infection is a multistep process.

True

Steps of Infection

* Establishment of  a presence - colonization/ incubation
* Prodromal - general S+S


* illness - specific S+S
* decline or convalescence

Degrees of Severity Acute Inflammation

* Immediate Transient response to minor injury - mild
* Immediate sustained response - moderate
* Delayed hemodynamic response - severe

Signs of immediate Transient response to minor injury - mild

redness (erythema), pain, heat, edema

Signs if Immediate sustained response - moderate

several days; results in damaged vessels

Signs of Delayed hemodynamic response - severe

increase in capillary permeability 4-24 hours after injury, e.g. radiation burns, burns

Healing in acute inflammatory response occurs in…?

2-3 Weeks

Predominant cell type at site of acute inflammation.

Neutrophils

How long does subacute inflammation last?

Persists longer than acute.

How long may chronic inflammation last?

May last for years.

Predominant cell types in chronic inflammation.

Lymphocytes and macrophages

What may chronic inflammation result from?

May result from changes in the immune system. Ex: autoimmune disease

Vascular Phase of Acute Infection Steps

* Rapid vasoconstriction
* Rapid Vasodilation
* Vascular Permeability increases

VASOACTIVE HYPEREMIA

occurs when excess blood builds up inside the vascular system

Acute Inflammation Cellular Phase Steps

1) Adhesion and Margination

2) Transmigration of WBC

3) Chemotaxis

Phagocytosis Step 1

Recognition and adherence to foreign antigen/pathogen

Phagocytosis Step 2

Engulfment and formation of phagosome

Phagocytosis Step 3

Fusion w/ lysosome to form phagolysosome

Phagocytosis Step 4

Destruction and digestion of foreign material

Complement Cascade - C3

Degranulation of mast cell; promotes phagocytosis; is a chemical attractant for WBC to inflammation; breaks down bacterial membrane

Clotting Cascade

All modes of clotting lead to activation of factor X and thrombin

Kinin Cascade

Bradykinin → histamine like effects; increased vascular permeability and induces pain

Serous Exudate

Watery exudate: indicates early inflammation, low protein

Fibrinous Exudate

Thick, clotted exudate indicates more advanced inflammation, large amounts of fibrinogen

Purulent Exudate (suppurative)

Pus: indicates a bacterial infection, degraded white cells, protein and tissue debris

Hemorrhagic Exudate

Exudate contains blood indicates bleeding, severe leakage of red cells from capillaries

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What are the two mechanisms of infection?

* Inadequate immune response - immune deficiency
* Hypersensitivity; so an inappropriate response.

Communicability

Ability to spread

Infectivity

Ability to invade and multiply

Virulence

Capacity for severe disease

Pathogenicity

Ability to produce disease

Portal of Entry

Route to invade host

Toxigenicity

Ability to produce toxins

What are bacteria described by?

* shape
* staining ability
* O2 need

Cytoplasm in bacteria

* reproductive and metabolic machinery
* cytoplasmic membrane flexible lipid wall

Bacteria cell wall

rigid

Bacteria replication

* self-replicating
* Asexual
* simple cell division

does bacteria have RNA or DNA?

both

What are the smallest intracellular pathogens?

virus

Structure of virus

* no organized cell structure
* protein coat surrounding a nucleic core
* RNA or DNA; never both
* some have lipoprotein envelope; influenza, herpesvirus, poxvirus

can viruses replicate out of host?

no viruses cannot replicate out of host cells.

Viral Replication process

* Copies of genetic material made
* New virions released from cell to infect other host cells
* Some remain latent in host cell until activated by stress, hormone changes, disease (e.g., herpes virus and cold sore)

Fungi Structure

Free living eukaryotic cell meaning it has a nucleus

where are fungi found?

in every environment on earth

Do fungi often cause illness?

NO. very few cause illness in healthy ppl.

* They are opportunistic so cause illness when host is compromised

Ex. of fungi

candida & histoplasmosis

Are fungi temperature sensitive?

yes! they are often temperature sensitive; outside body vs inside body

Factors that impact infection

* HAI
* MultiDrug Resistant Organisms (MDRO)
* Survival on environmental surfaces
* Direct and Indirect transmission

Virulence factors that enhance disease.

* Toxins
* Adhesion Factors
* Evasive Factors
* Invasive Factors

Toxins

produced by organisms

Adhesion Factors

anchoring organisms to host tissues and protecting against host defenses

Evasive Factors

protecting against host

Invasive Factors

Help penetrate host barrier

Pathology of Infection

* Enter host cells causing cell death

OR

* Inducing host responses - that while targeted against organisms cause collateral damage (inflammation)

Biofilm

structured community of bacteria

* access to nutrients - elimination of wasters
* Intracellular signaling and communication

Location of BioFilms

* dental plaque
* catheter infections
* implanted medical devices

MOA of antibiotics

* inhibits cell wall synthesis
* inhibits protein synthesis
* inhibits nucleic acid synthesis
* Interrupts metabolic pathway
* disrupts cell membrane permeability
* inhibits enzymes important in microorganism’s function

Antibiotic Resistance methods

* Genetic mutation


* Inactivation of antibiotic
* Penicillin Resistance
* Modification of Target Molecule
* Increasing active efflux of the antibiotic

Causes of Antibiotic Resistance

* Lack of compliance w/ therapeutic regimen
* Overuse
* Destruction of the normal microbiome

W/IN 6-12 Hrs of an MI what tissue changes occur?

* sub-cellular cyanosis and decreased temperature
* No healing

W/IN 18-24 Hrs of an MI what tissue changes occur?

* Tissue color changes to gray or brown
* Inflammation
* Intercellular enzyme release

W/IN 2-4 Days of an MI what tissue changes occur?

* Visible Necrosis
* Proteolytic enzymes remove debris
* catecholamines
* lipolysis & glycogenolysis increase glucose levels & FFAs to help myocardial recovery from anaerobic state

W/IN 4-10 Days of an MI what tissue changes occur?

* soft w/ fatty changes in center
* Hemorrhage in infarcted area
* debris cleared collagen matrix produces

W/IN 10-14 Days of an MI what tissue changes occur?

* Weak, fibrotic scar with some revascularization
* Healing continues but mushy and vulnerable to stress

W/IN 6 Weeks of an MI what tissue changes occur?

* scarring complete
* Tough inelastic scar replaces necrotic myocardium

HF is the interplay of 2 factors

* Inability of failing heart to maintain sufficient CO to support body functions
* Recruitment (and subsequent failure) of compensatory mechanisms designed to maintain cardiac reserve.

Antibiotic therapy based on culture and sensitivity of the organism, such as 

* Doxycycline
* Ciproflaxin
* LevoFLOXacin
* Azithromycin
* Ceftriaxone

Nitrofurantoin macrocrystals for patients with allergies to

sulfamethoxazole-trimethoprim or resistance to *E. coli*

What is given for UTIs during pregnancy?

Nitrofurantoin macrocrystals, amoxicillin, or cephalexin

What is bactrim often given in combo with for continuous antimicobial prophylaxis for chronic UTIs?

Nitrofurantoin Macrocrystals

Phenazopyridine is given for…

1-2 days for relief of dysuria.

NSTEMI

present w/ CP and no EKG changes w/ elevated troponins

STEMI

Elevated ST segment w/ CP but do not develop Q waves w/ elevated troponin

Absence of Q waves =

better prognosis as it indicates reperfusion

QwMI

Present w/ ST segment elevation and progress to have Q waves w/ elevated troponin.

Ischemia

lack of O2

Ischemia in EKG

* T wave Inversion or ST depression in leads facing the ischemic areas
* The T intervals are symmetrical, relatively narrow, and a bit pointed in ischemia
* ST depressions of >1-2mm and longer than 0.08 sec → ischemia

Myocardial Injury

Prolonged Ischemia

Myocardial Injury in EKG

* ST segment elevation
* > 1mm in standard leads or >2 mm in precordial leads

Infarction

cell death

MI in EKG

Significant Q

* 0.04 sec. or more in width
* 1/4 - 1/3 of the height of the R wave
* Usually develops in hours of onset of the infarction and may not be apparent for 1-2 days

Female pt. Symptoms of MI

* Indigestion
* Fatigue
* Pain described as pressure
* Dyspnea

Unstable Angina S+S

* Pain at rest >20 min
* New Onset
* Not relieved w/ NTG or rest
* Severe and prolonged than previous symptoms

Pathologic changes of Ischemia

ischemic areas cease to function in min

Pathologic changes of Injury

Irreversible damage/death to myocardial cells occurs w/in 20-40 min.

Pathologic changes of Infarction

Early reperfusion after onset of ischemia can prevent further ischemia and necrosis; once the cardiac cells die no coming back.

Acute Management via **Fibrinolytic therapy – tPA. Streptokinase, Urokinase Qualifications**

* Pt. must be at low risk for bleeding
* No recent trauma in three months

Acute Management via Percutaneous Coronary Interventions (PCI)

Balloon PTCA – percutaneous transluminal coronary angioplasty (with stent placement)

Acute Management via CABG - coronary artery bypass graft surgery

* open heart
* saphenous vein or mammary artery is used