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Green Patho > Foundational Concepts- Basics, Inflm and Infection > Flashcards

Foundational Concepts- Basics, Inflm and Infection Flashcards

1
Q

Etiology- Definition and 5 General categories

A

Etiology (Et)- Cause of disease /causative factors
o Idiopathic- unknown origin
o Congenital – d/t dev abn in utero, present at birth
o Genetic- hereditary, parent to offspring
o Acquired- post natal, d/t pathogens, toxins and injury
o Introgenic- d/t Tx or procedural error (ex catheterization and bladder infection.

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2
Q

Define Predisposition

A

promoting development of disease (ex. Smoking predisposes lung cancer)

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3
Q

Define Lesion

A

Local Pathological tissue change (could be anything from incision or pimple, internal or external)

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4
Q

Define Subclinical

A

Pathology present with no obvious mnfts

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5
Q

Injury refers to a l/o function- Extent of injury is dependent on:

A

Agent- (i.e pathogen or trauma)
Intensity
Duration

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6
Q

What are the 3 basic problems injury causes?

A
  • Deficiency (lack of 02 l/o fx) (ex MI or CVA)
  • Intoxication (toxins l/o fx)
  • Trauma (Altered str, L/o fx
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7
Q

1) Mechanism of Injury- Def. Free radical Production

A

Are toxic reactive chem fragments (ex 02-) that can create chem interference (target DNA, proteins and membranes)

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8
Q

2) Mechanisms of injury- Def. Hypoxia

A

Deficiency in 02- affects metabolism and ATP production (inhibits fx)

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9
Q

3) Mechanisms of injury- Def Ca+ Imbalance

A

Ca+ plays a role in many fx, altered concentration gradients cause l/o fx
Agent of injury- Ca+ influx and release from mitochodria. Increase of CA causes increased activity of Es and potential cell damage (Example of Es Affected- ATPase, phospholipidase, protease)

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10
Q

3 basic mechanisms of injury

A

1) Free radical production
2) Hypoxia
3) Ca+ imbalance

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11
Q

Define Atrophy

A

Decrease in size of cells= reduction in mass and tissue wasting
(NOTE: Atrophy refers to decrease in cell size, but a reduction in tissue mass can also be caused by a reduction in cell number. Whether the tissue is likely to reduce in size of cells or number of cells is dependent on tissue type and ease of cellular replication. Epithelial cells would reduce in number, muscle cells reduce size)

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12
Q

Define Hyperplasia

A

Increase in cell number= increase in mass of tissue

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13
Q

Define Hypertrophy

A

increase in cell size= enlargement of tissue mass

Note: Fig 5-2 heart enlargement (enlargement of heart is almost always pathological, except extreme atheletes

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14
Q

Define Metaplasia

A

Tissue replacement of normal differentiated tissue with another normal differentiated tissue.
(NOTE: key example is pseudo stratified columnar epithelial cells in resp. tract, damaged by smoke and replaced by stratified epithelial cell = more protection and less fx)

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15
Q

Defina Dysplasia

A

Faulty cell replacement in a tissue- could be faulty in terms of size, shape, or organization

  • Increase Mitotic index (high division rates)
  • Can be pre-cancerous
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16
Q

Define Anaplasia

A

Undifferentiated cell growth
o Assoc. w/ CA
(NOTE:differentiated refers to all cells grow to specialize to the same type within tissue)

17
Q

Define Apoptosis

A

(p.103) Controlled death/replacement. Also called programmed death, is built into genetics and normal. Death occurs after a certain number of divisions or after a time period.

18
Q

Acute inflame- 3 parts of Vascular Response and what mediates the response

A

Vasoconstriction (mediated by nervous system for stat response, constriction is brief to allow for clotting)

Vasodilation and Permeability Change
• Leukocytes, mast cells, + platelets release mediators (i.e. Histamine + prostaglandins-> Affect blood vessels and nerves.
o Histamine-Increases capillary permeability and increases capillary dilation.
o Prostaglandins do both these and also mediate pain

19
Q

Acute inflm- Describe Vasodialation

Surface manifestations and mediated by?

A

Vessel dilation resulting in increased in blood flow (hyperemia) EMIA- meaning in blood… in this case blood volume)

• Mnfts as Redness and Warmth (not immediate and not nervous system, done through mediators)

20
Q

Acute Inflm- What does increase permeability of vessels allow for?

A

Allows Exudate (fluid, blood and protein) to enter injured tissues. Fluid movement is described as a fluid shift. Fluid and protein shift cause swelling and pain -> which in turn causes patient to immobilize the area.

21
Q

Cardinal Signs of local Inflm

A
  • Redness (erythema- Eryth- RBC, Emia- blood)
  • Swelling
  • Warmth
  • Pain
  • L/o Fx
22
Q

Acute Inflm- 3 Key Progressive Steps of Cellular Response.

A
  • Diapedesis (emigration into tissue spaces)
  • Chemotaxis (locomotion along chemical gradient of Neutrophils and other WBC to injury site)
  • Phagocytosis (of cell debris and foreign particles)
23
Q

Exudate- Def and 5 Types

A
  • Serous – (Mostly fluid, low in proteins and cells. Mild acute inflm. Note: Both plasma and serum are fluid in blood- Serum w/o clotting factor and plasma w/ clotting factor)
  • Purulent/Suppurative- (High in Pus (dead neutrophils), WBC, and Necrotic debris. Cloudy w/ foul odor- Suggests bacterial infection and severe acute inflm)
  • Hemorrhagic- (High in RBC, Severe injury)
  • Fibrinous- (High in Fibrinogen, strands of sticky mesh)
  • Membranous- (dev mucous membrane, necrotic cells in Fibropurulent exudate)
24
Q

Tell Me About Fever- Benefits, Causes, Mediator

A

• Fever Is a systemic manifestation along with malaise, fatigue, headache often associated with infection

Benefits of Fever
• Enhances phagocytosis and Immune Response (IR)
• Inhibits Reproduction and growth of pathogens

Pathogenesis of Fever
• Not intentional, consequential but beneficial
• Pathologic Temp change and not easily brought down
• Most cases are related to infection and the toxins released by bacteria known as pyrogens
• Mediated by prostaglandin E2 (PGE2) migration to hypothalamus and increase set point of bodies thermoregulation

25
Q

Describe events leading to a Fever (pathogenesis)

A 
exogenous pyrogens (derived from outside the body) →induce host cells to produce fever-producing mediators, ie. stimulates the (a large cascade of) production of
endogenous pyrogens (released by the body called IL1 Interleukin 1, IL6 Interleukin 6, TNF Tumor.Necrosis.Factor)
→act to inc. the set point by binding to the receptor at the Hypothalamic receptor, mediated by PGE2 (Prostaglandin E2)
→resulting in the temp set point adjusted upwards
via cAMP (Adenosene MonoPhosphate, internal cellular messenger which helps the PGE2 bind)
note: if a fever develops in an absence of infection, then there will be no exogenous pyrgens eg/ type of anemia which causes excessive cell breakdown would make an additional source of pyrogens instead eg/ myocardial infarction, pulmonary emboli, neoplasm’s, trauma or Sx causing injured cells, or Leukemia or Hodgkin’s disease causing abnormal cells)
26
Q

Tell me about C-reactive Protean (CRP)

A
  • Marker for inflm, specifically serum marker [found in blood serum] (Note: Also a Marker for Atherosclerosis (Cardio Vascular Disease- CVD)
  • Protein produced in liver (hepatic protein)
  • Role in defense via complement (complement are inactive proteins produced by liver and circulating in blood which are activated during immune response)
27
Q

2 categories of medication associated with tx of acute inflame and their action on inflm.

A

o NSAID’s (non steroidal anti inflm drugs) Reduce prostaglandin synthesis -> Reduction in inflm and pain

o Steroidal (anti inflm drugs)
• Reduce Permeability, inhibits WBC and Masts cells moving to site of injury
• Reduces prostaglandins and histamine release
• Have major side effects and are dangerous in high does or over the long term

28
Q

Basic Tx’s for Inflm

A
  • Cold-> Reduces swelling (vasoconstriction)
  • Elevation and pressure- (reduces blood flow/exudate/pain)
  • Heat-> stimulates phagocytosis
  • Drugs-> NSAIDS and Steroids
29
Q

Mech of Infec.- 4 Major portals of Entry

A

Penetration, Direct contact, Ingestion, Inhalation

30
Q

Portals of Entry- Discuss Penetration + Examples

A

Entry from a break in the bodies surface barriers (i.e. skin or mucous membranes) Examples include abrasions, burns, punctures from any activity (accident, surgery, bites, etc) skin lesions (from a primary infectious process- chicken pox)

31
Q

Portals of Entry- Discuss Direct Contact + Examples

A

Entry from contact with infectious agents/tissues to intact mucous membranes (i.e. STI’s Gonorrrhea, Herpes, etc)
o Vertical transmission can occur between mother and child when mucous membranes come in contact during birth. (Congenital infections)

32
Q

Portals of Entry- Discuss Inhalation + Examples

A

Entry of infectious agent through the respiratory tract. Infectious agents must overcome protections such as sweeping ciliated epithelial cell, coughing and respiratory secretions of antibodies and enzymes to successfully gain entry. Examples includes bacterial pneumonia, menigitus, influenza.

33
Q

Portals of Entry- Discuss Ingestion + Examples

A

Entry of infectious agents through the oral cavity and gastrointestinal tract. Very commonly through contaminated food and water. Examples are bacterial, viral and parasitic infections- cholera, dysentery, hep A. Infectious agent must be able to survive low ph and gastric secretions aswell out compete bacteria within system to reproduce (infectious dose)

34
Q

6 Stages of Disease Course

A
  • Incubation- Pathogen begins active reproduction without causing symptoms in host
  • Prodromal- Symptoms first appear in host (fever, pain, myalgia, etc)
  • Acute- Period of most pronounced and specific symptoms of infection corresponding with rapid proliferation of pathogen. Period when tissue damage or even host death is most likely to occur
  • Convalescent- Period of containment and progressive elimination of pathogen. Tissue repair and symptom resolution begins
  • Resolution- Total elimination of pathogen from body as well as corresponding symptoms of disease
35
Q

Common strategies for Diagnosis of Infection

A
  • Culture- Artificial propagation of microorganism in lab setting to grow to detectable levels (microscope or other means). Usually in brth or agar plate)
  • Serology- Measuring levels of serum antibodies from sample of diseased host.
  • DNA and RNA Sequencing- Detection of DNA or RNA sequence specific to an infectious agent.
36
Q

Clinical Mnftns of Infection- Local and systemic

A
  • Symptoms are the outward expression of inflammation and immune responses can be characteristic of any infectious agent
  • Can be localized (rash, diarrhea, pneumonia) or systemic (fever, myalgia)
  • Systemic- Fever, ?

Can be obvious (chickenpox) or require further lab testing (WBC)

37
Q

Discuss Drug Tx- Bacterial Infection

4 ways drug may act on a prokaryote cell?

A

• Antibiotics-(bactericidal) Produced by other bacteria/fungi as a byproduct of metabolism generally only work on other prokaryotes. Organized into family of compounds. General gram negative or gram positive or broad spectrum antibiotics. May cause unwanted toxic side-effects. Rapid growth of diverse antibiotic resistances 4 basic mechanisms of action:
o Interference with a step in bacterial cell wall synthesis (penicillin)
o Inhibition of bacterial protein synthesis
o Interruption of nucleic acid synthesis
o Interference with normal metabolism

38
Q

Discuss Drug Tx- Viral Infections

A

Early efforts all toxic to eukaryotes cells since virus uses host cell enzymes for replication. Antiviral compounds target RNA and DNA synthesis. (inhibition of viral DNA polyamerase) Or target virus ability to bind to eukaryote cell or…. The list goes on

39
Q

The rules about Complications

A

What to Know:
o Potential to develop (may not)
o Be aware of what they are
o Avoid them, if they develop, deal with them

Green Patho (18 decks)

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