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HSC 411 > Exam 1 > Flashcards

Exam 1 Flashcards

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1
Q

Pathology

A

Study of disease, all aspects of disease

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2
Q

Pathophysiology

A

Study of abnormal functioning of diseased organs with application to diagnostic procedures and patient care

How the body functions in diseased conditions

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3
Q

Homeostasis

A

Relatively stable internal environment

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4
Q

Health

A

When our physical and mental capabilities can be fully utilized

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5
Q

Disease

A

Disruption in homeostasis - unhealthy state of body part, system, or body as a whole

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6
Q

Etiology

A

The study of disease causation

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7
Q

Genetic etiology

A

Defective genes are responsible for structural/functional defect

“error in genes”

EX) sickle cell, color blindness, muscular dystrophy

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8
Q

Congenital etiology

A

Genetic info intact, other factors of embryo’s intrauterine environment interfere with normal development.

“error in prenatal development”

May be caused by: medications, poor nutrition, drug/substance abuse

EX) fetal alcohol syndrome, atrial septic defect (ASD) spina bifida, cleft palate, anencephaly

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9
Q

Acquired etiology

A

Genes and development are normal; however, factors encountered later produce the disease.

Caused by “Something later in life”

What we do to ourselves to get disease, caused by lifestyle, bacteria, toxins, viruses, etc.

EX) tuberculosis, emphysema, and hepatitis

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10
Q

Idiopathic

A

If cause is unknown

EX) Alzheimer’s, multiple sclerosis, cancer

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11
Q

Medical history

A

Description of nature and timing of patients abnormalities

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12
Q

Symptoms

A

Subjective evidence as described by patient

Hard to measure, must take patients word

EX) pain, itchiness (pruritis), anxiety, numbness, vertigo, fatigue, nausea, etc.

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13
Q

Signs

A

Are detected by observer. Elevated blood pressure or irregular heart beat. Signs emerge during physical examination.

EX) pale, blue in color (cyanotic), listen to breathing, take temp, rash on skin, excessive sweating (diaphoresis)

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14
Q

Findings

A

Results from lab tests, CT imaging, or exploratory surgery that clarify clinical picture

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15
Q

Syndrome

A

Combination of signs and symptoms associated with a specific disease

“Cluster of signs and symptoms”

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16
Q

Pathogenesis

A

Pattern of disease development - from onset to manifestation

Time over which disease develop

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17
Q

Acute

A

Rapid onset, develop quickly, and usually are short duration

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18
Q

Chronic

A

Usually are longer duration. Onset can be sudden or insidious - onset is slow and concerns are not immediate

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19
Q

Chronic diseases are often characterized by:

A

Remission - signs and symptoms subside

Exacerbation - signs and symptoms return (can be the same signs or symptoms or different)

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20
Q

Sequela

A

A condition resulting from a disease

“aftermath of a disease”

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21
Q

Lesions

A

Somatic distribution of damage sites/anatomical derangement

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22
Q

Local lesions

A

Damage is confined to one region of body

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23
Q

Systemic lesions

A

Damage is more widely distributed

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24
Q

Focal lesions

A

Within disease organ, damage is confined to one of more distinct sites

EX) bronchopulmonary segments of lungs

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25
Q

Diffuse lesions

A

If lesions are more uniformly distributed throughout the organ

EX) entire lung is full of cancer

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26
Q

Diagnosis

A

Analysis of signs and symptoms, coupled with knowledge of Pathogenesis leads to (diagnosis) or the identification of patients disease

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27
Q

Therapy

A

Once diagnosis is established, (therapy) treatment of the disease with aim of cure or reducing signs and symptoms to level where normal functional capacity can be restored

-has aim of cure, alleviate suffering

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28
Q

Palliative treatment

A

Attempts to reduce suffering

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29
Q

Prognosis

A

Assessment of body’s response to therapy, knowledge of Pathogenesis, and clinical experience all combine for a prediction of patients outcome

Excellent prognosis - likely to recover

Poor - associated with higher morbidity or mortality

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30
Q

Framingham Study

A

Cohort study/longitudinal study
Set up by US Public Health Service to study the characteristics of people who would later develop coronary heart disease
5000 people aged 30-59 for a period of 20 years (predicted 1500 would have heart disease)

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31
Q

Levels of Prevention

A

Primary - remove risk factors
-prevents disease from occurring

Secondary - early detection and treatment
-Detects and cures disease in the asymptomatic phase

Tertiary - reduce complications
-reduces complications of disease

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32
Q

Causes of cell injury

A

Deficiency
Intoxication
Trauma

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33
Q

Deficiency

A

Lack of substance necessary to cell. Many factors play a role in deficiencies.

Some examples include: adequate oxygen, pH balance, ion balance, etc.

-ischemia and hypoxian

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34
Q

Ischemia

A

A decrease in blood supply due to either occlusion (blockage) or loss of pressure

“not enough blood”

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35
Q

Hypoxia

A

Inadequate oxygenation due to failure of respiratory, cardiovascular system, or red blood cells

“not enough oxygen”

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36
Q

Tisses differ in their ability to tolerate hypoxia:

A

Some tissues really sensitive to low oxygen

  • brain
  • heart
  • kidney

Others really resilient
-fiberblasts

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37
Q

Nutritional Deficiency

A

Lack of nutrient.

May be primary or secondary

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38
Q

Primary nutritional deficiency

A

Do not have in diet

EX) goiter - lack of iodine; “scurvy” - lack of vitamin C

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39
Q

Secondary nutritional deficiency

A

Taking enough in, but body is not able to use it

EX) diabetes

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40
Q

Infection

A

Microorganisms also consume substances essential for normal cell metabolism

EX) bacteria, fungi

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41
Q

Does ischemia lead to hypoxia?

A

Yes

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42
Q

Does hypoxia lead to ischemia

A

No

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43
Q

Intoxication

A

Presence of substance that interferes with cell function, poisoning

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44
Q

Toxins

A

Are injurious substances that interfere with normal function

“poison”

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45
Q

Two major origins of toxins

A

Exogenous - originate outside of cell

Endogenous - originate inside cell

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46
Q

Exogenous - biological

A

Produced by Microorganisms

EX) E. coli, MRSA, staff infection

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47
Q

Exogenous - non-biological

A

Injurious chemicals that originate outside the body

EX) drug overdose, CCl4, mercury, lead paint

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48
Q

Endogenous - genetic defect

A

Produces toxin

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49
Q

Endogenous - free radicals

A

Produced by normal cellular processes
Highly reactive chemical species
Can cause widespread damage
-have unpaired electron - trying to gain stability - highly reactive

Free radicals can be scavenged by antioxidants (vitamin E and C)

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50
Q

Endogenous - impaired circulation (ischemia)

A

Allows metabolic byproducts to accumulate to toxic levels

EX) CO2 and H+

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51
Q

Trauma

A

Loss of cells structural integrity, physical injury

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52
Q

Trauma - hypothermia

A

Due to extreme cold

EX) frostbite - blood becomes highly viscous (thick) and blood vessels vasoconstrict

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53
Q

Trauma - hyperthermia

A

Extreme heat damages cells by disrupting and coagulating (denaturing) proteins

EX) burns - source of heat can be direct contact with source, solar radiation, or electric current

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54
Q

Trauma - ioninizing radiation

A

Can produce toxic chemical fragments called free radical. Free radicals interrupt normal cellular function and damage proteins, especially susceptible is DNA. This leads to problems with reproduction of cell (mitosis) and organisms (meiosis).

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55
Q

Trauma - mechanical pressure

A

Forces cell membrane to explode or degenerate

EX) blood force trauma, breaks, car accident, etc.

Also could occur from a tumor - tumor puts pressure on surrounding cells and causes cells to die

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56
Q

Viruses - mechanism of action

A

Bits of DNA or RNA

Need host cell (cold = epithelial cells, HIV = helper T-cells)

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57
Q

Cellular Adaptation

A

Cell damage is often reversible because of adaptive responses

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58
Q

Adaptive responses

A

Altered size or number

  • Hypertrophy
  • atrophy
  • hyperplasia
  • metaplasia
  • Dysplasia
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59
Q

Hypertrophy

A

Process of cell and organ enlargement due to increased demands
Can be normal, pathological, or compensatory

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60
Q

Normal hypertrophy

A

Increased demand

EX) body builders

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61
Q

Pathological hypertrophy

A

Underlying pathological condition

EX) myocardial cells enlarge due to valvular stenosis (narrowing of heart valves)

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62
Q

Compensatory hypertrophy

A

Compensating for something

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63
Q

Atrophy

A

Decrease in cell size

Due to: disuse, ischemia, lack of neural or hormonal input

EX) bedridden patients lose muscle and skeletal mass, broken bones/cast, stroke-no neural imput

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64
Q

Hyperplasia

A

Process of producing new cells by mitosis in response to increased demand

“increased number of cells”

Must have the ability to undergo mitosis

Muscle cells do not have the ability to go through mitosis

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65
Q

Metaplasia

A

Change from one cell type to another - a response to chronic irritation/inflammation

Is reversible

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66
Q

Dysplasia

A

Disordered growth

  • cell types abnormal
  • always pathological

Next step: cancer

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67
Q

Altered functional capabilities

A

Alternative metabolism
Organelle changes
Intracellular accumulations/residual bodies

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68
Q

Alternative metabolism

A

For example, in hypoxia, cells switch from oxidative phosphorylation to glycolysis

Or, if there is a disruption of glucose, cells can switch to fat and/or protein

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69
Q

Organelle changes

A

Altering the complement of organelles to better meet a demand

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70
Q

Intracellular accumulations/residual bodies

A

“within cell accumulations”

Build up of substances that cells do not dispose of. This gives pathologists an idea about the history of damage.

EX) lipofusion granules

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71
Q

Hydrophic change

A

Damage leads to water entering cells to be sequestered into vacuoles
-reversible

If enough water enters, cell (and ER, Golgi, Mito) swells and cytoplasm gets paler. Condition is known as cloudy swelling or Hydrophic degeneration

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72
Q

Fatty change

A

Cell injury causes fat to accumulate. This causes cells to get bigger, which makes organ get bigger,
Eventually, cell ruptures and fat is deposited inside organ

Accumulation of lipid within non-adipocytes

EX) liver (#1 cause is alcohol damage)

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73
Q

Irreversible injury and cell death

A

A result of extreme membrane distortions, increased permeability, or lysosomal liberation

Best indicator of irreversible injury is an altered nucleus

74
Q

Pyknosis

A

Shrink and condense

75
Q

Karyorrhexis

A

Breaks up into small, dispersed fragments

76
Q

Karyolysis

A

Nucleus seems to fade and melt into cytoplasm

“nuclear dust”

77
Q

Apoptosis/PCD (programmed cell death

A

Cell suicide or controlled cell death.
Can be normal or pathological
-eliminates cells that are worn out, overproduced, or genetically damaged
-triggered by gene activation

EX) mutated cells stay alive and reproduce

78
Q

Necrosis

A

Characterized by cell membrane breakdown and tissue death
-Always pathological and unregulated

Neighboring cells are also affected
“messy”
Always causes inflammation

79
Q

Types of necrosis

A 
Coagulation necrosis 
Liquefaction necrosis 
Caseous necrosis 
Gangrenous necrosis 
Calcification necrosis
80
Q

Coagulation necrosis

A

Retains outlines of cells

Firm and relatively intact region of necrosis with relatively normal architecture

  • still have cell structure
  • pale, ghost-like cells

MOST COMMON

81
Q

Liquefaction necrosis

A

When phagocytes secrete enzymes that liquefy tissue, seen often in the brain post anoxia where extracellular proteins like collagen are lacking

  • liquid region of dead cells, tissue fluid, and phagocytes
  • seen in brain and some infections (mostly bacterial)
82
Q

Caseous necrosis

A

A form of coagulation necrosis seen most often in tuberculosis.
-rare

Pale, yellow, granular, “cheese-like” appearance

83
Q

Gangrenous necrosis

A

A complication of necrosis characterized by decay (visible decay of tissue)

Especially problematic in the extremities if blood flow is compromised

-dry, wet, and gas

84
Q

Dry gangrene

A

Extremity becomes dry and shrinks

85
Q

Wet gangrene

A

Superimposed bacterial infection

86
Q

Gas gangrene

A

Infection of the necrotic area with clostridium perfringens

Progresses very quickly

May produce foul smelling gas

87
Q

Calcification

A

Calcium deposition

bone forming in soft tissues

88
Q

Dystrophic calcification

A

Slow, gradual accumulation of Ca++ leads to rigidity and brittleness in necrotic tissue

EX) calcified arteries

Cells that are stressed/injured/dying - deposit calcium

89
Q

Assessment of functional loss

A

Functional deterioration of internal organs can be assessed by measuring subtle changes in body fluids
(look at blood, urine, saliva, CSF)

EX) elevate bilirubin may indicate functional deterioration of liver cells

90
Q

Detections of cell constituents released from injured cell

A

Injured cells may leak substances at faster rate, so high plasma levels may indicate cell injury

91
Q

Elevated plasma potassium can indicate:

A

Hemolysis, indicating large-scale rupture of cells

92
Q

High levels of creatine phosphate (CPK) indicates:

A

Skeletal, cardiac, or brain tissue damage

93
Q

Monitoring of electrical activity

A

Can visually examine electrical activity of internal structures and compare to normal pattern

  • Electrocardiogram (EKG) for heart
  • Electroencephalogram (EEG) for brain
  • Electromyogram (EMG) for muscle
94
Q

Direct tissue examination

A

A small sample of tissue is taken during a biopsy. Sample is examined for tissue organization and cell characteristics

95
Q

Body temperature reflects the difference between

A

Heat production and heat loss

96
Q

Core body temperature

A

97-99.5 deg Fahrenheit = thermostatic set point

97
Q

Core body temperature is regulated by:

A

The thermoregulatory center in the hypothalamus

Integrates input from thermal receptors and initiates output responses that conserve of generate body heat
-a negative feedback homeostatic mechanism

98
Q

Mechanisms of heat production (in cold conditions)

A 
Shivering
Vasoconstriction
Arrector Pili
Sweat glands are inactive 
Behavioral
99
Q

Mechanisms of heat loss (in hot conditions)

A

Sudoriferous glands activated

100
Q

Fever/pyrexia

A

An elevation in body temperature that is cause by a PGE induced upward displacement of the set point of the hypothalamic thermoregulatory center

101
Q

Febrile

A

Feverish

102
Q

Thermostatic failure

A

Fever above 105.5

103
Q

Etiology of fever

A

A symptom rather than a disease

104
Q

Pyrogens

A

Fever causing agents

105
Q

Exogenous pyrogens

A

Come from outside the body and trigger the release of PGE

EX) gram-negative bacteria have component called lipopolysaccharides (LPS)

106
Q

Endogenous pyrogens

A

Substances produced in inflammatory response that act on receptors in hypothalamus

Interleukin, TNF, and other cytokines travel through blood brain barrier to trigger PGE formation

Exogenous pyrogens stimulate endogenous pyrogens

107
Q

Manifestations/signs and symptoms of fever

A

Weakness, anorexia, myalgia, fatigue, pallor, shivering, headache, malaise (feel sick), tachycardia

108
Q

Benefits of fever

A

Increases in temperature may

  • interfere with pathogen
  • speed immune response
109
Q

Harmful effects of fever

A

Heart rate increases 10 bpm per 1 deg F with fever
-this puts big strain on people with heart problems

Fever causes convulsions in some children - febrile seizures

> 105 disrupts brain function
106 tissue damage
109 leads to death

110
Q

Treatment of fever

A

Antipyretic therapy

Acetylsalicylic acid (aspirin) or acetaminophen inhibits prostaglandin production in hypothalamus

This blocks set point elevation and maintains set point closer to norm

111
Q

Behavioral responses (fever)

A

Cold compresses, ice baths, breezes

FYI: “brain cooling” by cooling forehead and nasal region leading to cavernous sinus

112
Q

Hyperthermia

A

Describes an increase in body temperature that occurs without a change in the set point of the hypothalamic thermoregulatory center. It occurs when the thermoregulatory mechanisms are overwhelmed by heat production excessive environmental heat of impaired dissipation of heat

113
Q

In increasing levels of severity, hypothermia includes:

A

Heat cramps
Heat exhaustion
Heatstroke

114
Q

Heat cramps

A

Slow, painful, skeletal muscle cramps and spasms that last for 1-3 minutes. This is due to excess loss of water and salt; when it is after heavy sweating water alone is replaced. Tonicity is disturbed.

115
Q

Heat exhaustion

A

Related to a gradual loss of salt and water, usually following prolonged and heavy exertion in a hot environment

Symptoms include:
-thirst, fatigue, nausea, giddiness, possibly delirium, and GI symptoms

Treatment
-rest in a cool environment, drink plenty of water, salt replacement

116
Q

Heat stroke

A

A severe, life-threatening failure of the thermoregulatory mechanisms resulting in an excessive increase in body temperature (greater than 104 deg)

-absence of sweating, loss of consciousness

-children and elderly most susceptible
(elderly over 50 - 80% fatal. Impaired heat loss + failure of homeostatic mechanisms)

117
Q

Symptoms and treatment of heat stroke

A

Symptoms: include dizziness, weakness, disorientation, nausea, convulsions, and coma. Skin is hot and dry, then becomes cool with time

Treatment: must cool body rapidly by submersion in cold water, application of ice packs, or spraying with water and fanning. GET MEDICAL HELP IMMEDIATELY!

118
Q

Osmosis

A

Diffusion of water through a semipermeable membrane (water moves from higher to lower concentration)

Moves toward a higher solute concentration

119
Q

Plasma proteins - albumin

A

Maintain osmotic pressure in blood
Stays in blood and creates a sucking pressure to prevent fluid from leaving the cell
Produced by liver

If albumin decreases - blood vessels leak

EX) alcoholics with cirrhosis - “blood belly”
EX) starving children - makes albumin but uses it for energy - get big belly

120
Q

Filtration/hydrostatic pressure

A

Water pressure forcing substances through a membrane

Pushing pressure

EX) like a coffee filter

121
Q

2 main types of white blood cells

A

Granulocytes: NEB

Agranulocytes: ML

122
Q

Leukocytosis

A

Increase in WBC

123
Q

Leukopenia

A

Decrease in WBC

124
Q

Neutrophils

A

PMSs
Polymorphonuclear, segs, bands

60-70% of WBCs
Phagocytes
First cells to arrive at site of inflammation
Have lifespan of ~24 hours, and must be constantly produced
-self-destruct, apoptosis

125
Q

Eosinophils

A

1-3% of WBCs
Increase in number in allergic or parasitic worm infections
May help to control inflammation and allergic reactions

126
Q

Basophils

A

Less than 1% of WBCs
Granules contain histamine (vasodilator)

Similar to mast cells

  • contain histamine
  • all around body
127
Q

Polymorphonuclear

A

“many-shaped” nucleus

128
Q

Segs

A

Nuclei broke into different pieces

129
Q

Bands

A

Immature “baby” neutrophils
Nuclei not broken yet

Lots of bands, could be fighting infection

130
Q

Monocytes

A

3-8% of WBCs
Largest of all WBCs
Second cells to arrive at site of inflammation, within ~2 days are the predominant cell type in the inflamed area
Phagocytic and engulf great quantities of material
When leave circulation are called macrophages

Live for months/years

131
Q

Lymphocytes

A

20-30% of WBCs

Two types:

  1. B-cells - production of antibodies
  2. T-cells - cell mediated immunity
132
Q

Blood hydrostatic pressure (BHP)

A

(arterial end)
Pressure of blood/water. It is higher near arterial side, so pushes out fluid. The fluid formed is called tissue fluid/interstitial fluid

133
Q

Tissue osmotic pressure (TOP)

A

(arterial end)

[solute] Outside of vessel is higher, so water moves out

134
Q

Tissue hydrostatic pressure (THP)

A

(venous end)

Pressure outside of vessel is higher due to fluid being driven into confined spaces

135
Q

Blood osmotic pressure (BOP)

A

(venous end)

[plasma proteins] higher near vein end, so water is pulled back in

136
Q

Excess interstitial fluid is gathered by:

A

Lymphatic system and returned to circulatory system

Extra interstitial fluid leads to edema

137
Q

Inflammation

A

Protective tissue response to injury or invasion - “-itis”
EX) meningitis, hepatitis, tendonitis, arthritis, etc.

It is the local reaction of vascularized tissue to injury that is essential in the healing of wounds and infections. It is the bridge between injury and healing.

138
Q

What can cause inflammation

A

Deficiency
Intoxication
Trauma

Note: although there are a variety of causes of inflammation, the sequence of events is similar regardless of the triggering event, it is nonspecific

139
Q

Cardinal signs (of inflammation)

A
  1. rubor
  2. calor
  3. dolor
  4. tumor
  5. loss of function
140
Q

rubor

A

redness

lots of blood (vasodilation)
hyperemic response

141
Q

calor

A

heat

lots of blood - blood is warm

142
Q

dolor

A

pain

could be from chemicals (released from damaged tissue), pH - lactic acid, lots of fluid (swelling)

143
Q

tumor

A

swelling

caused by fluid in tissue spaces

144
Q

functions of the inflammatory response

A
  1. neutralize and destroy the noxious agent
  2. limit spread of infectious agents to surrounding tissues
  3. removal of necrotic tissue
  4. aid in healing process
  5. respond swiftly to threats
145
Q

vascular response (of inflammation)

A

hemodynamic changes triggered by chemical mediators (HISTAMINE)

  • vasodilation of arterioles and venules supplying the area
  • interstitial fluid formation/edema increased permeability of capillaries and venules due to increased space between endothelial cells
146
Q

cellular response (of inflammation)

A

movement of leukocytes (WBCs) into the injured area

147
Q

normal blood flow =

A

axial blood flow - elements cluster along long axis of vessel: plasma surrounds column

148
Q

how do WBCs get to the site of injury?

A 
margination
pavementing
emigration
chemotaxis 
phagocytosis
149
Q

margination of WBCs

A

as fluid leaves circulation, blood slows and the viscosity of the blood increases causing the leukocytes to move to the periphery of the blood vessel

150
Q

pavementing of WBCs

A

adherence of the marginated WBCs to the endothelium

“fried egg look”

151
Q

emigration of WBCs

A

through diapedesis, the leukocytes squeeze between endothelial cells and into the tissues

also called Extravasation

152
Q

chemotaxis of WBCs

A

migration in response to chemical signals

153
Q

phagocytosis of WBCs

A

ingestion and digestion of bacteria and cellular debris

154
Q

phagocytosis: cell types

A

Macrophages (monocytes)

Neutrophils

155
Q

phagocytosis: process

A

REK

  • recognize
  • engulf
  • kill
156
Q

chemical mediators

A

directly or indirectly elicit the vascular and cellular responses

  • Histamine
  • Arachidonic Acid Derivatives
  • Bradykinin
  • Lymphokines/Cytokines
157
Q

Histamine

A

released from mast cells

effects in inflammation: “vasoactive substance”

  • vasodilation (dilates arteries)
  • increases capillary permeability
  • short half-life = transient reaction (30 minutes)
158
Q

Arachidonic Acid Derivatives

A
  • found in phospholipids (of cell membrane)
  • phospholipase A2 act on phospholipids creating arachidonic acid

COX/Lipoxygenase pathways

159
Q

COX pathway

A

prostagladins (PG)

Effects in inflammation:

  • vasodilation
  • increase capillary permeability
  • fever
160
Q

Lipoxygenase pathway

A

Leukotrienes

Effects in inflammation:
-increases capillary permeability and chemotactic to WBCs

161
Q

Bradykinin

A

protein found in plasma (associated with complement clotting factor)

effects in inflammation:

  • vasodilation and increases capillary permeability
  • PAIN

EX) venom in bee sting is mostly bradykinin

162
Q

Lymphokines/Cytokines

A

substances released by lymphocytes that promote chemotaxis

163
Q

Why do we treat inflammation?

A

damage to normal tissue
pain and swelling impair function
can lead to scarring and loss of function
basis for many disease processes
(asthma, RA, DJD, allergies, Alz, athero, DM, etc.)

164
Q

inflammation: temperature

A

COLD is applied early to damaged area to reduce swelling and exudate formation
-manipulates area on the surface, blood vessels vasoconstrict, use IMMEDIATELY

HEAT is applied later to enhance phagocytosis
-makes tissue more elastic-less prone to injury, blood vessels vasodilate and bring blood and phagocytes, use AFTER swelling is gone

165
Q

inflammation: elevation and pressure

A

in limbs, elevation and pressure wraps decrease swelling and promote lymphatic drainage

166
Q

inflammation: pharmacology (drug therapy)

A

antihistamines

  • blocks histamine [receptors]
  • EX) take for allergies when histamine is constantly being released

NSAIDS (non-steroidal anti-inflammatory drugs)

  • inhibits COX pathway so prostaglandins are not produced
  • EX) ibuprofen, naproxen, aspirin
167
Q

acute inflammation exudates (listed)

A

serous exudate
fibrinous exudate
membranous exudate
purulent exudate

168
Q

exudate defined

A

protein rich fluid that is found in inflamed tissues

169
Q

serous exudate

A

mild injury
mostly plasma

ex) blister, joint swelling, rhinitis (runny nose)

170
Q

fibrinous exudate

A

commonly seen in serous membranes (organ or lining cavity)

increased fibrinogen
-forms thick and stringy exudate

EX) appendicitis, peritonitis, pleuritis

171
Q

membranous exudate

A

mucous membrane surfaces

EX) Thrush (oral cavity, patches of membranous inflammation)

common in very young and very old or immuno compromised individuals

172
Q

purulent or suppurative exudate

A

Pus = WBCs, bacteria, proteins, tissue debris

caused by pyogenic bacteria

  • releases lots of WBCs
  • liquefaction necrosis

abcess: local collection of pus that is encapsulated EX) pimple

173
Q

empyema

A

pus filled body cavity

174
Q

outcomes of acute inflammation

A
  1. 100% resolution - back to normal histology
  2. chronic inflammation - if the injurious agent persists
  3. scarring - loss of function
175
Q

chronic inflammation: characteristics

A

may last for weeks, months, or years

site of inflammation is infiltrated with lymphocytes and monocytes with few neutrophils (first to arrive and short life)

176
Q

chronic inflammation: causes

A

persistance irritants

  • may develop from recurrent or progressive acute process
  • foreign bodies such as asbestos, silica, or suture material
  • viruses, bacteria, fungi, parasites or idiopathic sources
177
Q

two patterns of chronic inflammation

A

nonspecific

granulomatous

178
Q

nonspecific inflammation

A

most common

involves diffuse accumulation of macrophages and lymphocytes and fibroblasts

fibroblasts proliferate secreting collagen with resulting scar formation. many times this will result in normal tissue (parenchymal tissue) being replaced with scar tissue with a net decrease in the function of the organ
(kidney, liver, lung, intestine, etc)

179
Q

granulomatous inflammation

A

organized accumulation of cells
-granuloma

type of inflammation occurs because the noxious agent is poorly digestible and/or difficult to control

seen in TB, some fungal infections, splinters, and other foreign bodies such as sutures, silica, talc, etc.

180
Q

granuloma

A

1-2 mm lesion with macrophages surrounded by lymphocytes

trying to “wall-off” or neutralize something

181
Q

epitheloid cells

A

large accumulations of macrophages (from monocytes)

182
Q

multi-nucleated giant cells

A

cells may clump = granuloma, or coalesce forming large cells with >200 nuclei

macrophages that have joined together to form one giant cell

HSC 411 (4 decks)

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