Exam 1 Flashcards
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1
Q
Pathology
A
Study of disease, all aspects of disease
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
3
Q
Homeostasis
A
Relatively stable internal environment
4
Q
Health
A
When our physical and mental capabilities can be fully utilized
5
Q
Disease
A
Disruption in homeostasis - unhealthy state of body part, system, or body as a whole
6
Q
Etiology
A
The study of disease causation
7
Q
Genetic etiology
A
Defective genes are responsible for structural/functional defect
“error in genes”
EX) sickle cell, color blindness, muscular dystrophy
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
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
10
Q
Idiopathic
A
If cause is unknown
EX) Alzheimer’s, multiple sclerosis, cancer
11
Q
Medical history
A
Description of nature and timing of patients abnormalities
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.
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)
14
Q
Findings
A
Results from lab tests, CT imaging, or exploratory surgery that clarify clinical picture
15
Q
Syndrome
A
Combination of signs and symptoms associated with a specific disease
“Cluster of signs and symptoms”
16
Q
Pathogenesis
A
Pattern of disease development - from onset to manifestation
Time over which disease develop
17
Q
Acute
A
Rapid onset, develop quickly, and usually are short duration
18
Q
Chronic
A
Usually are longer duration. Onset can be sudden or insidious - onset is slow and concerns are not immediate
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)
20
Q
Sequela
A
A condition resulting from a disease
“aftermath of a disease”
21
Q
Lesions
A
Somatic distribution of damage sites/anatomical derangement
22
Q
Local lesions
A
Damage is confined to one region of body
23
Q
Systemic lesions
A
Damage is more widely distributed
24
Q
Focal lesions
A
Within disease organ, damage is confined to one of more distinct sites
EX) bronchopulmonary segments of lungs
25
Diffuse lesions
If lesions are more uniformly distributed throughout the organ
EX) entire lung is full of cancer
26
Diagnosis
Analysis of signs and symptoms, coupled with knowledge of Pathogenesis leads to (diagnosis) or the identification of patients disease
27
Therapy
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
28
Palliative treatment
Attempts to reduce suffering
29
Prognosis
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
30
Framingham Study
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)
31
Levels of Prevention
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
32
Causes of cell injury
Deficiency
Intoxication
Trauma
33
Deficiency
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
34
Ischemia
A decrease in blood supply due to either occlusion (blockage) or loss of pressure
"not enough blood"
35
Hypoxia
Inadequate oxygenation due to failure of respiratory, cardiovascular system, or red blood cells
"not enough oxygen"
36
Tisses differ in their ability to tolerate hypoxia:
Some tissues really sensitive to low oxygen
- brain
- heart
- kidney
Others really resilient
-fiberblasts
37
Nutritional Deficiency
Lack of nutrient.
| May be primary or secondary
38
Primary nutritional deficiency
Do not have in diet
EX) goiter - lack of iodine; "scurvy" - lack of vitamin C
39
Secondary nutritional deficiency
Taking enough in, but body is not able to use it
EX) diabetes
40
Infection
Microorganisms also consume substances essential for normal cell metabolism
EX) bacteria, fungi
41
Does ischemia lead to hypoxia?
Yes
42
Does hypoxia lead to ischemia
No
43
Intoxication
Presence of substance that interferes with cell function, poisoning
44
Toxins
Are injurious substances that interfere with normal function
"poison"
45
Two major origins of toxins
Exogenous - originate outside of cell
Endogenous - originate inside cell
46
Exogenous - biological
Produced by Microorganisms
EX) E. coli, MRSA, staff infection
47
Exogenous - non-biological
Injurious chemicals that originate outside the body
EX) drug overdose, CCl4, mercury, lead paint
48
Endogenous - genetic defect
Produces toxin
49
Endogenous - free radicals
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)
50
Endogenous - impaired circulation (ischemia)
Allows metabolic byproducts to accumulate to toxic levels
EX) CO2 and H+
51
Trauma
Loss of cells structural integrity, physical injury
52
Trauma - hypothermia
Due to extreme cold
EX) frostbite - blood becomes highly viscous (thick) and blood vessels vasoconstrict
53
Trauma - hyperthermia
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
54
Trauma - ioninizing radiation
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).
55
Trauma - mechanical pressure
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
56
Viruses - mechanism of action
Bits of DNA or RNA
| Need host cell (cold = epithelial cells, HIV = helper T-cells)
57
Cellular Adaptation
Cell damage is often reversible because of adaptive responses
58
Adaptive responses
Altered size or number
- Hypertrophy
- atrophy
- hyperplasia
- metaplasia
- Dysplasia
59
Hypertrophy
Process of cell and organ enlargement due to increased demands
Can be normal, pathological, or compensatory
60
Normal hypertrophy
Increased demand
EX) body builders
61
Pathological hypertrophy
Underlying pathological condition
EX) myocardial cells enlarge due to valvular stenosis (narrowing of heart valves)
62
Compensatory hypertrophy
Compensating for something
63
Atrophy
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
64
Hyperplasia
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
65
Metaplasia
Change from one cell type to another - a response to chronic irritation/inflammation
Is reversible
66
Dysplasia
Disordered growth
- cell types abnormal
- always pathological
Next step: cancer
67
Altered functional capabilities
Alternative metabolism
Organelle changes
Intracellular accumulations/residual bodies
68
Alternative metabolism
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
69
Organelle changes
Altering the complement of organelles to better meet a demand
70
Intracellular accumulations/residual bodies
"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
71
Hydrophic change
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
72
Fatty change
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)
73
Irreversible injury and cell death
A result of extreme membrane distortions, increased permeability, or lysosomal liberation
Best indicator of irreversible injury is an altered nucleus
74
Pyknosis
Shrink and condense
75
Karyorrhexis
Breaks up into small, dispersed fragments
76
Karyolysis
Nucleus seems to fade and melt into cytoplasm
"nuclear dust"
77
Apoptosis/PCD (programmed cell death
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
Necrosis
Characterized by cell membrane breakdown and tissue death
-Always pathological and unregulated
Neighboring cells are also affected
"messy"
Always causes inflammation
79
Types of necrosis
```
Coagulation necrosis
Liquefaction necrosis
Caseous necrosis
Gangrenous necrosis
Calcification necrosis
```
80
Coagulation necrosis
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
Liquefaction necrosis
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
Caseous necrosis
A form of coagulation necrosis seen most often in tuberculosis.
-rare
Pale, yellow, granular, "cheese-like" appearance
83
Gangrenous necrosis
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
Dry gangrene
Extremity becomes dry and shrinks
85
Wet gangrene
Superimposed bacterial infection
86
Gas gangrene
Infection of the necrotic area with clostridium perfringens
Progresses very quickly
May produce foul smelling gas
87
Calcification
Calcium deposition
| bone forming in soft tissues
88
Dystrophic calcification
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
Assessment of functional loss
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
Detections of cell constituents released from injured cell
Injured cells may leak substances at faster rate, so high plasma levels may indicate cell injury
91
Elevated plasma potassium can indicate:
Hemolysis, indicating large-scale rupture of cells
92
High levels of creatine phosphate (CPK) indicates:
Skeletal, cardiac, or brain tissue damage
93
Monitoring of electrical activity
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
Direct tissue examination
A small sample of tissue is taken during a biopsy. Sample is examined for tissue organization and cell characteristics
95
Body temperature reflects the difference between
Heat production and heat loss
96
Core body temperature
97-99.5 deg Fahrenheit = thermostatic set point
97
Core body temperature is regulated by:
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
Mechanisms of heat production (in cold conditions)
```
Shivering
Vasoconstriction
Arrector Pili
Sweat glands are inactive
Behavioral
```
99
Mechanisms of heat loss (in hot conditions)
Sudoriferous glands activated
100
Fever/pyrexia
An elevation in body temperature that is cause by a PGE induced upward displacement of the set point of the hypothalamic thermoregulatory center
101
Febrile
Feverish
102
Thermostatic failure
Fever above 105.5
103
Etiology of fever
A symptom rather than a disease
104
Pyrogens
Fever causing agents
105
Exogenous pyrogens
Come from outside the body and trigger the release of PGE
EX) gram-negative bacteria have component called lipopolysaccharides (LPS)
106
Endogenous pyrogens
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
Manifestations/signs and symptoms of fever
Weakness, anorexia, myalgia, fatigue, pallor, shivering, headache, malaise (feel sick), tachycardia
108
Benefits of fever
Increases in temperature may
- interfere with pathogen
- speed immune response
109
Harmful effects of fever
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
Treatment of fever
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
Behavioral responses (fever)
Cold compresses, ice baths, breezes
FYI: "brain cooling" by cooling forehead and nasal region leading to cavernous sinus
112
Hyperthermia
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
In increasing levels of severity, hypothermia includes:
Heat cramps
Heat exhaustion
Heatstroke
114
Heat cramps
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
Heat exhaustion
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
Heat stroke
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
Symptoms and treatment of heat stroke
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
Osmosis
Diffusion of water through a semipermeable membrane (water moves from higher to lower concentration)
Moves toward a higher solute concentration
119
Plasma proteins - albumin
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
Filtration/hydrostatic pressure
Water pressure forcing substances through a membrane
Pushing pressure
EX) like a coffee filter
121
2 main types of white blood cells
Granulocytes: NEB
Agranulocytes: ML
122
Leukocytosis
Increase in WBC
123
Leukopenia
Decrease in WBC
124
Neutrophils
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
Eosinophils
1-3% of WBCs
Increase in number in allergic or parasitic worm infections
May help to control inflammation and allergic reactions
126
Basophils
Less than 1% of WBCs
Granules contain histamine (vasodilator)
Similar to mast cells
- contain histamine
- all around body
127
Polymorphonuclear
"many-shaped" nucleus
128
Segs
Nuclei broke into different pieces
129
Bands
Immature "baby" neutrophils
Nuclei not broken yet
Lots of bands, could be fighting infection
130
Monocytes
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
Lymphocytes
20-30% of WBCs
Two types:
1. B-cells - production of antibodies
2. T-cells - cell mediated immunity
132
Blood hydrostatic pressure (BHP)
(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
Tissue osmotic pressure (TOP)
(arterial end)
| [solute] Outside of vessel is higher, so water moves out
134
Tissue hydrostatic pressure (THP)
(venous end)
| Pressure outside of vessel is higher due to fluid being driven into confined spaces
135
Blood osmotic pressure (BOP)
(venous end)
| [plasma proteins] higher near vein end, so water is pulled back in
136
Excess interstitial fluid is gathered by:
Lymphatic system and returned to circulatory system
Extra interstitial fluid leads to edema
137
Inflammation
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
What can cause inflammation
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
Cardinal signs (of inflammation)
1. rubor
2. calor
3. dolor
4. tumor
5. loss of function
140
rubor
redness
lots of blood (vasodilation)
hyperemic response
141
calor
heat
lots of blood - blood is warm
142
dolor
pain
could be from chemicals (released from damaged tissue), pH - lactic acid, lots of fluid (swelling)
143
tumor
swelling
caused by fluid in tissue spaces
144
functions of the inflammatory response
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
vascular response (of inflammation)
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
cellular response (of inflammation)
movement of leukocytes (WBCs) into the injured area
147
normal blood flow =
axial blood flow - elements cluster along long axis of vessel: plasma surrounds column
148
how do WBCs get to the site of injury?
```
margination
pavementing
emigration
chemotaxis
phagocytosis
```
149
margination of WBCs
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
pavementing of WBCs
adherence of the marginated WBCs to the endothelium
"fried egg look"
151
emigration of WBCs
through diapedesis, the leukocytes squeeze between endothelial cells and into the tissues
also called Extravasation
152
chemotaxis of WBCs
migration in response to chemical signals
153
phagocytosis of WBCs
ingestion and digestion of bacteria and cellular debris
154
phagocytosis: cell types
Macrophages (monocytes)
| Neutrophils
155
phagocytosis: process
REK
- recognize
- engulf
- kill
156
chemical mediators
directly or indirectly elicit the vascular and cellular responses
- Histamine
- Arachidonic Acid Derivatives
- Bradykinin
- Lymphokines/Cytokines
157
Histamine
released from mast cells
effects in inflammation: "vasoactive substance"
- vasodilation (dilates arteries)
- increases capillary permeability
- short half-life = transient reaction (30 minutes)
158
Arachidonic Acid Derivatives
- found in phospholipids (of cell membrane)
- phospholipase A2 act on phospholipids creating arachidonic acid
COX/Lipoxygenase pathways
159
COX pathway
prostagladins (PG)
Effects in inflammation:
- vasodilation
- increase capillary permeability
- fever
160
Lipoxygenase pathway
Leukotrienes
Effects in inflammation:
-increases capillary permeability and chemotactic to WBCs
161
Bradykinin
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
Lymphokines/Cytokines
substances released by lymphocytes that promote chemotaxis
163
Why do we treat inflammation?
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
inflammation: temperature
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
inflammation: elevation and pressure
in limbs, elevation and pressure wraps decrease swelling and promote lymphatic drainage
166
inflammation: pharmacology (drug therapy)
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
acute inflammation exudates (listed)
serous exudate
fibrinous exudate
membranous exudate
purulent exudate
168
exudate defined
protein rich fluid that is found in inflamed tissues
169
serous exudate
mild injury
mostly plasma
ex) blister, joint swelling, rhinitis (runny nose)
170
fibrinous exudate
commonly seen in serous membranes (organ or lining cavity)
increased fibrinogen
-forms thick and stringy exudate
EX) appendicitis, peritonitis, pleuritis
171
membranous exudate
mucous membrane surfaces
EX) Thrush (oral cavity, patches of membranous inflammation)
common in very young and very old or immuno compromised individuals
172
purulent or suppurative exudate
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
empyema
pus filled body cavity
174
outcomes of acute inflammation
1. 100% resolution - back to normal histology
2. chronic inflammation - if the injurious agent persists
3. scarring - loss of function
175
chronic inflammation: characteristics
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
chronic inflammation: causes
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
two patterns of chronic inflammation
nonspecific
| granulomatous
178
nonspecific inflammation
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
granulomatous inflammation
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
granuloma
1-2 mm lesion with macrophages surrounded by lymphocytes
trying to "wall-off" or neutralize something
181
epitheloid cells
large accumulations of macrophages (from monocytes)
182
multi-nucleated giant cells
cells may clump = granuloma, or coalesce forming large cells with >200 nuclei
macrophages that have joined together to form one giant cell
