Pathology 1 Flashcards

1. Adaptation, Injury, and Death 2. Clinical apps 3. Repair and Inflammation (220 cards)

1
Q

Necrosis

A

Death of cells, tissues, or organs in a living person

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2
Q

Apoptosis

A

Programmed cell death of single cells

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3
Q

Ischemia

A

Reversible injury due to inadequate blood supply

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4
Q

Infarction

A

Irreversible necrosis due to ischemia not relieved in time

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5
Q

Treatment for liquefaction necrosis

A

Drainage

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6
Q

Treatment for caseous necrosis

A

Anti-fungal and anti-TB

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7
Q

Treatment for gangrenous necrosis

A

Amputation

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8
Q

Etiology

A

Cause

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9
Q

Morphology

A

Visible manifestation

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10
Q

Adaptation

A

Physiologic and morphologic changes, modulating function, bringing it to a new altered steady state of homeostasis

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11
Q

T or F: Most vital organs have a large reserve capacity

A

T

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12
Q

Injury

A

Reversible pathophysiologic and morphologic response to stress or noxious stimulus
Exceeds capacity of cell, tissue, or organ to adapt but isn’t enough to be lethal

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13
Q

Injurious reactive oxygen species (ROS) include _________ (4).

A

Superoxide
Hydrogen peroxide
Hydroxyl radical
Peroxynitrite

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14
Q

Why can reperfusion be injurious?

A

It brings oxygen that can be converted to ROS and calcium that can increase mitochondrial permeability

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15
Q

Features of coagulative necrosis

A

Preservation of ghost cell outline
Cytoplasm has increased eosinophilia
Nucleus has pyknosis, karyorrhexis, and karyolysis
Acute inflammatory response

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16
Q

Pyknosis

A

Condensation, shrinkage, and hyperbasophilia of a dead cell nucleus

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17
Q

Karyorrhexis

A

Fragmentation of a pyknotic dead nucleus

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18
Q

Karyolysis

A

Fading away of a dead nucleus

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19
Q

Features of liquefactive necrosis

A

Necrosis with conversion of solid tissue to liquid due to severe acute infection or toxicity

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20
Q

Abscess

A

Localized area of liquefactive necrosis

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21
Q

Microabscess

A

Localized area of liquefactive necrosis visible only microscopically

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22
Q

Features of caseous necrosis

A

Resembles cheese
Granular
Eosinophilic
No ghost cells

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23
Q

Features of gangrene

A

Form of coagulative necrosis with blackening and shrinkage

Usually distal extremity

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24
Q

Features of fat necrosis

A

Adipose tissue is digested by pancreatic lipase, creating chalky white saponification

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25
Which enzymes are essential for apoptosis?
Caspases
26
Features of apoptosis (4)
1. Cell shrinkage 2. Cytoplasmic hypereosinophilia 3. Chromatin condensation and karyorrhexis 4. Phagocytosis by macrophages
27
T or F: There is an inflammatory response in apoptosis.
F
28
Differences between apoptosis and necrosis in cell number
Apoptosis small clusters or single cells; Necrosis large groups of cells
29
Differences in apoptosis and necrosis in regard to cell membrane
Apoptosis: cell membrane intact Necrosis: cell membrane disrupted
30
What are the categories of disease?
``` VITAMIN D Vascular Infectious Toxic Autoimmune Metabolic Idiopathic Neoplastic Developmental ```
31
What is the most common type of vascular disease?
Atherosclerosis
32
What comprises infectious disease?
Any disease caused by a virus, bacterium, prion, fungus, protozoan, or parasite
33
Toxic disease includes ________.
Diseases due to toxins, poisons, or other noxious substances (alcohol, radiation, injury, natural toxins, therapeutic drugs)
34
What are autoimmune diseases?
Body's immune system attacks its own cells, tissues, or organs
35
Metabolic diseases include ________.
Malnutrition, obesity, diabetes, vitamin deficiencies, nutritional disorders, and disorders due to inherited enzyme abnormalities
36
Neoplasm
A tumor -- autonomous growth of cells uncontrolled y the normal controls on cell proliferation
37
10 aspects for the systematic study of disease
1. Definition 2. Epidemiology 3. Pathogenesis 4. Gross Pathology 5. Microscopic Pathology 6. Symptoms (subjective) 7. Signs (objective) 8. Diagnosis 9. Treatment 10. Prognosis
38
The first step in knowing a disease is _____.
Having a precise definition of it
39
The first step in knowing the epidemiology of a disease is ______.
Knowing how common it is
40
Differential Diagnosis
List of all other diseases that can mimic it by producing similar manifestations
41
Occam's Razor
A single diagnosis that explains all of a patient's symptoms, signs, and other manifestations of disease is most likely the correct diagnosis
42
What are the 5 most medically important electrolytes in order of importance?
K, Na, HCO3, Cl, Ca
43
Why is potassium important?
Abnormal levels impair the heart's electrical signaling mechanism for the synchronized contraction essential to pumping blood.
44
A sufficiently severe disturbance in potassium levels can cause _______.
Potassium pump may fail and the heart may arrest, leading to death
45
What symptoms can occur due to hypokalemia?
``` Muscle weakness Fatigue Myalgias Ileus (loss of normal peristalsis) Irritability Tachychardia (rapid heart rate) Possible respiratory muscle weakness ```
46
What symptoms can occur due to hyperkalemia?
``` Renal failure (MOST IMPORTANT) Mental malfunctioning Bradychardia (slow heart rate) Nerve malfunctions Muscle weakness Paralysis Cardiac arrest ```
47
T or F: Hypokalemia interferes with contractility of skeletal muscle.
T
48
Which is more likely to cause fatal cardiac arrhythmia, hypokalemia or hyperkalemia?
Hyperkalemia
49
(Low/High) levels of sodium cause water to enter cells in excess, resulting in swelling.
Low
50
Symptoms of hyponatremia
Because of swollen brain cells: | headache, malaise, nausea, confusion, lethargy, obtundation (reduced mental capacity), stupor, coma, seizures, and death
51
Symptoms of hypernatremia
Confusion, disorientation, lethargy, obtundation, coma | Severe: breathing issues
52
Muscles of respiration must have _______ to work (vague question... my b).
Stimulus from the brain
53
How is bicarbonate different from K, Na, and the other electrolytes?
It isn't an element, and it's created in the body by renal metabolism
54
What leads to bicarbonate deficiency, ultimately leading to acidosis?
Renal failure (most common!), diarrhea, alcoholic ketoacidosis, diabeticketoacidosis, shock, respiratory failure, and lactic acid buildup
55
Bicarbonate deficiency leads to (acidosis/alkalosis), and bicarbonate excess leads to (acidosis/alkalosis).
Deficiency: acidosis Excess: alkalosis
56
What leads to bicarbonate excess, ultimately leading to alkalosis?
Hyperventilation and vomiting (vomiting also depletes K)
57
What is the most important function of bicarbonate?
Maintenance of acid/base balance
58
What is the traditional method for measuring bicarbonate in the lab?
You can't measure them directly. 1. Treat blood sample with a strong acid 2. Strong acid breaks down the bicarb and releases CO2 3. CO2 is measured as a surrogate for bicarb
59
Other than bicarbonate, what is an important source of CO2?
Carbonic acid, accounts for 5%
60
How is CO2 as a stand-in for bicarbonate improved in the lab?
Expose blood sample to atmosphere with 40 mm Hg of CO2 and add oxygen to fully oxygenate the hemoglobin
61
T or F: Standard bicarbonate in the lab is not actually bicarbonate being measured.
T
62
Ischemia
Inadequacy of blood supply
63
When does total ischemia occur and what is the result?
When the heart stops pumping blood | Causes loss of consciousness
64
What is the earliest gross pathologic change of ischemia?
Darkening of color
65
What is enzyme diagnosis?
Diagnosis of injury based upon injured cells releasing some of their contents into the bloodstream
66
T or F: Blood testing is typically used in diagnosing injury to the kidneys.
F: Not used because renal cells don't have unique cellular contents
67
How is renal injury diagnosed?
By monitoring the output of its liquid product and the buildup of waste products in the bloodstream (urea and creatinine)
68
T or F: Blood testing is typically used in diagnosing injury to the pancreas.
T
69
How is lung injury diagnosed?
Functional assessment, biopsy
70
How is myocardial injury diagnosed?
Blood enzyme testing
71
How is brain injury diagnosed?
Radiological imaging studies (MRI, CT)
72
How is liver injury diagnosed?
Blood enzyme testing
73
How is small intestinal injury diagnosed?
Capsule endoscopy -- film the lumen of the GI tract
74
How is colon injury diagnosed?
Colonoscopy
75
How are stomach problems diagnosed?
Nasogastric Intubation -- pass a tube through the nose into the stomach Gastroscopy (specific diagnosis) Examine stool
76
What is one of the most problematic organs in which to diagnose injury, and why?
Jejunum of the small intestine: not accessible by endoscopy, injury must be really advanced to be diagnosed by radiological imaging or surgery
77
Amylase is secreted by _______.
Pancreas and salivary glands
78
Lipase function
Digests fats
79
Injury to the pancreas releases which enzyme(s) into the bloodstream in large amounts?
Amylase and Lipase
80
How can you diagnose mild, moderate, and severe pancreatitis?
Mild: radiologic imaging Moderate: causes edema visible on CT Severe: causes hemorrhage, liquefactive and fat necrosis visible on radiological imaging
81
T or F: Amylase is only present in the pancreas and salivary glands.
F: Also present in intestine, liver, kidney, muscle, fat, spleen, fallopian tube, heart, lung, and brain
82
T or F: Amylase is excreted in the urine.
T
83
What physiological changes can lead to increased amylase levels?
``` Pancreatitis Renal failure Appendicitis Out of control diabetes Ectopic pregnancy Tumors of the lung or ovary Salivary gland inflammation ```
84
Most of the lipase in serum is produced in ________ but some is secreted by ________(4).
Most is in pancreas, but some is secreted by lingual salivary glands (but not parotid), gastric mucosa, intestinal mucosa, and pulmonary mucosa
85
T or F: Lipase is present in leukocytes and adipose tissue cells.
T
86
With acute pancreatitis, which serum levels remain elevated longer: lipase or amylase?
Lipase
87
T or F: The higher the serum amylase or lipase, the higher likelihood that the diagnosis is pancreatitis.
T
88
What are the two organs for which blood testing is most often used to diagnose injury?
1. heart | 2. liver
89
ALT catalyzes the interconversion of _____.
Glu and Ala
90
AST catalyzes the interconversion of _____.
Glu and Asp
91
Liver injury is more likely to elevate the (ALT/AST) out of proportion to the (ALT/AST) than injury to any other organ.
ALT out of proportion to the AST
92
What's the de Ritis ratio, and what is it used for?
AST/ALT | Can be helpful in differentiating causes of hepatic injury
93
What diseases lower the de Ritis ratio from normal?
Acute hepatic injury
94
What diseases raise the de Ritis ratio from normal?
Chronic hepatic disease causing injury Hyperbilirubinemia Intrahepatic biliary obstruction Alcoholic liver disease
95
Where is gamma-glutamyltransferase (GGT) located and what is its function?
On the outer cell membranes of nearly all out cell types; functions to transport amino acids into cells
96
Which type of cell has the most GGT?
Hepatocytes
97
What is the relationship of GGT, ALT, and AST levels in cholestasis and alcoholic liver disease?
GGT increases more than AST and ALT increase
98
What is the relationship of GGT, ALT, and AST levels in extreme hepatic injury (i.e. viral infection or Tylenol overdose)?
ALT and AST increase more than GGT increases
99
What is the single best test for diagnosing liver disease? What if you can do a duo and a trio?
Single: ALT Duo: ALT, AST Trio: ALT, AST, GGT
100
What is the relationship of ALT, AST, and ALP levels in cholestatic liver diseases?
ALP is elevated out of proportion to ALT and AST
101
What is the relationship of ALP to GGT in alcoholic liver disease?
Less elevation of ALP than GGT
102
What is the relationship of ALP to GGT in malignant liver tumors.
Much more elevation of ALP than GGT
103
What is the function of alkaline phosphatase (ALP)?
Group of enzymes that transfer inorganic phosphate from donor to receptor molecules at an alkaline pH
104
In normal adults, most serum ALP is from ______.
Liver or Bone
105
What physiological changes cause elevated ALP levels?
Some bone diseases, especially Paget's bone disease Normal puberty Normal pregnancy (placental ALP) Some malignant tumors Cholestatic liver disease Alcoholic liver disease (smaller elevation)
106
What is the function of lactate dehydrogenase (LDH)?
Catalyzes the conversion of lactate to pyruvate by removing two hydrogens
107
What physiological changes cause elevated LDH levels?
``` Skeletal muscle injury Myocardial infarction Pulmonary infarction Some types of pneumonia Hepatitis Hemolysis (erythrocyte breakdown) ```
108
How effective is elevated LDH in making a diagnosis?
By itself it's not very effective, but plays a good role when combined with other tests
109
What is autolysis?
The morphologic response that all organs and tissues take on when a person dies No inflammation Gradual fading of the components of every cell
110
What usually causes infarcts?
Occlusion of an artery by a blood clot that formed at the site of occlusion (thrombosis) or traveled there (thromboembolism)
111
T or F: Occlusion of a vein usually causes infarction.
F: Because the body has alternative pathways for venous flow from most organs
112
Where does venous infarction usually occur?
Testes and ovaries
113
What factors influence whether reversible ischemia becomes irreversible infarction? (4)
1. Vulnerability of the tissue 2. Rate of development 3. Alternative blood supply 4. Blood oxygenation
114
What are causes of infarction other than arterial or venous occlusion?
Spasm of the artery Hemorrhage into a loose lesion of atherosclerosis Trauma involving blood vessels Strangulated hernia
115
What is a treatment for ischemia of leg muscles?
Exercise sufficient to cause the pain of leg ischemia (claudication)
116
T or F: Diseases that impair blood oxygenation in the lungs or blood oxygen-carrying capacity make ischemia anywhere in the body more likely to cause infarction faster.
T
117
What is the typical general appearance of an infarct?
Peripheral, subcapsular, and wedge-shaped | Base on the capsular surface and the apex at the site of the occluded artery
118
What are "white anemic" infarcts?
Infarcts typical of solid organs with end-arterial circulation Reperfusion may cause blood to pour into the infarct from necrotic edges of infarcted arteries
119
What are the mechanisms of "red hemorrhagic" infarcts?
1. Venous occlusion 2. Dual/anastomosing blood supply 3. Reperfusion
120
What is typical of a cerebral infarction?
It tends to develop liquefactive necrosis, probably due to the blood brain barrier.
121
_______ can render a cerebral infarction hemorrhagic.
Reperfusion
122
What is the current standard blood test for acute myocardial infarction?
Troponin
123
What is creatine phosphokinase (CPK/CK) and what is it composed of?
An enzyme that catalyzes the transfer of phosphate from creatine phosphate to ADP, creating ATP. It's composed of M and B dimers
124
Where is CK concentrated?
In muscle and brain
125
Start, Peak, and Normalization of CK-MB for MI
Start 3 hours Peak 24 hours Normalization 48 hours
126
Start, Peak, and Normalization of AST for MI
Start 24 hours Peak 48 hours Normalization 4 days
127
Start, Peak, and Normalization of LDH for MI
Start 24 hours Peak 72 hours Normalization 7 days
128
Start, Peak, and Normalization of Troponin for MI
Start 3 hours Peak 24 hours Normalization 10 days
129
For the diagnosis of acute MI, elevated troponin needs to be combined with 1 of the following: (4).
1. Symptoms of ischemia 2. EKG evidence of ischemia 3. Imaging evidence of ischemia 4. Identification of an intracoronary thrombus by angiography or autopsy
130
Why is it recommended to repeat troponin determination at least once when diagnosing myocardial infarction?
The sensitivity of the troponin level for the diagnosis of acute MI improves if it is assayed 10 hours after the onset of chest pain
131
_______ is primarily a term for the gross pathology of the most common form of ischemic necrosis.
Infarction
132
What is the most common cause of abscesses?
Necrotizing infections
133
Why aren't antibiotics able to treat microorganisms within an abscess?
Blood vessels are destroyed within an abscess so antibiotics can't get in
134
When does physiologic apoptosis occur?
Embryogenesis Involution Ending inflammation Deleting self-reactive lymphocytes
135
When does pathologic apoptosis occur?
``` In injury due to hypoxia, heat, radiation or chemotherapy Certain viral diseases Duct obstruction Transplant rejection Tumors ```
136
T or F: Both intrinsic and extrinsic pathways of apoptosis activate caspases.
T
137
What happens once cells have died by apoptosis?
Cell membrane remains intact No inflammatory response The cells become targets for phagocytosis by macrophages
138
Top 6 chief complaints
1. Abdominal pain 2. Chest pain 3. Dyspnea (shortness of breath) 4. Fatigue 5. Fever 6. Syncope (fainting)
139
Causes of Fatigue
``` Vascular: heart failure Infectious: mono, TB Toxic: drugs, alcoholic liver disease Autoimmune: lupus, myasthenia gravis Metabolic: hypothyroidism, hypoadrenalism Idiopathic: depression, sarcoidosis Neoplastic: anemia Developmental: renal failure due to genetic disease, etc. ```
140
Causes of Hypoglycemia
``` Sepsis Insulin Alcohol Hormone deficiency Hepatic failure ```
141
Causes of Hyponatremia
Vomiting Diarrhea Heart failure Hypoaldosteronism
142
Causes of Hyperkalemia
Renal failure Tissue necrosis Hypoaldosteronism
143
What are fibroblasts?
Cells that produce the interstitial ground substance of supporting tissue throughout the body
144
________ is the main fiber of the extracellular matrix.
Collagen
145
_______ are the key cellular players in the process of tissue repair.
Fibroblasts
146
Fibroblasts can differentiate into ________, but not _______.
Can differentiate into specialized connective tissue cells (i.e. osteocytes, chondrocytes, adipocytes) but not epithelial cells
147
The fibrous tissue that ______ produce to replace dead tissue is a scar.
Fibroblasts
148
Scar tissue lacks ______.
The specialized functional capacity of the tissue that it replaces
149
Scars are generally (smaller/larger) than the tissue they replace.
Smaller
150
________ are "collagen engineers".
Fibroblasts
151
What are myofibroblasts?
Fibroblasts that contain abundant contractile proteins; The effector cells of wound contraction
152
What is the general structure of active fibroblasts?
- Spindle-shaped, elongated, with tapering ends, usually sharply pointed, sometimes bifurcated, sometimes resembling a swallow tail, or star shaped - Large nuclei with prominent nucleoli
153
The cytoplasm of fibroblasts tends to be ______.
Basophilic because it has lots of RNA
154
How are fibroblasts recruited to and activated at sites of repair?
By transforming TGF-beta, FGF-2, and PDGF secreted by inflammatory cells
155
Inactive fibroblasts are sometimes called ______.
Fibrocytes
156
Can fibrocytes still serve repair functions?
Yes -- they are stable cells and ready to be called for duty at any time
157
What is the predominant type of white blood cells in the innate immune system response to infection?
Neutrophils
158
What is the predominant white blood cell type in acute inflammation?
Neutrophils
159
What are the first responder phagocytes?
Neutrophils
160
What are other names for neutrophils?
Segs, Polys, PMNs
161
T or F: Neutrophils can be part of chronic inflammation. Why or why not?
T: Partly because they can respond to necrosis
162
________ cause demargination of neutrophils and can increase the number of neutrophils measured.
Corticosteroids
163
What is neutrophilia?
An increased number of segmented neutrophils in the blood
164
What color are neutrophil granules?
Neutral duhhh. Not red or blue
165
What are neutrophil nuclei like?
Variably shaped nuclei segmented into 2 to 5 lobes
166
_________ neutrophils are associated with megaloblastic anemia due to vitamin B12 or folate deficiency.
Hypersegmented
167
Neutrophils with nuclei segmented into _____ or more lobes are hypersegmented.
6
168
What are bands?
Immature (adolescent) neutrophils
169
Where are bands a higher percent of the neutrophilic granulocytes?
In bone marrow
170
T or F: Bands are capable of phagocytosis.
T
171
What is bandemia?
When a person has a severe infection, the bone marrow releases bands into the blood in increasing numbers
172
The presence of increased numbers of immature leukocytes in the blood is referred to as _____.
A left shift
173
T or F: Corticosteroids can cause left shift.
F
174
T or F: Corticosteroids does not cause bandemia.
T
175
The earliest bone marrow precursor cells of granulocytes have ________ nuclei. As they mature, the nuclei become _______.
Round-oval become flattened on one side
176
How does the size of bands relate to the size of fully mature segmented neutrophils?
They're roughly the same size
177
How can the proportion of bands in a blood sample be determined?
Can only be determined by labor-intensive counting by a person with a microscope
178
What are macrophages?
Phagocytes derived from blood monocytes
179
What makes up the mononuclear phagocyte system?
``` Monocytes Macrophages Kupffer cells Sinus histiocytes (in lymph nodes and spleen) Microglial cells (in CNS) Alveolar macrophages (in lungs) ```
180
Who arrives at inflammation sites first: macrophages or neutrophils?
Neutrophils
181
Which type of cell is the dominant player in chronic inflammation?
Macrophage
182
M1 macrophages secrete __________ (4).
IL-1, IL-2, IL-23, and chemokines
183
M2 macrophages secrete _________.
Transforming growth factor beta and other growth factors that stimulate tissue repair and fibrosis
184
(M1/M2) macrophages are anti-inflammatory and (M1/M2) macrophages are pro-inflammatory.
M2: anti M1: pro
185
M2 macrophages are activated by ________ (2).
IL-3 and IL-4
186
T or F: Macrophage nuclei are typically segmented.
F: macrophage nuclei are never segmented
187
The color of the monocyte cytoplasm in peripheral blood smears is ________.
Blue-grey or sky blue
188
What color is the cytoplasm of macrophages in tissue?
Variably colored depending on what they eat
189
Macrophages at the site of a recent MI also contain _______(2).
Lipofuscin and hemosiderin
190
What increases the lifespan of a macrophage?
Being recruited to become tissue macrophages increases their lifespan from a day to months or years
191
What type of cell is the fundamental player in the adaptive immune system?
Lymphocyte
192
What are the most common types of lymphocyte?
T cells (carry out cell-mediated immunity) and B cells (carry out humeral immunity)
193
What do CD4+ T cells do?
They help B cells make antibodies and help macrophages destroy phagocytosed microbes
194
What do CD8+ T cells do?
They are directly involved in killing virus-infected cells and malignant tumor cells
195
Predominantly lymphocytic inflammation can be due to either _________ or ______.
Infection or autoimmune disease
196
What do lymphocytes look like?
They're small cells with round dense nuclei and scant cytoplasm
197
What are plasma cells?
Cells derived from activated B cells that produce large amounts of single-specificity antibody in adaptive immune response
198
T or F: Plasma cells are not normally present in peripheral blood.
T
199
What do plasma cells look like?
They have nuclear chromatin clumped around the periphery in a clock face configuration and a prominent perinuclear Golgi apparatus
200
What are eosinophils?
Granulocytic leukocytes found in the inflammation around parasitic infestations and allergic reactions
201
Eosinophils participate most in immune reactions mediated by Ig__.
E
202
The granules of eosinophils take up ______.
Eosin (red dye)
203
What are eosinophil nuclei like?
They only have 2 lobes usually
204
T or F: Mast cells participate in both acute and chronic inflammation.
T
205
Where are mast cells found?
Around blood vessels, nerves, and skin
206
What is the counterpart cell type to the mast cell?
Basophil
207
Mast cell granules are loaded with ______ (6).
``` Histamine Chemotactic factors for neutrophils and eosinophils Leukotrienes Proteases Platelet-activating factor Cytokines ```
208
Mast cell granules take up ______.
Hematoxylin (blue dye) and other basophilic dyes
209
What do histamine and leukotrienes do?
They cause vasodilation and endothelial cell contraction, mediating changes of inflammation
210
What are consequences of the action of histamine?
Person can suffer fatal laryngeal edema or anaphylactic shock
211
What are multinucleated giant cells?
They represent a syncytium of macrophages in a site of chronic inflammation
212
What are the most common types of multinucleated giant cells?
Foreign body type and Langhans type
213
When do foreign body multinucleated giant cells form?
When a single macrophage finds itself unable to engulf and phagocytose a large particle and it coalesces with other macrophages to try to ingest the particle
214
Langhans type multinucleated giant cells are associated with _______.
Immune granulomas
215
What is a granuloma?
An aggregate of activated macrophages working together
216
When do immune type granulomas form?
When persistent antigen induces a cell-mediated immune reaction
217
When do foreign body granulomas form?
When there's material too large or undigestible for clearance
218
What are the nuclei like in foreign body giant cells and in Langhans giant cells?
Foreign body: haphazardly arranged nuclei | Langhans: nuclei arranged in a semicircle peripherally
219
The macrophages that form Langhans giant cells have cytoplasm that is _______.
Epitheloid: smoother and more eosinophilic than typical macrophages
220
What are the cellular playerz in chronic inflammation? (6)
1. Macrophages 2. Lymphocytes 3. Plasma Cells 4. Eosinophils 5. Mast Cells 6. Multinucleated Giant Cells