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Pathology > Pathology 1 > Flashcards

Pathology 1 Flashcards

1. Adaptation, Injury, and Death 2. Clinical apps 3. Repair and Inflammation

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
Q

Which enzymes are essential for apoptosis?

A

Caspases

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26
Q

Features of apoptosis (4)

A
  1. Cell shrinkage
  2. Cytoplasmic hypereosinophilia
  3. Chromatin condensation and karyorrhexis
  4. Phagocytosis by macrophages
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27
Q

T or F: There is an inflammatory response in apoptosis.

A

F

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28
Q

Differences between apoptosis and necrosis in cell number

A

Apoptosis small clusters or single cells; Necrosis large groups of cells

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29
Q

Differences in apoptosis and necrosis in regard to cell membrane

A

Apoptosis: cell membrane intact
Necrosis: cell membrane disrupted

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30
Q

What are the categories of disease?

A 
VITAMIN D
Vascular
Infectious
Toxic
Autoimmune
Metabolic
Idiopathic
Neoplastic
Developmental
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31
Q

What is the most common type of vascular disease?

A

Atherosclerosis

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32
Q

What comprises infectious disease?

A

Any disease caused by a virus, bacterium, prion, fungus, protozoan, or parasite

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33
Q

Toxic disease includes ________.

A

Diseases due to toxins, poisons, or other noxious substances (alcohol, radiation, injury, natural toxins, therapeutic drugs)

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34
Q

What are autoimmune diseases?

A

Body’s immune system attacks its own cells, tissues, or organs

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35
Q

Metabolic diseases include ________.

A

Malnutrition, obesity, diabetes, vitamin deficiencies, nutritional disorders, and disorders due to inherited enzyme abnormalities

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36
Q

Neoplasm

A

A tumor – autonomous growth of cells uncontrolled y the normal controls on cell proliferation

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37
Q

10 aspects for the systematic study of disease

A
  1. Definition
  2. Epidemiology
  3. Pathogenesis
  4. Gross Pathology
  5. Microscopic Pathology
  6. Symptoms (subjective)
  7. Signs (objective)
  8. Diagnosis
  9. Treatment
  10. Prognosis
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38
Q

The first step in knowing a disease is _____.

A

Having a precise definition of it

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39
Q

The first step in knowing the epidemiology of a disease is ______.

A

Knowing how common it is

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40
Q

Differential Diagnosis

A

List of all other diseases that can mimic it by producing similar manifestations

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41
Q

Occam’s Razor

A

A single diagnosis that explains all of a patient’s symptoms, signs, and other manifestations of disease is most likely the correct diagnosis

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42
Q

What are the 5 most medically important electrolytes in order of importance?

A

K, Na, HCO3, Cl, Ca

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43
Q

Why is potassium important?

A

Abnormal levels impair the heart’s electrical signaling mechanism for the synchronized contraction essential to pumping blood.

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44
Q

A sufficiently severe disturbance in potassium levels can cause _______.

A

Potassium pump may fail and the heart may arrest, leading to death

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45
Q

What symptoms can occur due to hypokalemia?

A 
Muscle weakness
Fatigue
Myalgias
Ileus (loss of normal peristalsis)
Irritability 
Tachychardia (rapid heart rate)
Possible respiratory muscle weakness
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46
Q

What symptoms can occur due to hyperkalemia?

A 
Renal failure (MOST IMPORTANT)
Mental malfunctioning
Bradychardia (slow heart rate)
Nerve malfunctions
Muscle weakness
Paralysis
Cardiac arrest
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47
Q

T or F: Hypokalemia interferes with contractility of skeletal muscle.

A

T

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48
Q

Which is more likely to cause fatal cardiac arrhythmia, hypokalemia or hyperkalemia?

A

Hyperkalemia

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49
Q

(Low/High) levels of sodium cause water to enter cells in excess, resulting in swelling.

A

Low

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50
Q

Symptoms of hyponatremia

A

Because of swollen brain cells:

headache, malaise, nausea, confusion, lethargy, obtundation (reduced mental capacity), stupor, coma, seizures, and death

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51
Q

Symptoms of hypernatremia

A

Confusion, disorientation, lethargy, obtundation, coma

Severe: breathing issues

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52
Q

Muscles of respiration must have _______ to work (vague question… my b).

A

Stimulus from the brain

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53
Q

How is bicarbonate different from K, Na, and the other electrolytes?

A

It isn’t an element, and it’s created in the body by renal metabolism

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54
Q

What leads to bicarbonate deficiency, ultimately leading to acidosis?

A

Renal failure (most common!), diarrhea, alcoholic ketoacidosis, diabeticketoacidosis, shock, respiratory failure, and lactic acid buildup

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55
Q

Bicarbonate deficiency leads to (acidosis/alkalosis), and bicarbonate excess leads to (acidosis/alkalosis).

A

Deficiency: acidosis
Excess: alkalosis

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56
Q

What leads to bicarbonate excess, ultimately leading to alkalosis?

A

Hyperventilation and vomiting (vomiting also depletes K)

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57
Q

What is the most important function of bicarbonate?

A

Maintenance of acid/base balance

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58
Q

What is the traditional method for measuring bicarbonate in the lab?

A

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
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59
Q

Other than bicarbonate, what is an important source of CO2?

A

Carbonic acid, accounts for 5%

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60
Q

How is CO2 as a stand-in for bicarbonate improved in the lab?

A

Expose blood sample to atmosphere with 40 mm Hg of CO2 and add oxygen to fully oxygenate the hemoglobin

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61
Q

T or F: Standard bicarbonate in the lab is not actually bicarbonate being measured.

A

T

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62
Q

Ischemia

A

Inadequacy of blood supply

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63
Q

When does total ischemia occur and what is the result?

A

When the heart stops pumping blood

Causes loss of consciousness

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64
Q

What is the earliest gross pathologic change of ischemia?

A

Darkening of color

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65
Q

What is enzyme diagnosis?

A

Diagnosis of injury based upon injured cells releasing some of their contents into the bloodstream

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66
Q

T or F: Blood testing is typically used in diagnosing injury to the kidneys.

A

F: Not used because renal cells don’t have unique cellular contents

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67
Q

How is renal injury diagnosed?

A

By monitoring the output of its liquid product and the buildup of waste products in the bloodstream (urea and creatinine)

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68
Q

T or F: Blood testing is typically used in diagnosing injury to the pancreas.

A

T

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69
Q

How is lung injury diagnosed?

A

Functional assessment, biopsy

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70
Q

How is myocardial injury diagnosed?

A

Blood enzyme testing

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71
Q

How is brain injury diagnosed?

A

Radiological imaging studies (MRI, CT)

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72
Q

How is liver injury diagnosed?

A

Blood enzyme testing

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73
Q

How is small intestinal injury diagnosed?

A

Capsule endoscopy – film the lumen of the GI tract

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74
Q

How is colon injury diagnosed?

A

Colonoscopy

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75
Q

How are stomach problems diagnosed?

A

Nasogastric Intubation – pass a tube through the nose into the stomach
Gastroscopy (specific diagnosis)
Examine stool

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76
Q

What is one of the most problematic organs in which to diagnose injury, and why?

A

Jejunum of the small intestine: not accessible by endoscopy, injury must be really advanced to be diagnosed by radiological imaging or surgery

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77
Q

Amylase is secreted by _______.

A

Pancreas and salivary glands

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78
Q

Lipase function

A

Digests fats

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79
Q

Injury to the pancreas releases which enzyme(s) into the bloodstream in large amounts?

A

Amylase and Lipase

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80
Q

How can you diagnose mild, moderate, and severe pancreatitis?

A

Mild: radiologic imaging
Moderate: causes edema visible on CT
Severe: causes hemorrhage, liquefactive and fat necrosis visible on radiological imaging

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81
Q

T or F: Amylase is only present in the pancreas and salivary glands.

A

F: Also present in intestine, liver, kidney, muscle, fat, spleen, fallopian tube, heart, lung, and brain

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82
Q

T or F: Amylase is excreted in the urine.

A

T

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83
Q

What physiological changes can lead to increased amylase levels?

A 
Pancreatitis
Renal failure
Appendicitis
Out of control diabetes
Ectopic pregnancy
Tumors of the lung or ovary
Salivary gland inflammation
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84
Q

Most of the lipase in serum is produced in ________ but some is secreted by ________(4).

A

Most is in pancreas, but some is secreted by lingual salivary glands (but not parotid), gastric mucosa, intestinal mucosa, and pulmonary mucosa

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85
Q

T or F: Lipase is present in leukocytes and adipose tissue cells.

A

T

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86
Q

With acute pancreatitis, which serum levels remain elevated longer: lipase or amylase?

A

Lipase

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87
Q

T or F: The higher the serum amylase or lipase, the higher likelihood that the diagnosis is pancreatitis.

A

T

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88
Q

What are the two organs for which blood testing is most often used to diagnose injury?

A
  1. heart

2. liver

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89
Q

ALT catalyzes the interconversion of _____.

A

Glu and Ala

90
Q

AST catalyzes the interconversion of _____.

A

Glu and Asp

91
Q

Liver injury is more likely to elevate the (ALT/AST) out of proportion to the (ALT/AST) than injury to any other organ.

A

ALT out of proportion to the AST

92
Q

What’s the de Ritis ratio, and what is it used for?

A

AST/ALT

Can be helpful in differentiating causes of hepatic injury

93
Q

What diseases lower the de Ritis ratio from normal?

A

Acute hepatic injury

94
Q

What diseases raise the de Ritis ratio from normal?

A

Chronic hepatic disease causing injury
Hyperbilirubinemia
Intrahepatic biliary obstruction
Alcoholic liver disease

95
Q

Where is gamma-glutamyltransferase (GGT) located and what is its function?

A

On the outer cell membranes of nearly all out cell types; functions to transport amino acids into cells

96
Q

Which type of cell has the most GGT?

A

Hepatocytes

97
Q

What is the relationship of GGT, ALT, and AST levels in cholestasis and alcoholic liver disease?

A

GGT increases more than AST and ALT increase

98
Q

What is the relationship of GGT, ALT, and AST levels in extreme hepatic injury (i.e. viral infection or Tylenol overdose)?

A

ALT and AST increase more than GGT increases

99
Q

What is the single best test for diagnosing liver disease? What if you can do a duo and a trio?

A

Single: ALT
Duo: ALT, AST
Trio: ALT, AST, GGT

100
Q

What is the relationship of ALT, AST, and ALP levels in cholestatic liver diseases?

A

ALP is elevated out of proportion to ALT and AST

101
Q

What is the relationship of ALP to GGT in alcoholic liver disease?

A

Less elevation of ALP than GGT

102
Q

What is the relationship of ALP to GGT in malignant liver tumors.

A

Much more elevation of ALP than GGT

103
Q

What is the function of alkaline phosphatase (ALP)?

A

Group of enzymes that transfer inorganic phosphate from donor to receptor molecules at an alkaline pH

104
Q

In normal adults, most serum ALP is from ______.

A

Liver or Bone

105
Q

What physiological changes cause elevated ALP levels?

A

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
Q

What is the function of lactate dehydrogenase (LDH)?

A

Catalyzes the conversion of lactate to pyruvate by removing two hydrogens

107
Q

What physiological changes cause elevated LDH levels?

A 
Skeletal muscle injury
Myocardial infarction
Pulmonary infarction
Some types of pneumonia
Hepatitis
Hemolysis (erythrocyte breakdown)
108
Q

How effective is elevated LDH in making a diagnosis?

A

By itself it’s not very effective, but plays a good role when combined with other tests

109
Q

What is autolysis?

A

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
Q

What usually causes infarcts?

A

Occlusion of an artery by a blood clot that formed at the site of occlusion (thrombosis) or traveled there (thromboembolism)

111
Q

T or F: Occlusion of a vein usually causes infarction.

A

F: Because the body has alternative pathways for venous flow from most organs

112
Q

Where does venous infarction usually occur?

A

Testes and ovaries

113
Q

What factors influence whether reversible ischemia becomes irreversible infarction? (4)

A
  1. Vulnerability of the tissue
  2. Rate of development
  3. Alternative blood supply
  4. Blood oxygenation
114
Q

What are causes of infarction other than arterial or venous occlusion?

A

Spasm of the artery
Hemorrhage into a loose lesion of atherosclerosis
Trauma involving blood vessels
Strangulated hernia

115
Q

What is a treatment for ischemia of leg muscles?

A

Exercise sufficient to cause the pain of leg ischemia (claudication)

116
Q

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.

A

T

117
Q

What is the typical general appearance of an infarct?

A

Peripheral, subcapsular, and wedge-shaped

Base on the capsular surface and the apex at the site of the occluded artery

118
Q

What are “white anemic” infarcts?

A

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
Q

What are the mechanisms of “red hemorrhagic” infarcts?

A
  1. Venous occlusion
  2. Dual/anastomosing blood supply
  3. Reperfusion
120
Q

What is typical of a cerebral infarction?

A

It tends to develop liquefactive necrosis, probably due to the blood brain barrier.

121
Q

_______ can render a cerebral infarction hemorrhagic.

A

Reperfusion

122
Q

What is the current standard blood test for acute myocardial infarction?

A

Troponin

123
Q

What is creatine phosphokinase (CPK/CK) and what is it composed of?

A

An enzyme that catalyzes the transfer of phosphate from creatine phosphate to ADP, creating ATP. It’s composed of M and B dimers

124
Q

Where is CK concentrated?

A

In muscle and brain

125
Q

Start, Peak, and Normalization of CK-MB for MI

A

Start 3 hours
Peak 24 hours
Normalization 48 hours

126
Q

Start, Peak, and Normalization of AST for MI

A

Start 24 hours
Peak 48 hours
Normalization 4 days

127
Q

Start, Peak, and Normalization of LDH for MI

A

Start 24 hours
Peak 72 hours
Normalization 7 days

128
Q

Start, Peak, and Normalization of Troponin for MI

A

Start 3 hours
Peak 24 hours
Normalization 10 days

129
Q

For the diagnosis of acute MI, elevated troponin needs to be combined with 1 of the following: (4).

A
  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
Q

Why is it recommended to repeat troponin determination at least once when diagnosing myocardial infarction?

A

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
Q

_______ is primarily a term for the gross pathology of the most common form of ischemic necrosis.

A

Infarction

132
Q

What is the most common cause of abscesses?

A

Necrotizing infections

133
Q

Why aren’t antibiotics able to treat microorganisms within an abscess?

A

Blood vessels are destroyed within an abscess so antibiotics can’t get in

134
Q

When does physiologic apoptosis occur?

A

Embryogenesis
Involution
Ending inflammation
Deleting self-reactive lymphocytes

135
Q

When does pathologic apoptosis occur?

A 
In injury due to hypoxia, heat, radiation or chemotherapy
Certain viral diseases
Duct obstruction
Transplant rejection
Tumors
136
Q

T or F: Both intrinsic and extrinsic pathways of apoptosis activate caspases.

A

T

137
Q

What happens once cells have died by apoptosis?

A

Cell membrane remains intact
No inflammatory response
The cells become targets for phagocytosis by macrophages

138
Q

Top 6 chief complaints

A
  1. Abdominal pain
  2. Chest pain
  3. Dyspnea (shortness of breath)
  4. Fatigue
  5. Fever
  6. Syncope (fainting)
139
Q

Causes of Fatigue

A 
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
Q

Causes of Hypoglycemia

A 
Sepsis
Insulin
Alcohol 
Hormone deficiency
Hepatic failure
141
Q

Causes of Hyponatremia

A

Vomiting
Diarrhea
Heart failure
Hypoaldosteronism

142
Q

Causes of Hyperkalemia

A

Renal failure
Tissue necrosis
Hypoaldosteronism

143
Q

What are fibroblasts?

A

Cells that produce the interstitial ground substance of supporting tissue throughout the body

144
Q

________ is the main fiber of the extracellular matrix.

A

Collagen

145
Q

_______ are the key cellular players in the process of tissue repair.

A

Fibroblasts

146
Q

Fibroblasts can differentiate into ________, but not _______.

A

Can differentiate into specialized connective tissue cells (i.e. osteocytes, chondrocytes, adipocytes) but not epithelial cells

147
Q

The fibrous tissue that ______ produce to replace dead tissue is a scar.

A

Fibroblasts

148
Q

Scar tissue lacks ______.

A

The specialized functional capacity of the tissue that it replaces

149
Q

Scars are generally (smaller/larger) than the tissue they replace.

A

Smaller

150
Q

________ are “collagen engineers”.

A

Fibroblasts

151
Q

What are myofibroblasts?

A

Fibroblasts that contain abundant contractile proteins; The effector cells of wound contraction

152
Q

What is the general structure of active fibroblasts?

A
  • 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
Q

The cytoplasm of fibroblasts tends to be ______.

A

Basophilic because it has lots of RNA

154
Q

How are fibroblasts recruited to and activated at sites of repair?

A

By transforming TGF-beta, FGF-2, and PDGF secreted by inflammatory cells

155
Q

Inactive fibroblasts are sometimes called ______.

A

Fibrocytes

156
Q

Can fibrocytes still serve repair functions?

A

Yes – they are stable cells and ready to be called for duty at any time

157
Q

What is the predominant type of white blood cells in the innate immune system response to infection?

A

Neutrophils

158
Q

What is the predominant white blood cell type in acute inflammation?

A

Neutrophils

159
Q

What are the first responder phagocytes?

A

Neutrophils

160
Q

What are other names for neutrophils?

A

Segs, Polys, PMNs

161
Q

T or F: Neutrophils can be part of chronic inflammation. Why or why not?

A

T: Partly because they can respond to necrosis

162
Q

________ cause demargination of neutrophils and can increase the number of neutrophils measured.

A

Corticosteroids

163
Q

What is neutrophilia?

A

An increased number of segmented neutrophils in the blood

164
Q

What color are neutrophil granules?

A

Neutral duhhh. Not red or blue

165
Q

What are neutrophil nuclei like?

A

Variably shaped nuclei segmented into 2 to 5 lobes

166
Q

_________ neutrophils are associated with megaloblastic anemia due to vitamin B12 or folate deficiency.

A

Hypersegmented

167
Q

Neutrophils with nuclei segmented into _____ or more lobes are hypersegmented.

A

6

168
Q

What are bands?

A

Immature (adolescent) neutrophils

169
Q

Where are bands a higher percent of the neutrophilic granulocytes?

A

In bone marrow

170
Q

T or F: Bands are capable of phagocytosis.

A

T

171
Q

What is bandemia?

A

When a person has a severe infection, the bone marrow releases bands into the blood in increasing numbers

172
Q

The presence of increased numbers of immature leukocytes in the blood is referred to as _____.

A

A left shift

173
Q

T or F: Corticosteroids can cause left shift.

A

F

174
Q

T or F: Corticosteroids does not cause bandemia.

A

T

175
Q

The earliest bone marrow precursor cells of granulocytes have ________ nuclei. As they mature, the nuclei become _______.

A

Round-oval become flattened on one side

176
Q

How does the size of bands relate to the size of fully mature segmented neutrophils?

A

They’re roughly the same size

177
Q

How can the proportion of bands in a blood sample be determined?

A

Can only be determined by labor-intensive counting by a person with a microscope

178
Q

What are macrophages?

A

Phagocytes derived from blood monocytes

179
Q

What makes up the mononuclear phagocyte system?

A 
Monocytes
Macrophages
Kupffer cells
Sinus histiocytes (in lymph nodes and spleen)
Microglial cells (in CNS)
Alveolar macrophages (in lungs)
180
Q

Who arrives at inflammation sites first: macrophages or neutrophils?

A

Neutrophils

181
Q

Which type of cell is the dominant player in chronic inflammation?

A

Macrophage

182
Q

M1 macrophages secrete __________ (4).

A

IL-1, IL-2, IL-23, and chemokines

183
Q

M2 macrophages secrete _________.

A

Transforming growth factor beta and other growth factors that stimulate tissue repair and fibrosis

184
Q

(M1/M2) macrophages are anti-inflammatory and (M1/M2) macrophages are pro-inflammatory.

A

M2: anti
M1: pro

185
Q

M2 macrophages are activated by ________ (2).

A

IL-3 and IL-4

186
Q

T or F: Macrophage nuclei are typically segmented.

A

F: macrophage nuclei are never segmented

187
Q

The color of the monocyte cytoplasm in peripheral blood smears is ________.

A

Blue-grey or sky blue

188
Q

What color is the cytoplasm of macrophages in tissue?

A

Variably colored depending on what they eat

189
Q

Macrophages at the site of a recent MI also contain _______(2).

A

Lipofuscin and hemosiderin

190
Q

What increases the lifespan of a macrophage?

A

Being recruited to become tissue macrophages increases their lifespan from a day to months or years

191
Q

What type of cell is the fundamental player in the adaptive immune system?

A

Lymphocyte

192
Q

What are the most common types of lymphocyte?

A

T cells (carry out cell-mediated immunity) and B cells (carry out humeral immunity)

193
Q

What do CD4+ T cells do?

A

They help B cells make antibodies and help macrophages destroy phagocytosed microbes

194
Q

What do CD8+ T cells do?

A

They are directly involved in killing virus-infected cells and malignant tumor cells

195
Q

Predominantly lymphocytic inflammation can be due to either _________ or ______.

A

Infection or autoimmune disease

196
Q

What do lymphocytes look like?

A

They’re small cells with round dense nuclei and scant cytoplasm

197
Q

What are plasma cells?

A

Cells derived from activated B cells that produce large amounts of single-specificity antibody in adaptive immune response

198
Q

T or F: Plasma cells are not normally present in peripheral blood.

A

T

199
Q

What do plasma cells look like?

A

They have nuclear chromatin clumped around the periphery in a clock face configuration and a prominent perinuclear Golgi apparatus

200
Q

What are eosinophils?

A

Granulocytic leukocytes found in the inflammation around parasitic infestations and allergic reactions

201
Q

Eosinophils participate most in immune reactions mediated by Ig__.

A

E

202
Q

The granules of eosinophils take up ______.

A

Eosin (red dye)

203
Q

What are eosinophil nuclei like?

A

They only have 2 lobes usually

204
Q

T or F: Mast cells participate in both acute and chronic inflammation.

A

T

205
Q

Where are mast cells found?

A

Around blood vessels, nerves, and skin

206
Q

What is the counterpart cell type to the mast cell?

A

Basophil

207
Q

Mast cell granules are loaded with ______ (6).

A 
Histamine
Chemotactic factors for neutrophils and eosinophils
Leukotrienes
Proteases
Platelet-activating factor
Cytokines
208
Q

Mast cell granules take up ______.

A

Hematoxylin (blue dye) and other basophilic dyes

209
Q

What do histamine and leukotrienes do?

A

They cause vasodilation and endothelial cell contraction, mediating changes of inflammation

210
Q

What are consequences of the action of histamine?

A

Person can suffer fatal laryngeal edema or anaphylactic shock

211
Q

What are multinucleated giant cells?

A

They represent a syncytium of macrophages in a site of chronic inflammation

212
Q

What are the most common types of multinucleated giant cells?

A

Foreign body type and Langhans type

213
Q

When do foreign body multinucleated giant cells form?

A

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
Q

Langhans type multinucleated giant cells are associated with _______.

A

Immune granulomas

215
Q

What is a granuloma?

A

An aggregate of activated macrophages working together

216
Q

When do immune type granulomas form?

A

When persistent antigen induces a cell-mediated immune reaction

217
Q

When do foreign body granulomas form?

A

When there’s material too large or undigestible for clearance

218
Q

What are the nuclei like in foreign body giant cells and in Langhans giant cells?

A

Foreign body: haphazardly arranged nuclei

Langhans: nuclei arranged in a semicircle peripherally

219
Q

The macrophages that form Langhans giant cells have cytoplasm that is _______.

A

Epitheloid: smoother and more eosinophilic than typical macrophages

220
Q

What are the cellular playerz in chronic inflammation? (6)

A
  1. Macrophages
  2. Lymphocytes
  3. Plasma Cells
  4. Eosinophils
  5. Mast Cells
  6. Multinucleated Giant Cells

Pathology (4 decks)

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