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Pathology > Chapter 2: Tissue Deposits > Flashcards

Chapter 2: Tissue Deposits Flashcards

1
Q

State 6 Tissue Deposits Types

A 
Mucinous & Myxomatous Degeneration 
Hyalinosis 
Amyloidosis 
Pathologic Calcification
Gout
Pathological Pigmentation
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2
Q

Define Mucinous & Mycomatous Degeneration & state their occurrence

A 
Exaggerated Mucin Production 
In either:
Connective Tissue
Or
Epithelium
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3
Q

Define Mucin & State where is it secreted (2 points)

A

Glycoprotein

Mucous secreting cells:
Respiratory Tract
GIT cells

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4
Q

Describe Mucin Gross Examination (4 points)

A

Fluid
Pale Grey
Transparent
Slimy

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5
Q

Describe Mucin Microscopic Examination

A

H&E: Pale Blue

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6
Q

State Mucinous & Myxomatous Degeneration sites (2 points)

A

Mucinous→ Epithelium

Myxomatous→ Connective Tissue

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7
Q

Mention Epithelial Mucoid Degeneration occurrence examples (2 points)

A

Catarrhal Inflammation

Mucoid Adenocarcinoma

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8
Q

Mention Connective Tissue Myxomatous Degeneration occurrence examples (3 points)

A

Myxoma → Subcutaneous Tissue
Myxedema
Connective Tissue tumors

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9
Q

Describe Connective Tissue Myxomatous Degeneration Microscopic Examination (5 points)

A 
Few cells
Have processes
Star-shaped
Separated by:
Pale Blue Mucin
Rounded Hyperchromatic nuclei

Pale Cytoplasm

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10
Q

Define Hyalinosis & state their occurrence (2 points)

A 
Protein substance Deposition
In either:
Cells
Or 
Connective Tissue material
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11
Q

Describe the protein substance deposited in Hyalinosis (4 points)

A

Glassy
Homogenous
Structureless
Eosinophilic

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12
Q

State Hyalinosis 2 types

A

Cellular

Connective Tissue

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13
Q

Mention Cellular Hyalinosis sub-types & where are they found (3 points)

A

Mallory→ Chronic Alcoholics Liver
Corpora Amylacia→ Old Males Prostate
Russell Bodie→ Rhinoscleroma Plasma Cells

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14
Q

Mention Connective Tissue Hyalinosis sub-types & where are they found (4 points)

A

Blood Vessels Walls (Arterioles & Capillaries)→ Benign Hypertension

Old scars
Thrombi
Tumors

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15
Q

Define Amyloidosis & where is it found (2 points)

A

Extracellular amyloid abnormal deposition

In many tissues

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16
Q

Describe Amyloid (3 points)

A

Group of substances
Have Common physical structure
Biochemical composition of variable Fibrilar protein

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17
Q

Describe stained Amyloid appearance (2 points)

A

LM→

H&E: 
Extracellular
Homogenous
Structurless
Eosinophilic 
Hyaline material

Congo Red:
+ve

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18
Q

Describe Physical Amyloid Nature (2 points)

A

Amyloid forms:

Similar →
Morphological basis
Physical characteristics
Appearance

Heterogenous →
Chemically

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19
Q

State 2 main types of Amyloid Composition (Complex Proteins)

A

Fibril Proteins

Non-Fibrillar Components

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20
Q

Describe Fibril Protein Composition

A

About 95% Amyloid

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21
Q

State Fibril Proteins Types (3 points)

A

AL
AA
Other proteins

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22
Q

Describe AL Fibril protein (5 points)

A

Amyloid Light Chain

Derived from: Immunoglobulin light chain
Produced by: Immunoglobulin secreting cells
Seen: With plasma cell dycrasias
Included in: Primary Systemic Amyloidosis

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23
Q

Describe AA Fibril Protein (4 points)

A

Amyloid Associated

Synthesized in: Liver
Found in: Secondary Amyloidosis 
High level in:
Chronic Inflammatory 
Traumatic conditions
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24
Q

Describe Secondary Amyloidosis (2 points)

A

Includes largest diseases group

Associated with Amyloidosis

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25
Q

State the main other Fibril Proteins (3 points)

A

Transthyretin (TTR)
Aβ2-Microglobulin (Aβ2M)
Amyloid Protein (Aβ)

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26
Q

Describe Transthyretin [TTR] (5 points)

A 
Serum protein
Heredofamilial Amyloidosis most common form 
Example: Familial Amyloidosis
Polyneuropathies 
Synthesized in: Liver
Transports:
Thyroxine
Retinol
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27
Q

Describe Aβ2-Microglobulin (Aβ2M) occurrence

A

Long-term Hemodialysis

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28
Q

Describe Amyloid Protein occurrence[Aβ] (2 points)

A 
Alzheimer’s disease 
In→
Cerebral:
Plaques 
Blood Vessels
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29
Q

Describe Non-Fibrillar Components (2 points)

A 
5-10% Amyloid  
Constant →In All Amyloid types 
Responsible for Amyloid:
Stability
Staining properties
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30
Q

State 2 Amyloidosis Distribution Classification

A

Systemic

Localized

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31
Q

Mention Systemic Amyloidosis Types (4 points)

A

Primary (AL)
Secondary/Reactive/Inflammatory (AA)
Haemodialysis-Associated (Aβ2M)
Heredofamilial

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32
Q

Describe Primary Systemic Amyloidosis [AL] (3 points)

A 
Consists of AL Fibril Protein
Cases:
About 30%→Plasma Cell Dycrasias:
     About 10%→Multiple Myeloma 
     (Most common):
           Almost All→Either light chains      
           (Bence Jones Proteins):
           κ
           λ
           Both→ In serum & Urine
     Less often→Other Monoclonal          
     Gammopathies
Remaining 70% (True ‘Primary Idiopathic Amyloidosis’)→
Don’t have:
Evident B-cell proliferative disorder
Or
Any other associated diseases
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33
Q

Mention organs where Primary Amyloidosis is severe in (7 points)

A 
Heart
Kidney
Bowel 
Skin
Peripheral Nerves
Respiratory Tract
Skeletal Muscle
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34
Q

Describe Secondary/Reactive/Inflammatory Amyloidosis [AA] (4 points)

A 
Consists of AA Fibril Protein
Occur As:
Chronic Infectious Complication →
Tuberculosis 
Bronchiectasis 
Leprosy
Chronic:
Osteomyelitis 
Pyelonephritis 
Skin Infections

Non-Infectious Chronic Inflammatory conditions with Tissue Destruction →
Autoimmune disorders:
Rheumatoid Arthritis
Inflammatory Bowel Disease

Some Tumors →
Renal Cell Carcinoma
Hodgkin’s Disease

Familial Mediterranean Fever (AA)

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35
Q

Mention organs where Secondary/Reactive/Inflammatory Amyloidosis [AA] is typically distributed in (5 points)

A 
Solid Abdominal Viscera
Examples:
Kidney 
Liver
Spleen 
Adrenal
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36
Q

Describe Haemodialysis-Associated Amyloidosis [Aβ2M] (2 points)

A 
Derived from: β2-Microglobulin
Patients:
On Long-term dialysis 
For >10 years
For Chronic Renal Failure
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37
Q

Define β2-Microglobulin

A

Normal MHC component

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38
Q

Mention where is Haemodialysis-Associated Amyloidosis (Aβ2M) deposits found in (5 points)

A 
Vessel Walls:
Synovium
Joints
Tendon Sheaths
Subchondral Bones
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39
Q

State the 2 Heredofamilial Amyloidosis Types

A

Hereditary Polyneuropathic Amyloidosis (ATTR)

Familial Mediterranean Fever Amyloidosis (AA)

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40
Q

Describe Hereditary Polyneuropathic Amyloidosis [ATTR] (2 points)

A

Autosomal Dominant Disorder

Derived from: Transthyretin (ATTR) → Its structure contains a single amino acid substitution

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41
Q

Describe where is Hereditary Polyneuropathic Amyloidosis [ATTR] deposits found in & its results (5 points)

A

Peripheral & Autonomic Nerves

Muscular Weakness
Pain
Paraesthesia
Cardiomyopathy

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42
Q

Describe Familial Mediterranean Fever Amyloidosis [AA] (3 points)

A

Autosomal Recessive Disease
Inherited Disorder

In Mediterranean Region

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43
Q

Mention Localized Amyloidosis Types (3 points)

A

Senile:
Cardiac (ATTR)
Cerebral (Aβ, APrP)
Endocrine

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44
Q

Describe where is Senile Cardiac Amyloidosis [ATTR] found in (3 points)

A

50% >70 years old
Heart
Aorta

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45
Q

Describe Senile Cerebral Amyloidosis (Aβ, APrP) important diseases associated with it (2 points)

A

Alzheimer’s Disease (Aβ)

Down’s Syndrome

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46
Q

Describe Senile Endocrine Amyloidosis (2 points)

A

Some Endocrine lesions+ Amyloid Microscopic Deposits
Example:
Thyroid Medullary Carcinoma

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47
Q

Describe Amyloidosis Gross Appearance (2 points)

A

Affected organ:
Enlarged
Pale
Rubbery

Cut Surface:
Parenchyma →
Firm
Waxy
Iodine Test:
\+ve
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48
Q

Describe Amyloidosis Deposits Microscopic Appearance (2 points)

A

Small amounts →
In Extracellular locations:
Small blood vessels walls

Cause 𝐌𝐢𝐜𝐫𝐨scopic changes & effects

Large amounts →
Cause:
𝐌𝐚𝐜𝐫𝐨scopic changes & effects
Pressure Atrophy

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49
Q

Which organ Amyloidosis is the most common & most serious and Give and reason for that
(2 points)

A

Kidney

Ill effects on Renal functions

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50
Q

Describe Heart Amyloidosis (4 points)

A

In Primary Systemic Amyloidosis> Secondary Systemic Amyloidosis
Myocardial Fibers Pressure Atrophy
Impaired Ventricular Function
Restrictive Cardiomyopathy

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51
Q

Define Pathologic Calcification

A

Calcium slats deposition

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52
Q

What are the sites where Pathologic Calcification cannot be seen in?
(2 points)

A

Bone

Teeth

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53
Q

What are the 3 types of pathologic calcification?

A

Dystrophic
Metastatic
Stone formation

54
Q

Where are stones formed? (2 points)

A

Pathologic Calcification:
Dystrophic
Metastatic

55
Q

Describe the tissues where

dystrophic pathologic calcification can be seen in (3 points)

A

Non Viable

Diseased
Or
Necrotic

56
Q

How is the blood calcium level in dystrophic pathologic calcification?

A

Normal

57
Q

Give examples of sites where stoned are formed in dystrophic pathologic calcification (4 points)

A

Necrotic tissue
Atherosclerosis
Cells
Heart Valves

58
Q

What are the types of necrosis that have stones formed in them? (4 points)

A

Fat
Coagulative
Liquefactive
Caseous

59
Q

Where exactly are stones formed in Atherosclerosis?

A

Central Necrotic Core

60
Q

Where exactly are stones formed in cells?

A

Psammoma bodies

61
Q

What is the condition of the heart valves after stone formation?

A

Damaged

Aging

62
Q

Describe the tissues where

metastatic pathologic calcification can be seen in (2 points)

A

Normal

Viable

63
Q

What does metastatic pathologic calcification cause?

A

Hypercalcemia

64
Q

What causes Hypercalcemia? (4 points)

A

Increased PTH secretion
Bone Destruction
Vitamin D disorders
Excess Calcium intake

65
Q

Give examples to increased PTH secretion (2 points)

A

Ectopic PTH secretion

Increased Parathyroid tumor

66
Q

Give examples to bone destruction

3 points

A

Osteolytic tumors
Paget’s disease
Immobilization

67
Q

Give examples to Vitamin D disorders

2 points

A

Vitamin D toxicity

Sarcoidosis

68
Q

Give an example to excess calcium intake

A

Milk alkali syndrome

69
Q

What causes milk alkali syndrome?

2 points

A

Nephrocalcinosis
Renal stones

Antiacid Self-therapy

70
Q

What causes Nephrocalcinosis & Renal stones?

A

Milk

71
Q

Where is Calcium deposited in? (4 points)

A

Lungs
Kidneys
Stomach
Arteries

72
Q

What is the effect of depositing calcium in lungs?

A

Respiratory Failure

73
Q

What are the effects of depositing calcium in Kidneys? (2 points)

A

Kindey Failure

Nephrocalcinosis

74
Q

What are the effects of depositing calcium in Arteries? (2 points)

A

Ischemic Ulcers with

Necrosis

75
Q

Where exactly is calcium deposited in Arteries?

A

Skin small blood vessels

76
Q

State the name of the condition in which calcium is deposited in skin small blood vessels

A

Calciphylaxis

77
Q

What are the 2 substances involved in Gout formation?

A

Purine

Serum Uric Acid

78
Q

Describe Purine

A

Nucleoprotein

79
Q

What happens to Purine in Gout formation?

A

Its metabolism disturbed

80
Q

What is the effect of disturbed Purine metabolism on Serum uric acid?

A

Increases

81
Q

What does Serum uric acid form when increased?

A

Crystals deposits

82
Q

Where are Serum uric acid crystals deposits mainly found in?

A

Big toe’s Metatarsophalangeal joint

83
Q

State another site where Serum uric acid crystals deposits can be found in

A

Kidney

84
Q

What follows the deposition of Serum acid crystals?

A

Inflammation with foreign body giant cell reaction

85
Q

State the name given for the body giant cell

A

Tophi

86
Q

What are the effects of the deposition of Serum uric acid crystals in the Kidney?
(5 points)

A 
Urate stones
Interstitial Inflammation
Fibrosis
Chronic Renal Failure
Distal Convoluting Tubules damage
87
Q

What is caused when Distal Convoluting Tubules are damaged?

A

Polyuria

88
Q

What are the 2 types of Pathological Pigmentation?

A

Endogenous

Exogenous

89
Q

What causes pathological endogenous pigmentation? (4 points)

A

Lipofuscin
Melanin
Bilirubin
Hemosidrin

90
Q

What are the ways in which pathological endogenous pigmentation are presented in the body?

A

Inhalation
Ingestion
Tattoo

91
Q

What is the condition in which pathological endogenous pigmentation is presented in the body through inhalation?

A

Anthracosis

92
Q

What could be ingested leading to pathological endogenous pigmentation?

A

Lead poison

93
Q

What results in the formation of Lipofuscin?

A

The action of free radicals on cell membrane lipids

94
Q

Describe the structure of Lipofuscin

A

Complex

95
Q

What is Lipofuscin made of?

A

Lipid

Protein

96
Q

What is the color of the granules of Lipofuscin?

A

Brownish Yellow

97
Q

Describe the solubility of Lipofuscin

A

Insoluble

98
Q

What is Lipofuscin pigment described as?

A

Wear and Tear

99
Q

Where can Lipofuscin granules be found in?

A

Both sides of nucleus

100
Q

Where does Lipofuscin accumulate in?

A

Patients

Cells

101
Q

Which cells does Lipofuscin accumulate in?

A

Myocardial

102
Q

Which patients is Lipofuscin accumulation found in?

A

Elderly

103
Q

Where exactly is Lipofuscin accumulation found in Elderly patients?

A

Hepatocytes

104
Q

Where exactly does Lipofuscin accumulate in Myocardial cells?

A

Both nuclei poles

105
Q

Define Brown Atrophy?

A

Combination of:
Lipofuscin accumulation
Organs atrophy

106
Q

Define Hemosidrin

A

Hemoglobin derived pigment

107
Q

What does Hemosidrin consist of?

A

Ferritin aggregates

108
Q

What does Hemosidrin contain?

A

Iron

109
Q

What is the stain used to identify Hemosidrin in tissues?

A

Prussian Blue Dye

110
Q

What is the color of Hemosidrin when stained?

A

Golden Brown

111
Q

What is Hemosidrin considered as?

A

Physiologic iron store

112
Q

Where is Hemosidrin found in?

A

Tissue Macrophages

113
Q

Describe the amount of Hemosidrin in tissue macrophages

A

Small

114
Q

Which organs [having tissue macrophages] are Hemosidrin found in? (3 points)

A 
Liver
Bone marrow
Spleen
Pancreas
Skin
Heart
115
Q

Give an example to a Liver condition in which Hemosidrin deposits can be seen

A

Micronodular Cirrhosis

116
Q

Give an example to a Liver condition in which Hemosidrin deposits can be seen

A

Diabetes Mellitus

117
Q

What is the color of Hemosidrin when seen in a diabitic patient?

A

Bronze

118
Q

What are the 2 types of Hemosidrin

A

Local

Systemic

119
Q

Define Local Hemosidrosis

A

Local Hemosidrin Deposition

120
Q

What causes Local Hemosidrosis?

A

Local tissue hemorrhage

121
Q

Define Systemic Hemosidrosis

A

Generalized hemosidrin deposition

122
Q

Does Systemic Hemosidrosis causes tissue damage?

A

No

123
Q

What causes Systemic Hemosidrosis?

4 points

A

Hemorrhage
Multiple blood transfusion
Excessive dietary iron intake +
Alcohol consumption

124
Q

Define Hemochromatosis

A

More extensive Hemosidrin accumulation

125
Q

Where can Hemochromatosis be seen in?

A

Parenchymal cells

126
Q

What are the Parenchymal cells associated with when observing Hemochromatosis in them?
(3 points)

A

Tissue damage
Scarring
Organ Dysfunction

127
Q

What are the 2 Hemochromatosis types?

A

Primary

Secondary

128
Q

Describe Primary Hemochromatosis

A

Hereditary

129
Q

What causes Primary Hemochromatosis?

A

Gene mutation

130
Q

What does this gene mutation result in?

A

Duodenum excessive iron absorption

131
Q

Which patients can Secondary Hemochromatosis be seen in?

A

Hereditary hemolytic anemic patients

132
Q

When is Secondary Hemochromatosis seen with Hereditary hemolytic anemic patients?

A

After multiple blood transfusions

Pathology (11 decks)

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