Chapter 2: Tissue Deposits Flashcards
1
Q
State 6 Tissue Deposits Types
A
Mucinous & Myxomatous Degeneration Hyalinosis Amyloidosis Pathologic Calcification Gout Pathological Pigmentation
2
Q
Define Mucinous & Mycomatous Degeneration & state their occurrence
A
Exaggerated Mucin Production In either: Connective Tissue Or Epithelium
3
Q
Define Mucin & State where is it secreted (2 points)
A
Glycoprotein
Mucous secreting cells:
Respiratory Tract
GIT cells
4
Q
Describe Mucin Gross Examination (4 points)
A
Fluid
Pale Grey
Transparent
Slimy
5
Q
Describe Mucin Microscopic Examination
A
H&E: Pale Blue
6
Q
State Mucinous & Myxomatous Degeneration sites (2 points)
A
Mucinous→ Epithelium
Myxomatous→ Connective Tissue
7
Q
Mention Epithelial Mucoid Degeneration occurrence examples (2 points)
A
Catarrhal Inflammation
Mucoid Adenocarcinoma
8
Q
Mention Connective Tissue Myxomatous Degeneration occurrence examples (3 points)
A
Myxoma → Subcutaneous Tissue
Myxedema
Connective Tissue tumors
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
10
Q
Define Hyalinosis & state their occurrence (2 points)
A
Protein substance Deposition In either: Cells Or Connective Tissue material
11
Q
Describe the protein substance deposited in Hyalinosis (4 points)
A
Glassy
Homogenous
Structureless
Eosinophilic
12
Q
State Hyalinosis 2 types
A
Cellular
Connective Tissue
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
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
15
Q
Define Amyloidosis & where is it found (2 points)
A
Extracellular amyloid abnormal deposition
In many tissues
16
Q
Describe Amyloid (3 points)
A
Group of substances
Have Common physical structure
Biochemical composition of variable Fibrilar protein
17
Q
Describe stained Amyloid appearance (2 points)
A
LM→
H&E: Extracellular Homogenous Structurless Eosinophilic Hyaline material
Congo Red:
+ve
18
Q
Describe Physical Amyloid Nature (2 points)
A
Amyloid forms:
Similar →
Morphological basis
Physical characteristics
Appearance
Heterogenous →
Chemically
19
Q
State 2 main types of Amyloid Composition (Complex Proteins)
A
Fibril Proteins
Non-Fibrillar Components
20
Q
Describe Fibril Protein Composition
A
About 95% Amyloid
21
Q
State Fibril Proteins Types (3 points)
A
AL
AA
Other proteins
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
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
24
Q
Describe Secondary Amyloidosis (2 points)
A
Includes largest diseases group
Associated with Amyloidosis
25
State the main other Fibril Proteins (3 points)
Transthyretin (TTR)
Aβ2-Microglobulin (Aβ2M)
Amyloid Protein (Aβ)
26
Describe Transthyretin [TTR] (5 points)
```
Serum protein
Heredofamilial Amyloidosis most common form
Example: Familial Amyloidosis
Polyneuropathies
Synthesized in: Liver
Transports:
Thyroxine
Retinol
```
27
Describe Aβ2-Microglobulin (Aβ2M) occurrence
Long-term Hemodialysis
28
Describe Amyloid Protein occurrence[Aβ] (2 points)
```
Alzheimer’s disease
In→
Cerebral:
Plaques
Blood Vessels
```
29
Describe Non-Fibrillar Components (2 points)
```
5-10% Amyloid
Constant →In All Amyloid types
Responsible for Amyloid:
Stability
Staining properties
```
30
State 2 Amyloidosis Distribution Classification
Systemic
| Localized
31
Mention Systemic Amyloidosis Types (4 points)
Primary (AL)
Secondary/Reactive/Inflammatory (AA)
Haemodialysis-Associated (Aβ2M)
Heredofamilial
32
Describe Primary Systemic Amyloidosis [AL] (3 points)
```
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
```
33
Mention organs where Primary Amyloidosis is severe in (7 points)
```
Heart
Kidney
Bowel
Skin
Peripheral Nerves
Respiratory Tract
Skeletal Muscle
```
34
Describe Secondary/Reactive/Inflammatory Amyloidosis [AA] (4 points)
```
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)
35
Mention organs where Secondary/Reactive/Inflammatory Amyloidosis [AA] is typically distributed in (5 points)
```
Solid Abdominal Viscera
Examples:
Kidney
Liver
Spleen
Adrenal
```
36
Describe Haemodialysis-Associated Amyloidosis [Aβ2M] (2 points)
```
Derived from: β2-Microglobulin
Patients:
On Long-term dialysis
For >10 years
For Chronic Renal Failure
```
37
Define β2-Microglobulin
Normal MHC component
38
Mention where is Haemodialysis-Associated Amyloidosis (Aβ2M) deposits found in (5 points)
```
Vessel Walls:
Synovium
Joints
Tendon Sheaths
Subchondral Bones
```
39
State the 2 Heredofamilial Amyloidosis Types
Hereditary Polyneuropathic Amyloidosis (ATTR)
| Familial Mediterranean Fever Amyloidosis (AA)
40
Describe Hereditary Polyneuropathic Amyloidosis [ATTR] (2 points)
Autosomal Dominant Disorder
| Derived from: Transthyretin (ATTR) → Its structure contains a single amino acid substitution
41
Describe where is Hereditary Polyneuropathic Amyloidosis [ATTR] deposits found in & its results (5 points)
Peripheral & Autonomic Nerves
Muscular Weakness
Pain
Paraesthesia
Cardiomyopathy
42
Describe Familial Mediterranean Fever Amyloidosis [AA] (3 points)
Autosomal Recessive Disease
Inherited Disorder
In Mediterranean Region
43
Mention Localized Amyloidosis Types (3 points)
Senile:
Cardiac (ATTR)
Cerebral (Aβ, APrP)
Endocrine
44
Describe where is Senile Cardiac Amyloidosis [ATTR] found in (3 points)
50% >70 years old
Heart
Aorta
45
Describe Senile Cerebral Amyloidosis (Aβ, APrP) important diseases associated with it (2 points)
Alzheimer’s Disease (Aβ)
| Down’s Syndrome
46
Describe Senile Endocrine Amyloidosis (2 points)
Some Endocrine lesions+ Amyloid Microscopic Deposits
Example:
Thyroid Medullary Carcinoma
47
Describe Amyloidosis Gross Appearance (2 points)
Affected organ:
Enlarged
Pale
Rubbery
```
Cut Surface:
Parenchyma →
Firm
Waxy
Iodine Test:
+ve
```
48
Describe Amyloidosis Deposits Microscopic Appearance (2 points)
Small amounts →
In Extracellular locations:
Small blood vessels walls
Cause 𝐌𝐢𝐜𝐫𝐨scopic changes & effects
Large amounts →
Cause:
𝐌𝐚𝐜𝐫𝐨scopic changes & effects
Pressure Atrophy
49
Which organ Amyloidosis is the most common & most serious and Give and reason for that
(2 points)
Kidney
| Ill effects on Renal functions
50
Describe Heart Amyloidosis (4 points)
In Primary Systemic Amyloidosis> Secondary Systemic Amyloidosis
Myocardial Fibers Pressure Atrophy
Impaired Ventricular Function
Restrictive Cardiomyopathy
51
Define Pathologic Calcification
Calcium slats deposition
52
What are the sites where Pathologic Calcification cannot be seen in?
(2 points)
Bone
| Teeth
53
What are the 3 types of pathologic calcification?
Dystrophic
Metastatic
Stone formation
54
Where are stones formed? (2 points)
Pathologic Calcification:
Dystrophic
Metastatic
55
Describe the tissues where
| dystrophic pathologic calcification can be seen in (3 points)
Non Viable
Diseased
Or
Necrotic
56
How is the blood calcium level in dystrophic pathologic calcification?
Normal
57
Give examples of sites where stoned are formed in dystrophic pathologic calcification (4 points)
Necrotic tissue
Atherosclerosis
Cells
Heart Valves
58
What are the types of necrosis that have stones formed in them? (4 points)
Fat
Coagulative
Liquefactive
Caseous
59
Where exactly are stones formed in Atherosclerosis?
Central Necrotic Core
60
Where exactly are stones formed in cells?
Psammoma bodies
61
What is the condition of the heart valves after stone formation?
Damaged
| Aging
62
Describe the tissues where
| metastatic pathologic calcification can be seen in (2 points)
Normal
| Viable
63
What does metastatic pathologic calcification cause?
Hypercalcemia
64
What causes Hypercalcemia? (4 points)
Increased PTH secretion
Bone Destruction
Vitamin D disorders
Excess Calcium intake
65
Give examples to increased PTH secretion (2 points)
Ectopic PTH secretion
| Increased Parathyroid tumor
66
Give examples to bone destruction
| 3 points
Osteolytic tumors
Paget’s disease
Immobilization
67
Give examples to Vitamin D disorders
| 2 points
Vitamin D toxicity
| Sarcoidosis
68
Give an example to excess calcium intake
Milk alkali syndrome
69
What causes milk alkali syndrome?
| 2 points
Nephrocalcinosis
Renal stones
Antiacid Self-therapy
70
What causes Nephrocalcinosis & Renal stones?
Milk
71
Where is Calcium deposited in? (4 points)
Lungs
Kidneys
Stomach
Arteries
72
What is the effect of depositing calcium in lungs?
Respiratory Failure
73
What are the effects of depositing calcium in Kidneys? (2 points)
Kindey Failure
| Nephrocalcinosis
74
What are the effects of depositing calcium in Arteries? (2 points)
Ischemic Ulcers with
| Necrosis
75
Where exactly is calcium deposited in Arteries?
Skin small blood vessels
76
State the name of the condition in which calcium is deposited in skin small blood vessels
Calciphylaxis
77
What are the 2 substances involved in Gout formation?
Purine
| Serum Uric Acid
78
Describe Purine
Nucleoprotein
79
What happens to Purine in Gout formation?
Its metabolism disturbed
80
What is the effect of disturbed Purine metabolism on Serum uric acid?
Increases
81
What does Serum uric acid form when increased?
Crystals deposits
82
Where are Serum uric acid crystals deposits mainly found in?
Big toe’s Metatarsophalangeal joint
83
State another site where Serum uric acid crystals deposits can be found in
Kidney
84
What follows the deposition of Serum acid crystals?
Inflammation with foreign body giant cell reaction
85
State the name given for the body giant cell
Tophi
86
What are the effects of the deposition of Serum uric acid crystals in the Kidney?
(5 points)
```
Urate stones
Interstitial Inflammation
Fibrosis
Chronic Renal Failure
Distal Convoluting Tubules damage
```
87
What is caused when Distal Convoluting Tubules are damaged?
Polyuria
88
What are the 2 types of Pathological Pigmentation?
Endogenous
| Exogenous
89
What causes pathological endogenous pigmentation? (4 points)
Lipofuscin
Melanin
Bilirubin
Hemosidrin
90
What are the ways in which pathological endogenous pigmentation are presented in the body?
Inhalation
Ingestion
Tattoo
91
What is the condition in which pathological endogenous pigmentation is presented in the body through inhalation?
Anthracosis
92
What could be ingested leading to pathological endogenous pigmentation?
Lead poison
93
What results in the formation of Lipofuscin?
The action of free radicals on cell membrane lipids
94
Describe the structure of Lipofuscin
Complex
95
What is Lipofuscin made of?
Lipid
| Protein
96
What is the color of the granules of Lipofuscin?
Brownish Yellow
97
Describe the solubility of Lipofuscin
Insoluble
98
What is Lipofuscin pigment described as?
Wear and Tear
99
Where can Lipofuscin granules be found in?
Both sides of nucleus
100
Where does Lipofuscin accumulate in?
Patients
| Cells
101
Which cells does Lipofuscin accumulate in?
Myocardial
102
Which patients is Lipofuscin accumulation found in?
Elderly
103
Where exactly is Lipofuscin accumulation found in Elderly patients?
Hepatocytes
104
Where exactly does Lipofuscin accumulate in Myocardial cells?
Both nuclei poles
105
Define Brown Atrophy?
Combination of:
Lipofuscin accumulation
Organs atrophy
106
Define Hemosidrin
Hemoglobin derived pigment
107
What does Hemosidrin consist of?
Ferritin aggregates
108
What does Hemosidrin contain?
Iron
109
What is the stain used to identify Hemosidrin in tissues?
Prussian Blue Dye
110
What is the color of Hemosidrin when stained?
Golden Brown
111
What is Hemosidrin considered as?
Physiologic iron store
112
Where is Hemosidrin found in?
Tissue Macrophages
113
Describe the amount of Hemosidrin in tissue macrophages
Small
114
Which organs [having tissue macrophages] are Hemosidrin found in? (3 points)
```
Liver
Bone marrow
Spleen
Pancreas
Skin
Heart
```
115
Give an example to a Liver condition in which Hemosidrin deposits can be seen
Micronodular Cirrhosis
116
Give an example to a Liver condition in which Hemosidrin deposits can be seen
Diabetes Mellitus
117
What is the color of Hemosidrin when seen in a diabitic patient?
Bronze
118
What are the 2 types of Hemosidrin
Local
| Systemic
119
Define Local Hemosidrosis
Local Hemosidrin Deposition
120
What causes Local Hemosidrosis?
Local tissue hemorrhage
121
Define Systemic Hemosidrosis
Generalized hemosidrin deposition
122
Does Systemic Hemosidrosis causes tissue damage?
No
123
What causes Systemic Hemosidrosis?
| 4 points
Hemorrhage
Multiple blood transfusion
Excessive dietary iron intake +
Alcohol consumption
124
Define Hemochromatosis
More extensive Hemosidrin accumulation
125
Where can Hemochromatosis be seen in?
Parenchymal cells
126
What are the Parenchymal cells associated with when observing Hemochromatosis in them?
(3 points)
Tissue damage
Scarring
Organ Dysfunction
127
What are the 2 Hemochromatosis types?
Primary
| Secondary
128
Describe Primary Hemochromatosis
Hereditary
129
What causes Primary Hemochromatosis?
Gene mutation
130
What does this gene mutation result in?
Duodenum excessive iron absorption
131
Which patients can Secondary Hemochromatosis be seen in?
Hereditary hemolytic anemic patients
132
When is Secondary Hemochromatosis seen with Hereditary hemolytic anemic patients?
After multiple blood transfusions
