7. Disorders of the metabolism of lipids. Types of adipose degeneration Flashcards

(49 cards)

1
Q

What are Lipids?

A

Molecules containing HC

Make up Building Blocks of Structure + Function of Living Cells

E.g Fats / Oils / Waxes / Fat-Soluble Vitamins / Hormone

Make up 30% of Cytoplasm in Normal Cells

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2
Q

How do Lipids Cause Cellular Damage?

A

Lipid Accumulation in Unusual Locations / Unusual Composition + Unusual Amount

Lipids form Complex Structure with Proteins + Carbs

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3
Q

What are the 3 Types of Lipids?

A
  1. Neutral Lipids + Waxes = Triglycerides / Simple Lipids
  2. Complex Lipids = Phosphatides / Cerebrosides / Gangliosides + Sphingomyelins
  3. Sterols / Steroids
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4
Q

1| What are the Characteristics of Neutral Lipids + Waxes?

A

Neutral Lipids = ESTERS of Fatty Acids + Glycerin

The MAIN COMPONENT of Fat Deposits

Waxes = ESTERS of Fatty Acids; Have Movement; RARELY w/ Divalent Alcohols with a LONG STRAIGHT Chain

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5
Q

2| What are the Characteristics of Phosphatides (Complex Lipids)?

A

AKA Phospholipids = ESTERS of Fatty Acids + Glycerin w/ Nitrogenous Compounds / Inosite + Phosphoric Acid

LARGE Amounts in = Neural Tissue / Liver / Kidneys / Heart

OTHER Complex Lipids = Neural Tissue

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6
Q

3| What are the Characteristics of Steroids?

A

COMPLEX ESTERS of Fatty Acids w/ CYCLIC Alcohol

Cholesterol + Its Esters = Cholesters

Located in = Adrenal Cortex / CNS / Genital Glands

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7
Q

What are the 7 Physiological Functions of Lipids?

A

1) Direct Source of Energy
2) Protection + Covering = Eyelids / Heart Valves / Renal Capsules + Mesenterium
3) Maintain Body Temperature
4) Regulate Cell Communication + Neurotransmitter Signals
5) Make up Structural Part of Cell Membrane (Phospholipids + Cholesterol)
6) Energy Depot (85% are Triglycerides)
7) Synthesises = Bile Salts / Hormones / Prostaglandins + Eicosanoids

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8
Q

What is the Solubility of Lipids?

A

IN-Soluble = In Aqueous Solution + Acetic Acid

Soluble = Alcohol / Acetone / Benzole / Chloroform + Xylol

THEREFORE CANNOT be Studied in Alcohol Fixated Materials / Paraffin Fixatives

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9
Q

How do we Preserve Lipids?

A

Use Unfixed Tissue / Fixed in Formalin

AND THEN Cut on Freezing Microtome

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10
Q

What are the Staining Methods for Lipids?

A

(i) Sudan III (Oil Red)
(ii) Scharlactor (Red)
(iii) Sudan IV / Osmic Acid (Black)
(iv) Niblausulfate = Neutral Lipids (Blue)

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11
Q

Which 2 Microscopic Methods are Used to Test for Lipids?

A
  1. Polarised = Neutral Lipids are Isotopic; Cholesterol + Esters give Double Refraction of Light
  2. Electron = Ultrastructural Examination w/ Osmic Acid (Fixative)
    - HARDENS Lipids + Forms Lines during Cutting with Ultramicrotome Parallel Stretching
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12
Q

How is Fatty Degeneration Classified?

A

According to:

  1. Chemical Composition
  2. Localisation of Stromal + Parenchymal Cells
  3. Proliferation
  4. Acquired or Genetic
  5. Parenchymatous Fatty Degeneration
  6. Intracellular Fatty Degeneration
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13
Q

6| What is Intracellular Fatty Degeneration?

A

ABNORMAL Lipid Accumulation

WITHIN Parenchymal Cells

Organs Damaged = Heart / Liver / Kidneys

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14
Q

What are the 7 Causes of Fatty Degeneration?

A

MAIN = Hypoxia, which is DUE to

(i) EXCESSIVE Alcohol Intake
(ii) Chronic CV + Pulmonary Insufficiency; Anaemia
(iii) Hepatotoxins = Chloroform / Hepatotoxic Meds / Mushrooms
(iv) Malnutrition
(v) Infections = Sepsis / Diphtheria
(vi) Drugs = Oestrogen / Steroids
(vii) Late Period of Pregnancy

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15
Q

Where does Fat Dystrophy Occur?

A

Organs where PROTEIN Dystrophy Occur

  • Liver
  • Myocardium
  • Kidneys
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16
Q

What are Lipoproteins AND Lipoprotein Complexes?

A

Lipoproteins = Complex Particles w/ Central Core (Cholesterol Esters + Triglycerides), Surrounded by Free Chol + Phospholipids (Helping with Formation + Function)

Lipoprotein Complex = MASSIVE Macromolecules w/ Different Stage of Polymerisation

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17
Q

What is Lipophanerosis?

A

DIVISION of Layers of Protein-Lipid Complex

Via Appropriate Processing

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18
Q

What is the Pathogenesis of Fat Degeneration?

A

1) Processing w/ Special Methods is SPONTANEOUSLY REALISED in Living Cells, under influence of Agents LEADING to FAT Dystrophy
2) Liphanerosis = MAIN Mechanism for PARENCHYMATOUS Fat Degeneration
3) Infiltration + Absorption (Via PINOCYTOSIS) of Lipids OUTSIDE the Cell LEADS to Fat Degeneration
4) Lipoproteins FROM Blood Plasma / Products of Necrotic Cells GET INTO –> Intercellular Spaces + ENTER Cytoplasm Via PHAGOCYTOSIS
5) Transformation = Triglyceride Synthesis in PATHOLOGIC Conditions INSTEAD OF Carbs + Proteins

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19
Q

What is ‘Fatty Degeneration of the Liver’ also known as?

A

Liver Steatosis

Happens when MORE THAN 50% Hepatocytes contain NEUTRAL Lipids

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20
Q

What are the 4 Main Causes of Liver Steatosis?

A
  1. Alcoholic Steatosis
  2. Diabetes Mellitus

3 .Alimentary Damages

  1. Disorder of Small Intestines
21
Q

1| What is the Pathogenesis of Alcoholic Steatosis?

A

Fat Accumulation in Hepatocytes of Liver

DUE to Cell Damage from Chronic Alcoholism

22
Q

1| How does Chronic Alcoholism Cause Cellular Damage?

A

INCREASED Lipolysis + Free Fatty Synthesis

DECREASED Triglyceride Usage / FA Oxidation to KBs

BLOCKAGE of Lipoprotein Excretion

23
Q

2| How does Diabetes Mellitus Cause Liver Steatosis?

A

Complete / Relative DEFICIENCY of Insulin

{Insulin = Anti-Lipolytic Hormone}

LACK of Insulin = INCREASED Lipolysis in Depots + Entry of FAs in Liver

24
Q

3| How does Alimentary Damages Cause Liver Steatosis?

A

Inappropriate Diet = PROTEIN Deficiency LEADING to Fatty Liver Disease

LACK of PROTEIN = INHIBITED Lipoprotein Synthesis

E.g. Resections / Gastric Bypass

25
4| How does Disorders of Small Intestines Cause | Liver Steatosis?
Patients with SI Disorders = Enterocolitis DEFICIENCY of Proteins + Lipotropic Factors {Lipotropic Factors are needed for Lipoprotein Synthesis)
26
What are the MACROSOPIC Changes in Fatty LIVER? {Morphology}
Enlarged Liver w/ Rounded Margins Cut Surface = Pale Yellow + Slightly Bulges Greasy aka Goose Liver
27
What are the MICROSCOPIC Changes in Fatty LIVER? {Morphology}
Lipid Vacuoles in Cytoplasm of Hepatocytes = Empty Vacuoles Vacuoles initially Small (Microvesicular) --> Larger + Push Nucleus to Periphery of Cells (Macrovesicular) Hepatocytes w/ LARGE Lipid Vacuoles Rupture + Form Fatty Cysts Lipogranulomas Appear (Rarely)
28
What are the MACROSOPIC Changes in Fatty HEART? {Morphology}
Aka Tiger Heart Enlarged Heart Stretched + Flabby Chambers
29
What are the MICROSCOPIC Changes in Fatty HEART? {Morphology}
Dust-like Vacuoles in Cardiomyocytes Observed in Papillary Muscles + Trabecules of Ventricles in Form of Bands Surrounds Veins (Hypoxia is MOST SEVERE)
30
What are the MACROSOPIC Changes in Fatty KIDNEY? {Morphology}
Occurs in Nephrotic Syndrome Large, White Kidney Enlarged + Flabby Cortical Substance = Grey w/ Yellow Drops
31
What are the MICROSCOPIC Changes in Fatty KIDNEY? {Morphology}
Lipid Accumulates in CYTOPLASM of EPITHELIAL CELLS OF Convoluted Tubules
32
What is Stromal Fatty Infiltration?
AKA Lipomatosis Deposition of Mature Adipose Cells in Stromal CT Occurs in Obese People Organs Affected = 1. Heart 2. Pancreas
33
1| How does Stromal Fatty Infiltration, affect the Heart?
Subepicardial Fat COVERS Heart PREVENTING CT from Growing LEADING to Heart Rupture in Area of Fat Growth
34
2| How does Stromal Fatty Infiltration, affect the Pancreas?
Atrophy of B-Cells LEADS to Diabetes Mellitus
35
What Disease does Lipomatosis Occur?
{Lipomatosis = Local Enlargement of Adipose Tissue} In DEREUM'S DISEASE = Painful Fat Nodules appear in Subcut.Fat of Lower + Upper Extremities / Trunk
36
What is Obesity?
Lipid Accumulation of Specialized Cells OF Adipose Tissue
37
What is Obesity Classified into?
1. Depending on Excess of Patient Mass 2. According to Etiology (Cause) 3. According to Patient's Appearance 4. According to Morphological Peculiarities of Adipose Tissue
38
1| What are the 4 Degrees of Obesity?
1st Degree = Mass INCREASES by 20 - 29% 2nd Degree = Mass INCREASES by 30 - 49% 3rd Degree = Mass INCREASES by 50 - 99% 4th Degree = Mass INCREASES by 100% + More!
39
2| What are the 2 Types of Causes of Obesity?
a. Primary (Idiopathic) | b. Secondary
40
2b| What are the Types of Secondary Obesity
(i) Alimentary (ii) Cerebral (iii) Endocrine (iv) Inheritance in Gierke's Disease
41
3| What are the Kinds of Obesity, According to Patient's Appearance?
a. Symmetrical b. Upper c. Medial d. Lower
42
4| What are the Types of Obesity, According to Morphological Peculiarities of Adipose Tissue?
a. Hypertrophic Type | b. Hyperplastic Type
43
4a| What is Hypertrophic Type Obesity?
Tissue Enlargement DUE to INCREASE VOLUME OF Fatty Cells
44
4b| What is Hyperplastic Type Obesity?
Tissue Enlargement DUE to INCREASE NUMBER OF Fatty Cells
45
What Kind of Complication is Obesity?
SEVERE Complication of Endocrine + Nervous Diseases
46
What is Another Complication of Obesity?
Alimentary Obesity = Unfavourable for Organism Patients with Alimentary Obesity DEVELOP Ischaemic Heart Diseases
47
What is Cachexia?
SHARP REDUCTION in Amount of Adipose Tissue IN Whole Organism
48
What does Cholesterol Metabolism Disturbances Lead to?
Atherosclerosis - Where Vessel Wall is THICKENED DUE to Formation of Atherosclerotic Plaque (Lipids + Fibrotic Tissue)
49
What are Xantelsmas?
Specific Skin Lesion Observed in HYPERCHOLESTEROLEMIA Occurs in Eyelids Microscopically = Cholesterol Ester Accumulation in Cytoplasm of Skin's MACROPHAGES --> FOAMY / PSEUDOXANTOMATOUS Cells