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General Pathology > 7. Disorders of the metabolism of lipids. Types of adipose degeneration > Flashcards

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

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
Q

4| How does Disorders of Small Intestines Cause

Liver Steatosis?

A

Patients with SI Disorders = Enterocolitis

DEFICIENCY of Proteins + Lipotropic Factors

{Lipotropic Factors are needed for Lipoprotein Synthesis)

26
Q

What are the MACROSOPIC Changes in Fatty LIVER?

{Morphology}

A

Enlarged Liver w/ Rounded Margins

Cut Surface = Pale Yellow + Slightly Bulges

Greasy aka Goose Liver

27
Q

What are the MICROSCOPIC Changes in Fatty LIVER?

{Morphology}

A

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
Q

What are the MACROSOPIC Changes in Fatty HEART?

{Morphology}

A

Aka Tiger Heart

Enlarged Heart

Stretched + Flabby Chambers

29
Q

What are the MICROSCOPIC Changes in Fatty HEART?

{Morphology}

A

Dust-like Vacuoles in Cardiomyocytes

Observed in Papillary Muscles + Trabecules of Ventricles in Form of Bands

Surrounds Veins (Hypoxia is MOST SEVERE)

30
Q

What are the MACROSOPIC Changes in Fatty KIDNEY?

{Morphology}

A

Occurs in Nephrotic Syndrome

Large, White Kidney

Enlarged + Flabby

Cortical Substance = Grey w/ Yellow Drops

31
Q

What are the MICROSCOPIC Changes in Fatty KIDNEY?

{Morphology}

A

Lipid Accumulates in CYTOPLASM of EPITHELIAL CELLS

OF Convoluted Tubules

32
Q

What is Stromal Fatty Infiltration?

A

AKA Lipomatosis

Deposition of Mature Adipose Cells in Stromal CT

Occurs in Obese People

Organs Affected =

  1. Heart
  2. Pancreas
33
Q

1| How does Stromal Fatty Infiltration, affect the Heart?

A

Subepicardial Fat COVERS Heart

PREVENTING CT from Growing

LEADING to Heart Rupture in Area of Fat Growth

34
Q

2| How does Stromal Fatty Infiltration, affect the Pancreas?

A

Atrophy of B-Cells LEADS to Diabetes Mellitus

35
Q

What Disease does Lipomatosis Occur?

A

{Lipomatosis = Local Enlargement of Adipose Tissue}

In DEREUM’S DISEASE = Painful Fat Nodules appear in Subcut.Fat of Lower + Upper Extremities / Trunk

36
Q

What is Obesity?

A

Lipid Accumulation of Specialized Cells

OF Adipose Tissue

37
Q

What is Obesity Classified into?

A
  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
Q

1| What are the 4 Degrees of Obesity?

A

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
Q

2| What are the 2 Types of Causes of Obesity?

A

a. Primary (Idiopathic)

b. Secondary

40
Q

2b| What are the Types of Secondary Obesity

A

(i) Alimentary
(ii) Cerebral
(iii) Endocrine
(iv) Inheritance in Gierke’s Disease

41
Q

3| What are the Kinds of Obesity, According to Patient’s Appearance?

A

a. Symmetrical
b. Upper
c. Medial
d. Lower

42
Q

4| What are the Types of Obesity, According to Morphological Peculiarities of Adipose Tissue?

A

a. Hypertrophic Type

b. Hyperplastic Type

43
Q

4a| What is Hypertrophic Type Obesity?

A

Tissue Enlargement

DUE to INCREASE VOLUME

OF Fatty Cells

44
Q

4b| What is Hyperplastic Type Obesity?

A

Tissue Enlargement

DUE to INCREASE NUMBER

OF Fatty Cells

45
Q

What Kind of Complication is Obesity?

A

SEVERE Complication of

Endocrine + Nervous Diseases

46
Q

What is Another Complication of Obesity?

A

Alimentary Obesity = Unfavourable for Organism

Patients with Alimentary Obesity DEVELOP Ischaemic Heart Diseases

47
Q

What is Cachexia?

A

SHARP REDUCTION in Amount of Adipose Tissue

IN Whole Organism

48
Q

What does Cholesterol Metabolism Disturbances Lead to?

A

Atherosclerosis

  • Where Vessel Wall is THICKENED DUE to Formation of Atherosclerotic Plaque (Lipids + Fibrotic Tissue)
49
Q

What are Xantelsmas?

A

Specific Skin Lesion

Observed in HYPERCHOLESTEROLEMIA

Occurs in Eyelids

Microscopically = Cholesterol Ester Accumulation in Cytoplasm of Skin’s MACROPHAGES –> FOAMY / PSEUDOXANTOMATOUS Cells

General Pathology (13 decks)

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