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8 PATH 2 > LECTURE 1 > Flashcards

LECTURE 1 Flashcards

1
Q

What is Normal Diuresis of the Kidney?

A

1.3-1.6 L/day

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2
Q

Where are the kidneys located?

A

Retroperitoneal (behind the peritoneum) at the level of the lower ribs (T12-L3) right side slight lower

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3
Q

What can affect the kidneys due to its posterior superficial location?

A

Temperature

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4
Q

Why is the Capsule important for clinical issues?

A

It contains nociceptors and baroreceptors

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5
Q

What can happen to the capsule that would cause issues?

A

Distention of the capsule can be caused by inflammation, tumor, kidney stones, etc. (back pain)

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6
Q

What is contained in the cortex?

A

Glomerulus system with filtration and collecting system

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7
Q

What does the medulla contain?

A

Pyramids, collecting systems

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8
Q

What are the 4 compartments of the kidney?

A

1) Glomeruli
2) Tubules
3) Interstitial Tissue
4) Kidney Vessels

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9
Q

What are the the Glomeruli?

A

In cortex - filtration of blood via juxtaglomerular cells

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10
Q

How are the Glomeruli damaged?

A

Immunopathological (immunopathologically mediated)

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11
Q

What are the Tubules?

A

Collecting systems/channels - the glomeruli are made of tubules

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12
Q

How are the tubules affected?

A

Infection and Toxins

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13
Q

How is Interstitial Tissue affected?

A

Infection and Toxins

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14
Q

What are the 2 types of kidney disorders?

A

Primary (starts in one component) and Secondary (develop in all of them)

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15
Q

What are the 4 main functions of the kidney?

A

1) Excretion
2) Regulation
3) Maintenance
4) Secretion

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16
Q

What is Excretion?

A

Excretion of waste products of metabolism (MAJOR FUNCTION)

  • Toxic to the body: Excess can result in intoxication, even death
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17
Q

What is Regulation?

A

Regulation of the body’s concentration of water and salt

  • Can determine if body is wider or slimmer
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18
Q

What is Maintenance?

A

Kidneys maintain appropriate acid balance (pH) of plasma

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19
Q

What is the normal environment of the blood?

A

Plasma good portion of the blood (serum = plasma without clotting factor)

  • Normal environment of blood is weak basic - pH can vary depending on plasma pH changes
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20
Q

What is Secretion in regard to the Kidneys?

A

Secretes hormones (Erythropoietin, prostaglandins, calcitriol) and enzyme renin

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21
Q

What happens with Renal Failure?

A

Suppression of Erythropoietin production, results in LOSS of Hematopoietin

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22
Q

What does Renin do, what is it made by?

A

Regulation of BP, made by JUXTAGLOMERULAR CELLS

  • decreases the glomerular filtration rate (GFR) and decreases pressure in the afferent arteriole
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23
Q

What is Erythropoietin?

A

Promote formation and production of RBC’s in the bone marrow - can cause anemia (always with renal failure)

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24
Q

What are Prostaglandins?

A

Can be created by many organs, mainly by kidneys. Formation of various hormones and neurotransmitters - mediators of inflammation

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25
Q

What is the aka of Glomerulonephritis?

A

Glomerular Diseases, Glomerulopathy

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26
Q

What are most Glomeruli issues the result of?

A

Inflammation (can also be non-inflammatory)

  • *Also could be degeneration of the glomeruli (usually associated with an autoimmune pathology) -> Suppression of immune system
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27
Q

What is primary glomerular disease?

A

Begins in the kidney primarily then spreads to other organs

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28
Q

What is secondary glomerular diseases?

A

Kidney is involved as a result of a systemic disease

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29
Q

How does blood flow through the Glomerular structure?

A

Afferent arterioles enter glomerulus, blood flows into the Bowman’s capsule and then into the tubules, blood flows out of the glomerulus through afferent arteriole (arteriole -> capillary -> arteriole)

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30
Q

What are Juxtaglomerular Cells?

A

“Hormone Producing Cells”

Near the beginning of afferent arterioles. Controls BP in arterioles because blood only diffuses out at an optimum BP

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31
Q

What do Juxtaglomerular Cells produce?

A

RENIN

  • This begins the formation of angiotensin II, which increases the BP (KGB of the kidney) “keeps eye on the pressure in the arteriole”
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32
Q

What must pressure be above in order for filtration in glomeruli to occur?

A

50 mmHg **** QUIZ

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33
Q

What is the Endothelial layer of the Arteriole?

A

Inner layer, line the arterioles and have holes between the endothelial cells

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34
Q

What are on Endothelial Cells?

A

FENESTRAE, “window”

  • These promote filtration of the blood through the walls of the capillaries
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35
Q

What is the Glomerular Basement Membrane?

A

GBM (middle layer)

  • Location of connection of all things: endothelial cells lie here
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36
Q

What are visceral epithelial cells aka?

A

Podocytes

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37
Q

What is the function of Visceral Epithelial cells (aka Podocytes)?

A

Special function and anatomical structure - foot processes/pedicles with filtration slits between them ** QUIZ

  • This is important for formation of urine (waste products) and for filtration of blood
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38
Q

Foot process + slit =

A

Podocyte

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39
Q

What are Parietal Epithelial cells?

A

Epithelial cells that line the inner surface of the Bowman’s capsule - smooth cells

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40
Q

What are Mesangial Cells?

A

A type of stromal cell that occupies the space within the glomeruli

  • They can replicate, fight infection, and can become sclerotic if there is excess PROLIFERATION OF CT (healing)
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41
Q

What is the space between the visceral epithelial cells?

A

Mesangial Cells

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42
Q

What cells produce Erythropoietin?

A

Mesangial cells

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43
Q

What can the Mesangial cells do?

A

Contract to pull the capillaries together to organize the glomeruli (provide structural support)

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44
Q

The healing of the glomeruli —>

A

Can proliferate and close the gap through differentiation like fibroblasts (but still maintain contractility)

  • Contains monocytes/macrophages
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45
Q

What are the 3 Pathogenic Mechanisms of Glomerulonephritis?

A

1) Circulating Immune Complex Deposition
2) Anti-GBM (Glomerular Basement Membrane) Glomerulonephritis
3) Heymann’s Glomerulonephritis

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46
Q

What type of Hypersensitivity reaction is Circulating Immune Complex Deposition?

A

Classic Type III (immune complex mediated type).

  • OUTSIDE GLOMERULI **
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47
Q

Where does Circulating Immune Complex Deposition occur?

A

Formation of Immune complexes outside of the kidney - takes place only in the circulation OUTSIDE the kidney

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48
Q

How does the Immune Complex formation occur in Circulating Immune Complex Deposition ?

A

Appearance of antigens in the blood - antibodies are made, meet and bind to the antigens

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49
Q

What happens in the antibody/antigen complex in Circulating Immune Complex Deposition?

A

It attaches to the wall of the vessels

  • Immune complexes are deposited between the basement membrane and endothelial cells = SUBINTIMAL SPACE aka SUBENDOTHELIAL DEPOSITS
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50
Q

What does the immune complex attract in Circulating Immune Complex Deposition ?

A

It attracts phagocytic cells but the cells can’t engulf the complex because it is bound to the vascular wall (FRUSTRATED PHAGOCYTOSIS)

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51
Q

What is Frustrated Phagocytosis?

A

Release proteolytic enzymes (lysosomal) into the surrounding area = can result in the injury and inflammation of the vascular wall = VASCULITIS**

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52
Q

What is VASCULITIS?

A

Proteins digest the vascular wall

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53
Q

Frustrated Phagocytosis occurs in what pathogenic mechanism of Glomerulonephritis?

A

Circulating Immune Complex Formation

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54
Q

What type of Hypersensitivity reaction is Anti-GBM Glomerulonephritis?

A

Type II Complement dependent

  • INSIDE GLOMERULUS**
  • ANTIBODY DEPENDENT**
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55
Q

Explain the antibodies and antigens in Anti-GBM Glomerulonephritis?

A

Antigen of GBM are not self for the body*

Antibodies against antibodies of GBM*

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56
Q

What happens to the antibodies in Anti-GBM Glomerulonephritis?

A

Formation of antibodies against the glomerular basement membrane - attraction of neutrophils and a RELEASE of phagocytic cells

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57
Q

VASCULITIS occurs in what type of Glomerulonephritis?

A

Circulating Immune Complex Deposition and Anti-GBM Glomerulonephritis

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58
Q

What happens to phagocytic cells in Anti-GBM Glomerulonephritis?

A

Phagocytic cells can’t be dissolved so enzymes are released that destroy the basement membrane (GBM), epithelial cells and the podocytes

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59
Q

What happens to the glomerular basement membrane in Anti-GBM Glomerulonephritis ?

A

Antigens of the glomerular basement membrane start to be attacked - antibodies flow into the kidney and the reaction is inside the kidneys - bind to antibodies of GBM —> Frustrated Phagocytosis

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60
Q

Is Frustrated Phagocytosis and VASCULITIS a part of Anti-GBM Glomerulonephritis?

A

YES

  • Antibodies produced by antigen binding - binds complement - attracts phagocytic cells (PMN) - hydrolytic enzymes and activated oxygen -> disruption of basement membrane = VASCULITIS
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61
Q

Where does Heymann’s Glomerulonephritis occur?

A

INSIDE GLOMERULUS

  • NOT a Hypersensitivity (auto aggression)
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62
Q

What is Heymann’s Glomerulonephritis characterized by?

A

The development of antibodies against:

1) Antigens of the visceral epithelial cells AKA podocytes
2) Antigens that can be deposited between the glomerular basement membrane and podocytes

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63
Q

Between the glomerular basement membrane and podocytes, is called what?

A

Subepithelial deposits

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64
Q

What is special about the subepithelial deposits?

A

A lot of the components of the blood cells are removed through this area

  • It has waste products, bacteria, viruses etc. stored in this area

(Between PODOCYTES and BASEMENT MEMBRANE)

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65
Q

What does Heymann’s CMN lead to?

A

Destruction of the podocytes

  • It is marked by an autoimmune reaction against the antigens located within the podocytes
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66
Q

Does Heymann’s Glomerulonephritis cause VASCULITIS?

A

YES

  • Leads to the reaction of the phagocytic cells with this debris stored in this area -> leads to the same VASCULITIS reaction

(Same Mechanism)

  • Formation of phagocytic cells and release of enzymes BOTH good and bad cells are killed
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67
Q

Glomeruli capillaries are very permeable to water, but impermeable to ______

A

Blood cells, proteins, albumins, etc

  • If protein is in urine = PATHOLOGY
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68
Q

What is Nephritic Syndrome?

A

Damage of the glomeruli wall is characterized by paradoxical situation

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69
Q

What is Nephritic syndrome characterized by?

A
  • Increased permeability of RBC’s (found in the urine = hematuria (with RBC’s)
  • Decreased permeability of water
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70
Q

What is Nephritic Syndrome caused by? ***

A

Damage to the glomeruli ** QUIZ

71
Q

What are the 3 clinical conditions of Nephritic Syndrome?

A

1) Hematuria
2) Oliguria
3) Hypertension

72
Q

What is Hematuria?

A

Increased permeability of the glomerular wall to RBC’s

  • Blood in the urine with RBC casts (covered by huge amount of RBCs/copy) ; water can’t go through wall; less production of urine
73
Q

What is Oliguria?

A

Limited or diminished amount of urine production - Dramatic decrease in permeability of water

= Decreased in volume of urine

74
Q

What is the actual numerical decrease in Oliguria?

A

Normal = 1.3 - 1.6

OLIGURIA = < 400 mL ***

75
Q

What does Oliguria result in?

A

Azotemia

76
Q

What is Azotemia?

A

Increased concentration of nitrogen products

77
Q

What is the major factor of Oliguria ?

A

Waste products are dissolved in the water, and water exits the glomeruli and are eliminated with the urine -> If the rate of elimination of waste products is decreased, then the waste products accumulate

78
Q

What is actual Azotemia?

A

Nitrogen (azote) containing products that are waste products of metabolism

79
Q

What is the Biochemical *** abnormality of Azotemia?

A

Biochemical abnormality that refers to an elevation of Blood Urea Nitrogen (BUN) and creatinine levels which are closely related to a decreased glomerular filtration rate.

80
Q

What is aka of Toxic elements?

A

Nitrogen products

81
Q

What are Nitrogen products?

A

Toxic factors that are a result of the normal function of the human body. Patient FEELS NORMAL***

82
Q

What is the overall summary of Azotemia and Nitrogen?

A

Increased nitrogen products in the blood circulation due to the decreased capability to be removed from the body -> AZOTEMIA (nitrogen containing waste products in the blood) -> the concentration increases steadily — no symptoms until critical point/amount -> patient does not feel the minor intoxication until the “tipping point” , then they feel the effects of the intoxication ***

83
Q

What the concentration of azotemia is high, it results in ______

A

UREMIA

84
Q

What is Uremia?

A

Azotemia + combination/clinical manifestation of clinical signs and symptoms and then renal failure

85
Q

What are the symptoms of Uremia?

A

Nausea, vomiting, skin problems, or urine smell of the mouth

86
Q

What is Hypertension?

A

Juxtaglomerular cells regulate BP in the body (pressure within arterioles to push the blood through )

87
Q

What is the number the juxtaglomerular cells regulate BP in the body ?

A

> 50 mm Hg

88
Q

When is Renin produced?

A

When there is a decrease in pressure in the afferent arterioles and a decrease in glomerular filtration rate

89
Q

What does Renin production increase?

A

BP, though angiotensin II’s effect through vasoconstriction and aldosterone secretion -> Na+ retention

90
Q

What is an inevitable component of Nephritic syndrome?

A

Hypertension is an inevitable component of Nephritic syndrome

91
Q

Juxtaglomerular cells only take into account _______

A

The afferent BP -> will continue to elevate more and more -> leads to more and more filtration -> leads to hypertension due to renin

92
Q

What is the Net filtration pressure of the Glomerulus?

A

10 mmHg

Glomerular Hydrostatic P (60 mm Hg) - Bowman’s Capsule pressure (18 mm Hg) - Glomerular oncotic pressure (32 mm Hg)

93
Q

What is the most powerful hypertensive substance in the body?

A

Angiotensin II

94
Q

What are the diseases associated with Nephritic Syndrome?

A

Acute Proliferative (poststreptococcal, postinfectious) Glomerulonephritis

  • Beta Hemolytic Streptococcus Group A (pyogenes)
  • Acute and Chronic Tonsillitis
  • Molecular Mimicry
  • Rapidly Progressive (crescentic ) Glomerulonephritis
95
Q

What can Acute Proliferative (poststreptococcal, postinfectious) Glomerulonephritis be caused by?

A

The infectious antibodies of streptococcus

96
Q

What can antibodies destroy in Acute Proliferative (poststreptococcal, postinfectious) Glomerulonephritis?

A

The antibodies can destroy the glomerular well (Strep Throat)

97
Q

What are people with Strep Throat prone to?

A

Beta Hemolytic Streptococcus Group A (pyogenes)

98
Q

In some people the structure of glomeruli _______

A

May be similar to antigenic structure of streptococcal wall; Immune Complex triggered; confuses the immune system instead of fighting intruders, they fight the self tissue (molecular mimicry)

99
Q

What is molecular mimicry sometimes curable with?

A

Corticosteroids

100
Q

Explain Chronic Tonsillitis:

A

Tonsils are a good location for infection - enlargement of the palatine tonsils due to infectious inflammation (increased temperature and swelling)

101
Q

Explain the process of infection in Chronic Tonsillitis:

A

6 accumulations of lymphoid tissues: tonsils -> identify possible intruders to the immune system

  • the 2 visible tonsils are (palatine tonsils)

** Curable in infants and children

102
Q

What is Molecular Mimicry?

A

Some people have glomerular walls that have antigens which look like streptococci =

One of the mechanism of autoimmune diseases; caused by infection indirectly through confusion of similarity

103
Q

Where can Molecular Mimicry develop?

A

It can develop in children or adults (50% of adult cases are transferred into chronic Glomerulonephritis, but only 1% of children cases are transferred)

  • Effects typically 1st-2nd decade of life in boys
104
Q

What is the treatment of Molecular Mimicry?

A

Corticosteroids - after a few weeks of Tx, the kids will recover 99% of the time, the adults will recover 50% of the time

105
Q

What is the treatment of Acute Proliferative (poststreptococcal, postinfectious) Glomerulonephritis ?

A

Corticosteroids - after a few weeks of Tx, the kids will recover 99% of the time, the adults will recover 50% of the time

106
Q

What are the signs of Acute Proliferative Glomerulonephritis (poststreptococcal, postinfectious) ?

A
  • Swelling underneath the eyes (common with kidney problems)
  • Hematuria - - Urine brown/red
  • Hypertension
  • Oliguria -> Azotemia (biochemical tests only)
  • Edema -> Specifically underneath the eye
107
Q

What would you think about young people in your office with swelling under their eyes?

A

You need to rule out kidney issues, these patients may have a Low serum complement level (hypocomplementemia) -> Typical for Type III hypersensitivity rxn

108
Q

What does lab show on Acute Proliferative GMN aka Acute Poststreptococcal GMN aka Postinfectious GMN?

A

Low serum complement level (hypocomplementemia), elevated serum antistreptolysin O titers

109
Q

What is the MOST DANGEROUS Nephritic syndrome?

A

Rapidly Progressive (crescentic ) Glomerulonephritis

110
Q

Rapidly Progressive GMN aka

A

Crescentic GMN

111
Q

What is Rapidly Progressive GMN characterized by?

A

Rapid and progressive loss of renal function associated with severe oliguria and (if untreated) death from renal failure within weeks to months

112
Q

What does the prognosis depend on in Rapidly Progressive (crescentic) GMN?

A

It depends on the amount of glomeruli with crescents ( > 80% fatal) - become crescent shaped and obstruct the lumen of proximal convoluted tubule

  • Urine builds up inside the kidney -> Increased hydrostatic pressure with GBM -> Prevent circulation of blood
113
Q

What is the main symptom of Rapidly Progressive (crescentic) Glomerulonephritis ?

A

Hyperplasia of parietal epithelial cells of Bowman’s capsule

114
Q

What is Hyperplasia of parietal epithelial cells of Bowman’s capsule?

A

Increased production of cells can result in narrowing or closure of the tubules -> accumulation of urine -> increased hydrostatic pressure -> pressure atrophy

115
Q

Where is Secondary Glomerulonephritis developed ?

A

Not developed in the kidney primarily

116
Q

What are the 3 types of Rapidly Progressive GMN aka Crescentic GMN?

A

1) Type 1: Anti-GBM
2) Type 2: Immune Complex - Mediated Deposition
3) Type 3: Pauci-Immune

117
Q

What is Type I of Rapidly Progressive GMN aka Crescentic GMN?

A

Anti-GBM

118
Q

Type I (anti-GBM) of Rapidly Progressive GMN definition:

A

Development of Aggression against the basement membrane

119
Q

What type of Hypersensitivity Reaction is Type I (anti-GBM)?

A

Type II Hypersensitivity

120
Q

What are the 2 kinds of diseases in Type 1 Anti-GBM?

A

1) Idiopathic (>50%)

2) Goodpasture’s Syndrome

121
Q

What is Goodpasture’s Syndrome characterized by?

A

Development of autoimmune aggression against lung and kidney basement membranes (against glomeruli and alveoli)

  • antibodies against alveolar and glomerular basement membranes
122
Q

What is happening to the alveoli in Goodpasture’s Syndrome?

A

Alveoli are supposed to be filled with air , but are now filled with exudate because of damage to the basement membrane; they are permeable, blood from capillaries go into alveoli; inflammation of lung tissue, cough, trying to cough up the mucous

  • Hemoptysis (blood in sputum)
123
Q

Plasmapheresis is associated with _____

A

Goodpasture’s Syndrome

124
Q

What is used to treat Goodpasture’s Syndrome, how does it work?

A

Plasmapheresis (treats autoimmune diseases as well)

  • Remove antibodies from the blood (using centrifuges to remove the plasma) and give drugs to prevent more formation of antibodies
125
Q

Antibodies in Goodpasture’s syndrome forms against what membranes?

A

1) Alveolar Basement Membrane

2) Glomerular Basement Membrane

126
Q

Alveolar Basement membrane (good pasture’s syndrome) is associated with what symptom?

A

Hemoptysis (coughing up blood/ sputum containing blood)

  • Inflammation of membrane causes the formation of exudates (fluids and cells) in the alveoli -> can no longer exchange air
127
Q

Glomerular Basement Membrane (associated with Goodpasture’s Syndrome) :

A

Destruction of tissue around the membranes (crescents) -> glomerular tissue dies & replaced by CT (not functional)

128
Q

What type of Hypersensitivity reaction is Type II (Immune Complex-Mediated Deposition / Diseases) ?

A

Idiopathic 50%

Type III Hypersensitivity

129
Q

What 2 diseases are associated with Type 2: Immune Complex Mediated Deposition?

A

1) Systemic Lupus Erythematosus (SLE)

2) Henoch - Schonlein Purpura aka Hemorrhagic VASCULITIS

130
Q

What is Systemic Lupus Erythematosus?

A

Classic aggressive autoimmune disease that involves young ladies (20s), more common in African Americans

131
Q

What is the MOST COMMON cause of Systemic Lupus Erythematosus (SLE) ?

A

Ultraviolet radiation MC***

  • Sulfosalicylic drugs
  • Vaccination
132
Q

What is Systemic Lupus Erythematosus characterized by?

A

Aggressive autoimmune reaction against antigens of the cell nucleus and cytoplasm (any cell in the body can be affected)

133
Q

What are the Tests for Systemic Lupus Erythematosus?

A
  • Antinuclear antibodies (ANA) - - ANA against double stranded DNA and ANA against Smith - antigen (anti-Sm-antibodies); pathoneumonic finding
134
Q

What does SLE mostly involve?

A

Unusual arthritis, the skin, lungs, kidney, and cerebral vessels - - results in serious hypertension and possibly stroke

  • Survival rate has gone from 50 - 85%
135
Q

What is the primary manifestation of SLE?

A

Butterfly like skin rash/dermatitis

  • Also includes Alopecia
136
Q

SLE with kidney involvement =

A

Lupus Nephritis

137
Q

What does Lupus Nephritis involve?

A

Kidneys, develops quickly/rapidly - major cause of death in this disease - if treatment is not sufficient for a year, death will occur. Treatment should be as early as possible*

138
Q

What is also possible with Lupus Nephritis?

A

VASCULITIS of cerebral vessels -> cerebral VASCULITIS = death

139
Q

What is the survival rate of Lupus Nephritis?

A

85-90% (was 50%)

140
Q

What is the treatment for Lupus Nephritis?

A

Corticosteroids (results in Cushing’s Syndrome: moon-like face) and immunosuppressors

  • Immunosuppressors are a dangerous treatment which can suppress the immune system too much leading to infections, shingles, etc.
141
Q

Henoch-Schonlein Purpura aka

A

Hemorrhagic VASCULITIS

142
Q

Where does Henoch-Schonlein Purpura aka Hemorrhagic VASCULITIS develop?

A

In late adolescent males

143
Q

What are the 4 manifestations of Henoch-Schonlein Purpura aka Hemorrhagic VASCULITIS?

A

1) Articular
2) Abdominal
3) Skin
4) Kidney

144
Q

What is Articular Syndrome of Henoch-Schonlein Purpura ?

A

Characterized by sub clinical arthritis or joint pain (arthralgia)

145
Q

What is skin/Cutaneous Syndrome of Henoch-Schonlein Purpura?

A

Development of Purpura (subcutaneous hemorrhage < 2cm) rash - in the buttock and abdomen

146
Q

What is Abdominal Syndrome associated with Henoch-Schonlein Purpura?

A

Hemorrhagic inflammation of stomach and duodenal walls (gastroduodenitis)

147
Q

What is Kidney syndrome associated with Henoch-Schonlein Purpura?

A

Crescentic Glomerulonephritis: development of rapidly Progressive Glomerulonephritis (crescents) -> the addition of kidney syndrome, makes worse

  • Survival rate is decreased to 70% survival rate with kidney syndrome
148
Q

What happens with IgA in Henoch Schonlein Purpura?

A

IgA deposition in the Mesangium (part of IgA nephropathy)

149
Q

Type 3 of Rapidly Progressive GMN aka Crescentic GMN =

A

Pauci Immune

150
Q

What are the diseases associated with Pauci Immune?

A
  • Wegener’s Granulomatosis
  • Polyarteritis Nodosa
  • IgA Nephropathy aka Berger’s Disease
  • Alport Syndrome
151
Q

What Hypersensitivity is Type 3 Pauci - Immune related to?

A

It is NOT related to a specific type of hypersensitivity

152
Q

What is Type III (Pauci Immune) characterized by?

A

The development of VASCULITIS (MOST DANGEROUS!!)

153
Q

What is the pathogenesis of Type III Pauci Immune?

A

Very autoimmune disease

154
Q

What are a major sign of VASCULITIS in Type III (pauci immune)?

A

Antineutrophil ctoplasmic autoantibodies (found in the peripheral blood)

155
Q

T/F, more than 50% of Type III (Pauci Immune) is Idiopathic?

A

TRUE

156
Q

What is Wegener’s Granulomatosis?

A

Very aggressive disease, autoimmune pathology (rare)

157
Q

What are the 3 clinical symptoms of Wegener’s Granulomatosis?

A

1) Necrotizing VASCULITIS of upper respiratory tract
2) Necrotizing VASCULITIS of lower respiratory tract
3) Rapidly progressive GMN

158
Q

What are the symptoms of Necrotizing VASCULITIS of upper respiratory tract?

A
  • Destruction and decay of soft tissues and bones (facial bones) *** horrible smell
  • aging, elderly females
  • MELTING of bones of face which can lead to infection and suppurative inflammation (the patient is undergoing decay) = WET GANGRENE*****
159
Q

WHat are the symptoms of Necrotizing VASCULITIS of Lower respiratory tract?

A

Results in cavitation of the lungs

  • Dissolution / destruction of tissue
160
Q

What are the symptoms of Rapidly progressive GMN?

A

POOR prognosis (patient will die due to acute renal failure or 2ndary complications)

  • Affects middle aged males (can be women in older age)
  • There is now treatment
161
Q

What is Polyarteritis Nodosa?

A

Characterized by VASCULITIS of the vessels throughout the body -> the involvement of middle and small sized arteries with bulging/pouching of their walls

162
Q

T/f Polyarteritis (periarteritis) Nodosa is idiopathic?

A

TRUE

163
Q

Is Polyarteritis (periarteritis) Nodosa more common in young than old?

A

More common in young

164
Q

What organ/tissue is involved in Polyarteritis/Periarteritis Nodosa ?

A

Any organ/tissue can be involved in this disease

***** NO INVOLVEMENT OF LUNGS OR ARCH OF AORTA

165
Q

Nodosa =

A

Pouching of the walls

166
Q

What can node formation lead to in Polyarteritis (Periarteritis) Nodosa?

A

Node formation can lead to ischemia

  • Associated with compression of adjacent vessels, by the nodes
167
Q

How does pouching occur in Polyarteritis (Periarteritis) Nodosa?

A

Due to thinning of the wall due to VASCULITIS -> more vulnerable to distension -> Hemorrhaging into neighboring tissue OR can compress adjacent tissues (microinfarctions of the organs) ->

NECROSIS **

168
Q

What is VASCULITIS ?

A
  • Inflammation of vascular wall -> spreads into the lumen of the vessel -> Ischemia -> Infarction
169
Q

Wet Gangrene is associated with what Type 3 Pauci Immune disease?

A

Polyarteritis Nodosa aka Periarteritis Nodosa

170
Q

What organ is most commonly involved in Polyarteritis Nodosa aka Periarteritis Nodosa?

A

Kidney is the organ most commonly involved

  • Inflammation -> connective tissue formation -> decrease in normal size of the kidney
  • Leads to destruction of vessels, ruptures/hemorrhage’s, microinfarction, decreased lumen size, compression of surrounding tissues, and wet gangrene
171
Q

In Polyarteritis Nodosa, The Kidney has what major symptom?

A

Rapidly Progressing GMN

  • CT in the kidney (repair) shrinks the kidney = see CRESCENTS
172
Q

IgA Nephropathy aka

A

Berger’s Disease

173
Q

What is the MC disease worldwide?

A

IgA nephropathy

8 PATH 2 (10 decks)

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