LECTURE 1 Flashcards
1
Q
What is Normal Diuresis of the Kidney?
A
1.3-1.6 L/day
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
3
Q
What can affect the kidneys due to its posterior superficial location?
A
Temperature
4
Q
Why is the Capsule important for clinical issues?
A
It contains nociceptors and baroreceptors
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)
6
Q
What is contained in the cortex?
A
Glomerulus system with filtration and collecting system
7
Q
What does the medulla contain?
A
Pyramids, collecting systems
8
Q
What are the 4 compartments of the kidney?
A
1) Glomeruli
2) Tubules
3) Interstitial Tissue
4) Kidney Vessels
9
Q
What are the the Glomeruli?
A
In cortex - filtration of blood via juxtaglomerular cells
10
Q
How are the Glomeruli damaged?
A
Immunopathological (immunopathologically mediated)
11
Q
What are the Tubules?
A
Collecting systems/channels - the glomeruli are made of tubules
12
Q
How are the tubules affected?
A
Infection and Toxins
13
Q
How is Interstitial Tissue affected?
A
Infection and Toxins
14
Q
What are the 2 types of kidney disorders?
A
Primary (starts in one component) and Secondary (develop in all of them)
15
Q
What are the 4 main functions of the kidney?
A
1) Excretion
2) Regulation
3) Maintenance
4) Secretion
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
17
Q
What is Regulation?
A
Regulation of the body’s concentration of water and salt
- Can determine if body is wider or slimmer
18
Q
What is Maintenance?
A
Kidneys maintain appropriate acid balance (pH) of plasma
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
20
Q
What is Secretion in regard to the Kidneys?
A
Secretes hormones (Erythropoietin, prostaglandins, calcitriol) and enzyme renin
21
Q
What happens with Renal Failure?
A
Suppression of Erythropoietin production, results in LOSS of Hematopoietin
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
23
Q
What is Erythropoietin?
A
Promote formation and production of RBC’s in the bone marrow - can cause anemia (always with renal failure)
24
Q
What are Prostaglandins?
A
Can be created by many organs, mainly by kidneys. Formation of various hormones and neurotransmitters - mediators of inflammation
25
What is the aka of Glomerulonephritis?
Glomerular Diseases, Glomerulopathy
26
What are most Glomeruli issues the result of?
Inflammation (can also be non-inflammatory)
- *Also could be degeneration of the glomeruli (usually associated with an autoimmune pathology) -> Suppression of immune system
27
What is primary glomerular disease?
Begins in the kidney primarily then spreads to other organs
28
What is secondary glomerular diseases?
Kidney is involved as a result of a systemic disease
29
How does blood flow through the Glomerular structure?
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)
30
What are Juxtaglomerular Cells?
“Hormone Producing Cells”
Near the beginning of afferent arterioles. Controls BP in arterioles because blood only diffuses out at an optimum BP
31
What do Juxtaglomerular Cells produce?
RENIN
- This begins the formation of angiotensin II, which increases the BP (KGB of the kidney) “keeps eye on the pressure in the arteriole”
32
What must pressure be above in order for filtration in glomeruli to occur?
50 mmHg ****** QUIZ
33
What is the Endothelial layer of the Arteriole?
Inner layer, line the arterioles and have holes between the endothelial cells
34
What are on Endothelial Cells?
FENESTRAE, “window”
- These promote filtration of the blood through the walls of the capillaries
35
What is the Glomerular Basement Membrane?
GBM (middle layer)
- Location of connection of all things: endothelial cells lie here
36
What are visceral epithelial cells aka?
Podocytes
37
What is the function of Visceral Epithelial cells (aka Podocytes)?
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
38
Foot process + slit =
Podocyte
39
What are Parietal Epithelial cells?
Epithelial cells that line the inner surface of the Bowman’s capsule - smooth cells
40
What are Mesangial Cells?
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)
41
What is the space between the visceral epithelial cells?
Mesangial Cells
42
What cells produce Erythropoietin?
Mesangial cells
43
What can the Mesangial cells do?
Contract to pull the capillaries together to organize the glomeruli (provide structural support)
44
The healing of the glomeruli —>
Can proliferate and close the gap through differentiation like fibroblasts (but still maintain contractility)
- Contains monocytes/macrophages
45
What are the 3 Pathogenic Mechanisms of Glomerulonephritis?
1) Circulating Immune Complex Deposition
2) Anti-GBM (Glomerular Basement Membrane) Glomerulonephritis
3) Heymann’s Glomerulonephritis
46
What type of Hypersensitivity reaction is Circulating Immune Complex Deposition?
Classic Type III (immune complex mediated type).
- OUTSIDE GLOMERULI **
47
Where does Circulating Immune Complex Deposition occur?
Formation of Immune complexes outside of the kidney - takes place only in the circulation OUTSIDE the kidney
48
How does the Immune Complex formation occur in Circulating Immune Complex Deposition ?
Appearance of antigens in the blood - antibodies are made, meet and bind to the antigens
49
What happens in the antibody/antigen complex in Circulating Immune Complex Deposition?
It attaches to the wall of the vessels
- Immune complexes are deposited between the basement membrane and endothelial cells = SUBINTIMAL SPACE aka SUBENDOTHELIAL DEPOSITS
50
What does the immune complex attract in Circulating Immune Complex Deposition ?
It attracts phagocytic cells but the cells can’t engulf the complex because it is bound to the vascular wall (FRUSTRATED PHAGOCYTOSIS)
51
What is Frustrated Phagocytosis?
Release proteolytic enzymes (lysosomal) into the surrounding area = can result in the injury and inflammation of the vascular wall = VASCULITIS**
52
What is VASCULITIS?
Proteins digest the vascular wall
53
Frustrated Phagocytosis occurs in what pathogenic mechanism of Glomerulonephritis?
Circulating Immune Complex Formation
54
What type of Hypersensitivity reaction is Anti-GBM Glomerulonephritis?
Type II Complement dependent
- INSIDE GLOMERULUS****
- ANTIBODY DEPENDENT****
55
Explain the antibodies and antigens in Anti-GBM Glomerulonephritis?
Antigen of GBM are not self for the body*
Antibodies against antibodies of GBM*
56
What happens to the antibodies in Anti-GBM Glomerulonephritis?
Formation of antibodies against the glomerular basement membrane - attraction of neutrophils and a RELEASE of phagocytic cells
57
VASCULITIS occurs in what type of Glomerulonephritis?
Circulating Immune Complex Deposition and Anti-GBM Glomerulonephritis
58
What happens to phagocytic cells in Anti-GBM Glomerulonephritis?
Phagocytic cells can’t be dissolved so enzymes are released that destroy the basement membrane (GBM), epithelial cells and the podocytes
59
What happens to the glomerular basement membrane in Anti-GBM Glomerulonephritis ?
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
60
Is Frustrated Phagocytosis and VASCULITIS a part of Anti-GBM Glomerulonephritis?
YES
- Antibodies produced by antigen binding - binds complement - attracts phagocytic cells (PMN) - hydrolytic enzymes and activated oxygen -> disruption of basement membrane = VASCULITIS
61
Where does Heymann’s Glomerulonephritis occur?
INSIDE GLOMERULUS
- NOT a Hypersensitivity (auto aggression)
62
What is Heymann’s Glomerulonephritis characterized by?
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
63
Between the glomerular basement membrane and podocytes, is called what?
Subepithelial deposits
64
What is special about the subepithelial deposits?
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)
65
What does Heymann’s CMN lead to?
Destruction of the podocytes
- It is marked by an autoimmune reaction against the antigens located within the podocytes
66
Does Heymann’s Glomerulonephritis cause VASCULITIS?
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
67
Glomeruli capillaries are very permeable to water, but impermeable to ______
Blood cells, proteins, albumins, etc
- If protein is in urine = PATHOLOGY
68
What is Nephritic Syndrome?
Damage of the glomeruli wall is characterized by paradoxical situation
69
What is Nephritic syndrome characterized by?
- Increased permeability of RBC’s (found in the urine = hematuria (with RBC’s)
- Decreased permeability of water
70
What is Nephritic Syndrome caused by? ***
Damage to the glomeruli **** QUIZ
71
What are the 3 clinical conditions of Nephritic Syndrome?
1) Hematuria
2) Oliguria
3) Hypertension
72
What is Hematuria?
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
What is Oliguria?
Limited or diminished amount of urine production - Dramatic decrease in permeability of water
= Decreased in volume of urine
74
What is the actual numerical decrease in Oliguria?
Normal = 1.3 - 1.6
OLIGURIA = < 400 mL ***
75
What does Oliguria result in?
Azotemia
76
What is Azotemia?
Increased concentration of nitrogen products
77
What is the major factor of Oliguria ?
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
What is actual Azotemia?
Nitrogen (azote) containing products that are waste products of metabolism
79
What is the Biochemical *** abnormality of Azotemia?
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
What is aka of Toxic elements?
Nitrogen products
81
What are Nitrogen products?
Toxic factors that are a result of the normal function of the human body. Patient FEELS NORMAL***
82
What is the overall summary of Azotemia and Nitrogen?
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
What the concentration of azotemia is high, it results in ______
UREMIA
84
What is Uremia?
Azotemia + combination/clinical manifestation of clinical signs and symptoms and then renal failure
85
What are the symptoms of Uremia?
Nausea, vomiting, skin problems, or urine smell of the mouth
86
What is Hypertension?
Juxtaglomerular cells regulate BP in the body (pressure within arterioles to push the blood through )
87
What is the number the juxtaglomerular cells regulate BP in the body ?
> 50 mm Hg
88
When is Renin produced?
When there is a decrease in pressure in the afferent arterioles and a decrease in glomerular filtration rate
89
What does Renin production increase?
BP, though angiotensin II’s effect through vasoconstriction and aldosterone secretion -> Na+ retention
90
What is an inevitable component of Nephritic syndrome?
Hypertension is an inevitable component of Nephritic syndrome
91
Juxtaglomerular cells only take into account _______
The afferent BP -> will continue to elevate more and more -> leads to more and more filtration -> leads to hypertension due to renin
92
What is the Net filtration pressure of the Glomerulus?
10 mmHg
Glomerular Hydrostatic P (60 mm Hg) - Bowman’s Capsule pressure (18 mm Hg) - Glomerular oncotic pressure (32 mm Hg)
93
What is the most powerful hypertensive substance in the body?
Angiotensin II
94
What are the diseases associated with Nephritic Syndrome?
Acute Proliferative (poststreptococcal, postinfectious) Glomerulonephritis
- Beta Hemolytic Streptococcus Group A (pyogenes)
- Acute and Chronic Tonsillitis
- Molecular Mimicry
- Rapidly Progressive (crescentic ) Glomerulonephritis
95
What can Acute Proliferative (poststreptococcal, postinfectious) Glomerulonephritis be caused by?
The infectious antibodies of streptococcus
96
What can antibodies destroy in Acute Proliferative (poststreptococcal, postinfectious) Glomerulonephritis?
The antibodies can destroy the glomerular well (Strep Throat)
97
What are people with Strep Throat prone to?
Beta Hemolytic Streptococcus Group A (pyogenes)
98
In some people the structure of glomeruli _______
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
What is molecular mimicry sometimes curable with?
Corticosteroids
100
Explain Chronic Tonsillitis:
Tonsils are a good location for infection - enlargement of the palatine tonsils due to infectious inflammation (increased temperature and swelling)
101
Explain the process of infection in Chronic Tonsillitis:
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
What is Molecular Mimicry?
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
Where can Molecular Mimicry develop?
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
What is the treatment of Molecular Mimicry?
Corticosteroids - after a few weeks of Tx, the kids will recover 99% of the time, the adults will recover 50% of the time
105
What is the treatment of Acute Proliferative (poststreptococcal, postinfectious) Glomerulonephritis ?
Corticosteroids - after a few weeks of Tx, the kids will recover 99% of the time, the adults will recover 50% of the time
106
What are the signs of Acute Proliferative Glomerulonephritis (poststreptococcal, postinfectious) ?
- Swelling underneath the eyes (common with kidney problems)
- Hematuria - - Urine brown/red
- Hypertension
- Oliguria -> Azotemia (biochemical tests only)
- Edema -> Specifically underneath the eye
107
What would you think about young people in your office with swelling under their eyes?
You need to rule out kidney issues, these patients may have a Low serum complement level (hypocomplementemia) -> Typical for Type III hypersensitivity rxn
108
What does lab show on Acute Proliferative GMN aka Acute Poststreptococcal GMN aka Postinfectious GMN?
Low serum complement level (hypocomplementemia), elevated serum antistreptolysin O titers
109
What is the MOST DANGEROUS Nephritic syndrome?
Rapidly Progressive (crescentic ) Glomerulonephritis
110
Rapidly Progressive GMN aka
Crescentic GMN
111
What is Rapidly Progressive GMN characterized by?
Rapid and progressive loss of renal function associated with severe oliguria and (if untreated) death from renal failure within weeks to months
112
What does the prognosis depend on in Rapidly Progressive (crescentic) GMN?
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
What is the main symptom of Rapidly Progressive (crescentic) Glomerulonephritis ?
Hyperplasia of parietal epithelial cells of Bowman’s capsule
114
What is Hyperplasia of parietal epithelial cells of Bowman’s capsule?
Increased production of cells can result in narrowing or closure of the tubules -> accumulation of urine -> increased hydrostatic pressure -> pressure atrophy
115
Where is Secondary Glomerulonephritis developed ?
Not developed in the kidney primarily
116
What are the 3 types of Rapidly Progressive GMN aka Crescentic GMN?
1) Type 1: Anti-GBM
2) Type 2: Immune Complex - Mediated Deposition
3) Type 3: Pauci-Immune
117
What is Type I of Rapidly Progressive GMN aka Crescentic GMN?
Anti-GBM
118
Type I (anti-GBM) of Rapidly Progressive GMN definition:
Development of Aggression against the basement membrane
119
What type of Hypersensitivity Reaction is Type I (anti-GBM)?
Type II Hypersensitivity
120
What are the 2 kinds of diseases in Type 1 Anti-GBM?
1) Idiopathic (>50%)
| 2) Goodpasture’s Syndrome
121
What is Goodpasture’s Syndrome characterized by?
Development of autoimmune aggression against lung and kidney basement membranes (against glomeruli and alveoli)
- antibodies against alveolar and glomerular basement membranes
122
What is happening to the alveoli in Goodpasture’s Syndrome?
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
Plasmapheresis is associated with _____
Goodpasture’s Syndrome
124
What is used to treat Goodpasture’s Syndrome, how does it work?
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
Antibodies in Goodpasture’s syndrome forms against what membranes?
1) Alveolar Basement Membrane
| 2) Glomerular Basement Membrane
126
Alveolar Basement membrane (good pasture’s syndrome) is associated with what symptom?
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
Glomerular Basement Membrane (associated with Goodpasture’s Syndrome) :
Destruction of tissue around the membranes (crescents) -> glomerular tissue dies & replaced by CT (not functional)
128
What type of Hypersensitivity reaction is Type II (Immune Complex-Mediated Deposition / Diseases) ?
Idiopathic 50%
Type III Hypersensitivity
129
What 2 diseases are associated with Type 2: Immune Complex Mediated Deposition?
1) Systemic Lupus Erythematosus (SLE)
| 2) Henoch - Schonlein Purpura aka Hemorrhagic VASCULITIS
130
What is Systemic Lupus Erythematosus?
Classic aggressive autoimmune disease that involves young ladies (20s), more common in African Americans
131
What is the MOST COMMON cause of Systemic Lupus Erythematosus (SLE) ?
Ultraviolet radiation MC***
- Sulfosalicylic drugs
- Vaccination
132
What is Systemic Lupus Erythematosus characterized by?
Aggressive autoimmune reaction against antigens of the cell nucleus and cytoplasm (any cell in the body can be affected)
133
What are the Tests for Systemic Lupus Erythematosus?
- Antinuclear antibodies (ANA) - - ANA against double stranded DNA and ANA against Smith - antigen (anti-Sm-antibodies); pathoneumonic finding
134
What does SLE mostly involve?
Unusual arthritis, the skin, lungs, kidney, and cerebral vessels - - results in serious hypertension and possibly stroke
- Survival rate has gone from 50 - 85%
135
What is the primary manifestation of SLE?
Butterfly like skin rash/dermatitis
- Also includes Alopecia
136
SLE with kidney involvement =
Lupus Nephritis
137
What does Lupus Nephritis involve?
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
What is also possible with Lupus Nephritis?
VASCULITIS of cerebral vessels -> cerebral VASCULITIS = death
139
What is the survival rate of Lupus Nephritis?
85-90% (was 50%)
140
What is the treatment for Lupus Nephritis?
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
Henoch-Schonlein Purpura aka
Hemorrhagic VASCULITIS
142
Where does Henoch-Schonlein Purpura aka Hemorrhagic VASCULITIS develop?
In late adolescent males
143
What are the 4 manifestations of Henoch-Schonlein Purpura aka Hemorrhagic VASCULITIS?
1) Articular
2) Abdominal
3) Skin
4) Kidney
144
What is Articular Syndrome of Henoch-Schonlein Purpura ?
Characterized by sub clinical arthritis or joint pain (arthralgia)
145
What is skin/Cutaneous Syndrome of Henoch-Schonlein Purpura?
Development of Purpura (subcutaneous hemorrhage < 2cm) rash - in the buttock and abdomen
146
What is Abdominal Syndrome associated with Henoch-Schonlein Purpura?
Hemorrhagic inflammation of stomach and duodenal walls (gastroduodenitis)
147
What is Kidney syndrome associated with Henoch-Schonlein Purpura?
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
What happens with IgA in Henoch Schonlein Purpura?
IgA deposition in the Mesangium (part of IgA nephropathy)
149
Type 3 of Rapidly Progressive GMN aka Crescentic GMN =
Pauci Immune
150
What are the diseases associated with Pauci Immune?
- Wegener’s Granulomatosis
- Polyarteritis Nodosa
- IgA Nephropathy aka Berger’s Disease
- Alport Syndrome
151
What Hypersensitivity is Type 3 Pauci - Immune related to?
It is NOT related to a specific type of hypersensitivity
152
What is Type III (Pauci Immune) characterized by?
The development of VASCULITIS (MOST DANGEROUS!!)
153
What is the pathogenesis of Type III Pauci Immune?
Very autoimmune disease
154
What are a major sign of VASCULITIS in Type III (pauci immune)?
Antineutrophil ctoplasmic autoantibodies (found in the peripheral blood)
155
T/F, more than 50% of Type III (Pauci Immune) is Idiopathic?
TRUE
156
What is Wegener’s Granulomatosis?
Very aggressive disease, autoimmune pathology (rare)
157
What are the 3 clinical symptoms of Wegener’s Granulomatosis?
1) Necrotizing VASCULITIS of upper respiratory tract
2) Necrotizing VASCULITIS of lower respiratory tract
3) Rapidly progressive GMN
158
What are the symptoms of Necrotizing VASCULITIS of upper respiratory tract?
- 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
WHat are the symptoms of Necrotizing VASCULITIS of Lower respiratory tract?
Results in cavitation of the lungs
- Dissolution / destruction of tissue
160
What are the symptoms of Rapidly progressive GMN?
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
What is Polyarteritis Nodosa?
Characterized by VASCULITIS of the vessels throughout the body -> the involvement of middle and small sized arteries with bulging/pouching of their walls
162
T/f Polyarteritis (periarteritis) Nodosa is idiopathic?
TRUE
163
Is Polyarteritis (periarteritis) Nodosa more common in young than old?
More common in young
164
What organ/tissue is involved in Polyarteritis/Periarteritis Nodosa ?
Any organ/tissue can be involved in this disease
***** NO INVOLVEMENT OF LUNGS OR ARCH OF AORTA
165
Nodosa =
Pouching of the walls
166
What can node formation lead to in Polyarteritis (Periarteritis) Nodosa?
Node formation can lead to ischemia
- Associated with compression of adjacent vessels, by the nodes
167
How does pouching occur in Polyarteritis (Periarteritis) Nodosa?
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
What is VASCULITIS ?
- Inflammation of vascular wall -> spreads into the lumen of the vessel -> Ischemia -> Infarction
169
Wet Gangrene is associated with what Type 3 Pauci Immune disease?
Polyarteritis Nodosa aka Periarteritis Nodosa
170
What organ is most commonly involved in Polyarteritis Nodosa aka Periarteritis Nodosa?
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
In Polyarteritis Nodosa, The Kidney has what major symptom?
Rapidly Progressing GMN
- CT in the kidney (repair) shrinks the kidney = see CRESCENTS
172
IgA Nephropathy aka
Berger’s Disease
173
What is the MC disease worldwide?
IgA nephropathy
