Path 2 first quiz Flashcards
functions of the kidney
Blood pH
water and salt concentration
waste elimination
hormones
hormones of the kidney
Renin-BP
erythropoeitin
prostaglandings
prostaglandins
precursors for hormones
forms RBCs
erythropoietin
four compartments
glomeruli-filtration of blood:Renin-BP
tubules-collection system
Interstitial tissues
Vessels of the kidney
glomular pathology
usually immunological
pathology of the tubules
due to bacterial toxins
pseudo fenstration
holes in endothelial tissue that filter blood
between 2 _____ are filtration slits and they are important for the formation of _____
podocyte, urine
Mesangial cells are a type of _____ cell that occupies space within the ______
stromal, glomeruli
this cell can replicate, fight infection, and become sclerotic if there is excess proliferation
mesangial cells
antibody-antigen complex attaches to the wall of vessels. deposited between basement membrane and endothelial cells
circulating immune complex deposition
subentimal layer
between basement membrane and endothelial cells
circulating immune complex deposition is a type ___ hypersensitivity
III
prevents normal filtration of the blood due to
circulating immune complex deposition
Heymann’s glomerular nephritis is not a _____ reaction
hypersensitivity
Anti-GBM glomerulonephritis
Type 2 hypersensitivity-destroys podocytes
are very permeable to water, but impermeable to blood cells, proteins, albumins
Glomeruli
for unknown reasons, the glomeruli is damaged and there is increased
permeability of RBC’s and decreased permeability of water.
In nephritic syndrome
blood in the urine, with red blood casts
Hematuria
(limited or diminished amount of urine produced)
Oliguria
production of renin is the first step in a cascade. The end product is the formation of Angiotensin
II, which leads to the____ in the blood pressure.
increase
elevated blood levels of
blood urea nitrogen AKA: BUN and creatinine which is closely related to reduced glomerular
filtration rate
azotemia
antibodies of streptococcus is produced and the antibodies can also
destroy the glomerular wall
Acute Proliferative Glomerulonephritis
Some viral infections (measles, etc) in children may also result in this condition. It is curable
with corticosteroids
Acute Proliferative Glomerulonephritis
50% of cases of this in the adult is transferred
into chronic glomerularnephritis and only 1% in children
Acute Proliferative Glomerulonephritis
swelling underneath the eyes – common with
kidney problem
MOST DANGEROUS. it is a complex of
disorders (not a disease) characterized by rapid and progressive kidney pathology (oligouria) and
death within weeks or months.
Rapidly Progressive (Crescentic) Glomerulonephritis
glomeruli will become crescent shaped and obstruct the lumen of the proximal convoluted
tubule and urine will build up inside the kidney and increase hydrostatic pressure within the
glomerular basement membrane. This prevents circulation of the blood. (the prognosis of the
disease is based in the amount of crescent cells – 80% or more is fatal)
Rapidly Progressive (Crescentic) Glomerulonephritis
idiopathic more than 50%
Type I- (Anti-GBM)- ( type II
hypersensitivity reaction)
characterized by development of
autoimmune aggression against two basement membranes. The Abs will form against
Ags of the membranes. (lungs and kidney)
Good pasture’s syndrome (anti-GCM)
This is curable, via plasmapheresis
Good pasture’s syndrome
if there is protein in the urine =
PATHOLOGY
development of aggression against the basement membrane ( type II
hypersensitivity reaction)
Type I- (Anti-GBM)
it is associated with Type III hypersensitivity
reactions.
Type II- (Immune Complex Deposition)
Systemic lupus erythematosus is associated with
Type II- (Immune Complex Deposition)
classic autoimmune disease that involves young ladies
– 20s. It is more common in African Americans
Systemic lupus erythematosus
Causes – UV radiation, intake of
sulfasalysitic drugs, vaccination
Systemic lupus erythematosus
It mostly involves the skin, lungs, kidney
and cerebral vessels. Results in serious hypertension and possibly stroke. Primary
manifestation of systemic lupus is the butterfly rash. Lupus Nephritis – involvement of
the kidneys, develops quickly. This is the major cause of death in this disease. Vasculitis
of cerebral vessels is possible in SLE
Systemic lupus erythematosus
● survival is 90% at the present time
● TMT – corticosteroid therapy
Systemic lupus erythematosus
characterized by the development of vasculitis. It is inflammation of
the vascular wall. MOST DANGEROUS. Manifested by anti-neutrophil plasmocytic
auto-antibodies. This tells us there is an autoimmune disorder that results in vasculitis.
Type III - (Pauci-immune)
develops in middle aged males (can be women in older
age). It is characterized by necrotizing vasculitis of the upper and lower respiratory tract
and rapidly progressing of glomerulonephritis (kidneys). You see a melting of the bones
of the face which can lead to infection and supperative inflammation. The patient is
undergoing decay. Patient will die due to acute renal failure, or secondary
complications.
Wegener’s Granulematosus
characterized by vasculitis of the vessels throughout the body (middle and small sized arteries). With the pouching of the arteriole wall,
which gives it the name nodosa. Because of the inflammation causes weakness of the wall and pouching. The pouching of the walls can lead to rupture of the wall and obstruction of the lumen. These nodes are on every organ of the body and causes death. This disease can manifest in any organ except the lungs and the arch of the
aorta . INCURABLE. NETTER PICTURE
Polyarteritis (Periarteritis) Nodosa
Hematuria following an acute respiratory infection. Many cases month after month. Could also be caused by an acute intestinal or urinary infection. The patient will experience pain in the loin (lumbar spine). One of the most common diseases associated with gross hematuria. MOST COMMON glomerular disease worldwide. Hallmark is the deposition of IgA immune complexes into the
immune mesagium. (50% increase in IgA). There will also be increased concentration of IgA in the blood and IgA immune complexes in the blood. Can manifest with Henoch-Schonlein Purpura. If not controlled can switch to chronic glomerulonephritis.
IgA Nephropathy (Berger’s Disease)
Type III - (Pauci-immune)
Wegener's Granulematosus Polyarteritis (Periarteritis) Nodosa IgA Nephropathy (Berger’s Disease)
Henoch-Schonlein Purpura (hemorrhagic vasculitis)- usually develops in boys in their 20’s. It is characterized by four clinical syndromes:
abdominal syndrome
cutaneous syndrome
articular syndrome
crescentic glomerulonephritis
abdominal syndrome
it is characterized by hemorrhagic inflammation of
the stomach and duodedenal walls (gastroduodenitis).
cutaneous syndrome
subcutaneous hemorrhages in the buttock and
abdomen – leads to the development of purpura rash
articular syndrome
characterized by subclinical arthritis or at least pain
in the joints.
crescentic glomerulonephritis
if the patient has the first three
syndromes - and if you add crescatic glomerular nephritis makes the
prognosis much worse – 70%.
