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Flashcards in Path 2 first quiz Deck (50):
1

functions of the kidney

Blood pHwater and salt concentrationwaste eliminationhormones

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hormones of the kidney

Renin-BPerythropoeitin prostaglandings

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prostaglandins

precursors for hormones

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forms RBCs

erythropoietin

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four compartments

glomeruli-filtration of blood:Renin-BPtubules-collection systemInterstitial tissuesVessels of the kidney

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glomular pathology

usually immunological

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pathology of the tubules

due to bacterial toxins

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pseudo fenstration

holes in endothelial tissue that filter blood

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between 2 _____ are filtration slits and they are important for the formation of _____

podocyte, urine

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Mesangial cells are a type of _____ cell that occupies space within the ______

stromal, glomeruli

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this cell can replicate, fight infection, and become sclerotic if there is excess proliferation

mesangial cells

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antibody-antigen complex attaches to the wall of vessels. deposited between basement membrane and endothelial cells

circulating immune complex deposition

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subentimal layer

between basement membrane and endothelial cells

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circulating immune complex deposition is a type ___ hypersensitivity

III

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prevents normal filtration of the blood due to

circulating immune complex deposition

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Heymann's glomerular nephritis is not a _____ reaction

hypersensitivity

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Anti-GBM glomerulonephritis

Type 2 hypersensitivity-destroys podocytes

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are very permeable to water, but impermeable to blood cells, proteins, albumins

Glomeruli

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for unknown reasons, the glomeruli is damaged and there is increasedpermeability of RBC's and decreased permeability of water.

In nephritic syndrome

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blood in the urine, with red blood casts

Hematuria

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(limited or diminished amount of urine produced)

Oliguria

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production of renin is the first step in a cascade. The end product is the formation of AngiotensinII, which leads to the____ in the blood pressure.

increase

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elevated blood levels ofblood urea nitrogen AKA: BUN and creatinine which is closely related to reduced glomerularfiltration rate

azotemia

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antibodies of streptococcus is produced and the antibodies can alsodestroy the glomerular wall

Acute Proliferative Glomerulonephritis

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Some viral infections (measles, etc) in children may also result in this condition. It is curablewith corticosteroids

Acute Proliferative Glomerulonephritis

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50% of cases of this in the adult is transferredinto chronic glomerularnephritis and only 1% in children

Acute Proliferative Glomerulonephritis

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swelling underneath the eyes – common with

kidney problem

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MOST DANGEROUS. it is a complex ofdisorders (not a disease) characterized by rapid and progressive kidney pathology (oligouria) anddeath within weeks or months.

Rapidly Progressive (Crescentic) Glomerulonephritis

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glomeruli will become crescent shaped and obstruct the lumen of the proximal convolutedtubule and urine will build up inside the kidney and increase hydrostatic pressure within theglomerular basement membrane. This prevents circulation of the blood. (the prognosis of thedisease is based in the amount of crescent cells – 80% or more is fatal)

Rapidly Progressive (Crescentic) Glomerulonephritis

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idiopathic more than 50%

Type I- (Anti-GBM)- ( type IIhypersensitivity reaction)

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characterized by development ofautoimmune aggression against two basement membranes. The Abs will form againstAgs of the membranes. (lungs and kidney)

Good pasture’s syndrome (anti-GCM)

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This is curable, via plasmapheresis

Good pasture’s syndrome

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if there is protein in the urine =

PATHOLOGY

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development of aggression against the basement membrane ( type IIhypersensitivity reaction)

Type I- (Anti-GBM)

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it is associated with Type III hypersensitivityreactions.

Type II- (Immune Complex Deposition)

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Systemic lupus erythematosus is associated with

Type II- (Immune Complex Deposition)

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classic autoimmune disease that involves young ladies– 20s. It is more common in African Americans

Systemic lupus erythematosus

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Causes – UV radiation, intake ofsulfasalysitic drugs, vaccination

Systemic lupus erythematosus

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It mostly involves the skin, lungs, kidneyand cerebral vessels. Results in serious hypertension and possibly stroke. Primarymanifestation of systemic lupus is the butterfly rash. Lupus Nephritis – involvement ofthe kidneys, develops quickly. This is the major cause of death in this disease. Vasculitisof cerebral vessels is possible in SLE

Systemic lupus erythematosus

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● survival is 90% at the present time● TMT – corticosteroid therapy

Systemic lupus erythematosus

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characterized by the development of vasculitis. It is inflammation ofthe vascular wall. MOST DANGEROUS. Manifested by anti-neutrophil plasmocyticauto-antibodies. This tells us there is an autoimmune disorder that results in vasculitis.

Type III - (Pauci-immune)

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develops in middle aged males (can be women in olderage). It is characterized by necrotizing vasculitis of the upper and lower respiratory tractand rapidly progressing of glomerulonephritis (kidneys). You see a melting of the bonesof the face which can lead to infection and supperative inflammation. The patient isundergoing decay. Patient will die due to acute renal failure, or secondarycomplications.

Wegener's Granulematosus

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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 theaorta . INCURABLE. NETTER PICTURE

Polyarteritis (Periarteritis) Nodosa

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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 theimmune 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)

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Type III - (Pauci-immune)

Wegener's GranulematosusPolyarteritis (Periarteritis) NodosaIgA Nephropathy (Berger’s Disease)

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Henoch-Schonlein Purpura (hemorrhagic vasculitis)- usually develops in boys in their 20's. It is characterized by four clinical syndromes:

abdominal syndromecutaneous syndromearticular syndromecrescentic glomerulonephritis

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abdominal syndrome

it is characterized by hemorrhagic inflammation ofthe stomach and duodedenal walls (gastroduodenitis).

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cutaneous syndrome

subcutaneous hemorrhages in the buttock andabdomen – leads to the development of purpura rash

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articular syndrome

characterized by subclinical arthritis or at least painin the joints.

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crescentic glomerulonephritis

if the patient has the first threesyndromes - and if you add crescatic glomerular nephritis makes theprognosis much worse – 70%.