Stupid Charts Flashcards by Jessica Carson

Q

A.

A

Joint instability

conformation abnormality

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Q

B.

A

chronic irritation to joint capsule

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Q

C.

A

chronic synovitis (pmns, leukocytes, macrophages, synoviocytes)

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Q

D.

A

increased chemical mediators: IL1, PG, NO, TNF-alpha

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Q

E.

A

villous hyperplasia, joint capsule fibrosis, periarticular osteophytes

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Q

F.

A

increased wear on cartilage

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Q

G.

A

Chondrocyte clones

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Q

H.

A

chondrocyte degeneration/necrosis and chondromalacia (fibrillation and thinning of articular cartilage)

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Q

I.

A

decreased squeeze film lubrication

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Q

J.

A

deterioration of synovial fluid

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Q

K.

A

decreased boundary lubrication and nutrition by synovial fluid

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Q

L.

A

decreased matrix production, increased matrix breakdown

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Q

M.

A

increased subchondrial bone compression

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Q

N.

A

subchondral hyperostosis

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Q

A.

A

Chronic antigenemia (ex. Persistent viral infection)

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Q

B.

A

Ag on subepithelial side of GBM due to 1. size, 2. shape, 3, charge

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Q

C.

A

Ab production

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Q

D.

A

In situ formation of Ag-Ab complexes

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Q

E.

A

C’ - membrane attack complex

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Q

F.

A

damage to podocyte foot processes causing retraction

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Q

G.

A

filtration apparatus breakdown leading to albumin leaking

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Q

H.

A

proteinuria (albuminuria)

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Q

I.

A

hypoproteinemia (hypoalbuminemia)

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Q

J.

A

decrease POPP leading to adema and ascites

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K.

increase in lipoprotein production by liver causing hypercholesterolemia

L.

nephrotic syndrome

M.

thickening of GBM

N.

glomerulosclerosis

O.

loss of nephrons

P.

CRF

A.

Nephrotoxin

B.

Kills PCT epithelium in most nephrons at the same time

C.

1. necrotic segment leaks 2. nephron occluded by debris 3. decreased local glomerular blood flow

D.

decreased SNGFR in effected nephrons

E.

decreased TGFR

F.

1. decrease in urine production causing anuria 2. increase in retention of metabolic wastes (BUN, creatinine, K, and others)

G.

bradycardia, vomiting, Malaise

H.

Metabolic acidosis: decreased NH3 production, decreased H excretion, decreased HCO3 production

A.

loss of nephrons over time

B.

hypertrophy of viable nephrons (supernephrons)

C.

increased SNGFR

D.

increased flow rate (20x) solute overload decreased solute resorption

E.

decreased medullary osmolality impaired counter current multiplier

F.

filtrate not modified

G.

large volume of unconcentrated urine (polyuria and isosthenuria)

H.

dehydration to polydispia

I.

fibrosis

J.

decreased TGFR

K.

Overperfusion injury/ glomerulosclerosis

L.

1. azotemia (increased BUN, creatinine) 2. hyperphosphatemia 3. accumulation of uremic toxins

M.

vascular injury

N.

oral ammonia production via urea splitting oral bacteria

O.

oral/GI mucosal ulcers

P.

decreased erythropoietin leading to nonregenerative anemia

Q.

Ca-P complex/precipitation soft tissue mineralization decreased Ca and Vitamin D3

R.

Secondary renal hyperparathyroidism leading to fibrous osteodystrophy

A.

failure of passive transfer

B.

umbilical infection (+/- omphalophlebitis)

C.

bacteremia

D.

localization in metaphyseal vessels: capillary loops and marginal defense mechanisms

E.

fibrinopurulent and necrotizing inflammation in metaphysis

F.

extension into physis, +/- epiphysis

G.

chondronecrosis and destruction of physis

H.

chemical mediators: IL1, IL6, PG, TNFalpha

I.

increased local osteoclastic bone resorption

J.

radiographic bone lysis

K.

osteonecrosis

L.

sequestrum formation