Stupid Charts Flashcards by Jessica Carson

Q

A.

A

Joint instability

conformation abnormality

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

B.

A

chronic irritation to joint capsule

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

C.

A

chronic synovitis (pmns, leukocytes, macrophages, synoviocytes)

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

D.

A

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

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

E.

A

villous hyperplasia, joint capsule fibrosis, periarticular osteophytes

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

F.

A

increased wear on cartilage

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

G.

A

Chondrocyte clones

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

H.

A

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

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

I.

A

decreased squeeze film lubrication

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

J.

A

deterioration of synovial fluid

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

K.

A

decreased boundary lubrication and nutrition by synovial fluid

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

L.

A

decreased matrix production, increased matrix breakdown

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

M.

A

increased subchondrial bone compression

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

N.

A

subchondral hyperostosis

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

A.

A

Chronic antigenemia (ex. Persistent viral infection)

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

B.

A

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

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

C.

A

Ab production

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

D.

A

In situ formation of Ag-Ab complexes

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

E.

A

C’ - membrane attack complex

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

F.

A

damage to podocyte foot processes causing retraction

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

G.

A

filtration apparatus breakdown leading to albumin leaking

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

H.

A

proteinuria (albuminuria)

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

I.

A

hypoproteinemia (hypoalbuminemia)

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

J.

A

decrease POPP leading to adema and ascites

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

K.

A

increase in lipoprotein production by liver causing hypercholesterolemia

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

L.

A

nephrotic syndrome

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

M.

A

thickening of GBM

How well did you know this?

1

Not at all

2

3

4

5

Perfectly

Q

N.

A

glomerulosclerosis

Q

O.

A

loss of nephrons

Q

P.

A

CRF

Q

A.

A

Nephrotoxin

Q

B.

A

Kills PCT epithelium in most nephrons at the same time

Q

C.

A

necrotic segment leaks
nephron occluded by debris
decreased local glomerular blood flow

Q

D.

A

decreased SNGFR in effected nephrons

Q

E.

A

decreased TGFR

Q

F.

A

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

Q

G.

A

bradycardia, vomiting, Malaise

Q

H.

A

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

Q

A.

A

loss of nephrons over time

Q

B.

A

hypertrophy of viable nephrons (supernephrons)

Q

C.

A

increased SNGFR

Q

D.

A

increased flow rate (20x)

solute overload

decreased solute resorption

Q

E.

A

decreased medullary osmolality

impaired counter current multiplier

Q

F.

A

filtrate not modified

Q

G.

A

large volume of unconcentrated urine (polyuria and isosthenuria)

Q

H.

A

dehydration to polydispia

Q

I.

A

fibrosis

Q

J.

A

decreased TGFR

Q

K.

A

Overperfusion injury/ glomerulosclerosis

Q

L.

A

azotemia (increased BUN, creatinine)
hyperphosphatemia
accumulation of uremic toxins

Q

M.

A

vascular injury

Q

N.

A

oral ammonia production via urea splitting oral bacteria

Q

O.

A

oral/GI mucosal ulcers

Q

P.

A

decreased erythropoietin leading to nonregenerative anemia

Q

Q.

A

Ca-P complex/precipitation

soft tissue mineralization

decreased Ca and Vitamin D3

Q

R.

A

Secondary renal hyperparathyroidism leading to fibrous osteodystrophy

Q

A.

A

failure of passive transfer

Q

B.

A

umbilical infection (+/- omphalophlebitis)

Q

C.

A

bacteremia

Q

D.

A

localization in metaphyseal vessels: capillary loops and marginal defense mechanisms

Q

E.

A

fibrinopurulent and necrotizing inflammation in metaphysis

Q

F.

A

extension into physis, +/- epiphysis

Q

G.

A

chondronecrosis and destruction of physis

Q

H.

A

chemical mediators: IL1, IL6, PG, TNFalpha

Q

I.

A

increased local osteoclastic bone resorption

Q

J.

A

radiographic bone lysis

Q

K.

A

osteonecrosis

Q

L.

A

sequestrum formation