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Pathology Pre-Midterm > Module 2-Path > Flashcards

Module 2-Path Flashcards

1
Q

What is an amyloid?

A

Extracellular protein deposits found most commonly in the kidney

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2
Q

What is the pathogenesis of amyloidosis?

A

Protein misfolding for AL amyloidosis

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3
Q

In amyloidosis the organ is initially enlarged but then what happens?

A

Atrophies

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4
Q

What does localized amyloidosis mean?

A

Affects one organ

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5
Q

What are the individual organs that localized amyloidosis affects?

A
  1. Kidneys: affected kidney turns brown with iodine stain –> proteinurina, enlargement and failure
  2. Senile Cardiac Amyloidosis and Familial Amyloidotic Neuropathies –> Transthretin
  3. Liver: deposits in Space of Disse (hepatomegaly)
  4. Alzheimers –> Beta2 Amyloid, Beta Amyloid or ABeta (you also see TAU proteins but these are intracellular)
  5. Spleen –> white pulp (sago spleen, see tapioca like granules); sinusoids/red pulp (lardaceous spleen) –> splenomegaly (s
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6
Q

What are some examples of systemic amyloidosis?

A

Systemic: affects multiple organs

  • Multiple Myeloma -> w/Bence Jones Proteins –> AL amyloid
  • Chronic Inflammatory Conditions -> Crohns, Ulcerative Colitis, TB, Osteomyelitis, RA) –> AA amyloid
  • -Dialysis patients form B-2 microglobulin
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7
Q

what is the difference between AL and AA amyloid?

A 
AL amyloid (amyloid light chains): composed of immunoglobin light chains 
AA amyloid (amyloid associated): composed of non immunoglobin protein derived from SAA (Serum-amyloid associated protein) 
these are usually always chronic inflammatory diseases
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8
Q

Is AL or AA associated with primary amyloidosis?

A

Immunocyte dyscrasias is primary amyloidosis

deposition of AL in extracellular spaces throughout the body

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9
Q

Is AL or AA associated with secondary amyloidosis?

A

Reactive systemic amyloidosis aka secondary amylodiosis
deposition of AA protein in extracellular space
associated with chronic inflammation
secondary condition to autoimmune and neoplasmas

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10
Q

How does amyloidosis of the kidney present?

A

Generalized edema due to loss of proteins –> Nephrotic syndrome (in the kidney most common)

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11
Q

How does amyloidosis of the heart present?

A

Usually deposits into the myocardium so you get arrhythmias

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12
Q

What are the various stains for amyloidosis?

A

EM: non branching fibrils (beta pleated sheets) and non branching component made up of alpha 1 glycoprotein
H and E stain: amorphous, glassy pink (hyline), extracellular protein
Congo Red: salmon pink/red if this is subject to polarized light looks like apple green birefringement

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13
Q

Dystrophic calcification involves what kind of tissues?

A

Dead or dying tissues due to injury

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14
Q

Where is dystrophic calcification commonly seen?

A

Atherosclerotic plaques, enzymatic fat necrosis, damaged cardiac valves, mercury poisoning, congenital CMV, aging (degenerative with wear and tear) and Rheumatic Fever

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15
Q

What is the presentation of dystrophic calcification ?

A

Aortic stenosis, repeated syncope, SOB, CHF and murmur

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16
Q

What are the calcium levels for dystrophic calcification?

A

Ca2+ levels are normal

exception is fat necrosis of pancreas = hypocalcemia

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17
Q

What is the H and E stain for dystrophic calcification?

A

Ca2+ stains deep blue (Basophilic)

18
Q

Where is another common site for dystrophic calcification?

A

Breast, indicative of breast cancer

19
Q

In the picture for aortic stenosis, the area of necrosis is due to what?

A

Initial intracellular Ca comes from mitochondria of dying or dead cells = initiating factor for extracellular accumulation of Ca phosphate
Collagen enhances crystallization rate

20
Q

How does the calcium appear in aortic stenosis?

A

Salts seen as white granules/clumps/gritty deposits

21
Q

In metastatic calcification, Ca2+ levels are what?

A

Elevated in normal tissues

22
Q

What are the four main causes for metastatic calcification?

A
  1. Primary hyperparathyroidism: Increased PTH –> bone reabsorption, hydroxylation of Vit D & reabsorption of calcium in renal tubule with the excretion of phosphates
  2. Sarcoidoisis: non-caseating granuloma; activates vitamin D precursors which increases renal and intestinal absorption of Ca2+ as well as bone reabsorption
  3. Chronic Renal Failure
  4. Vitamin D intoxication
23
Q

What is the main etiology or cause of acute gout?

A

Idiopathic

24
Q

What are some pre-disposing factors for gout?

A 
Obesity
Red Wine 
Red Meat 
Alcohol 
Lesch Nyhan (HGPRT deficiency) 
Thiazides
25
Q

Does hyperuricemia (High uric acid levels) always lead to gout?

A

Does not always lead to gout, but to get gout, you have to have high uric acid levels

26
Q

Primary gout includes 90% and Secondary causes of gout includes 10%. Name some primary and secondary causes?

A

Primary –> unknown enzyme defect; HGPRT deficiency

Secondary –> Increased Na turnover, chronic renal disease and inborn errors of metabolism

27
Q

What is the pathogenesis for acute gout?

A

Macrophages engulf uric acid crystals –> complement activation –> bring in neutrophils via secretion of IL-8 (then signs of inflammation)

28
Q

For acute gout is there edema usually?

A

Edematous soft tissue with acute inflammatory infiltrate

29
Q

What is the best investigation for gout?

A

Joint Aspiration/atherocentesis

30
Q

What is the most common location for gout?

A

1st metatarsal joint of the big toe

31
Q

What pathway is defective in Gout?

A

Disorder of purine metabolism

Increased uric acid levels due to overproduction or reduced excretion or both

32
Q

What are the crystals seen in gout?

A

Monosodium Urate Crystals
Negatively Birefringment (yellow)
Needle shaped crystals

33
Q

In regards to pseudogout (chondrocalcinosis), what are some characteristics?

A

Calcium Pyrophosphate Crystals
Loves the knee
Positive Birefringement (blue crystals)
Rhomboid crystals

34
Q

Is Chronic Gout (or tophous gout) painful?

A

Nope just lost of function
No bradykinin, no pain
No pain normally but every chronic inflammation can have an episode of acute on chronic inflammation which causes pain

35
Q

Is there swelling with chronic gout?

A

Nope

No histamine –> no swelling or redness

36
Q

Takes about how long for chronic gout to develop?

A

about 20 years

37
Q

In chronic gout you will see foreign body granuloma (With foreign body giant cells), explain the process

A

Just like for any chronic inflammation

Fibroblasts deposit collagen –> joint becomes fibrosed –> decreased ROM

38
Q

Chronic gout involves granulation tissue so what hypersensitivity is it?

A

type IV

39
Q

A classic symptom of chronic gout is Tophaceous deposits in soft tissues, which common soft tissues?

A

ear, nose cartilage and skin of fingertips

40
Q

What are some complications of chronic gout?

A

Joint destruction and other complication is renal failure (tubules get damaged by uric acid crystals) and kidney stones

Pathology Pre-Midterm (35 decks)

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