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Flashcards in PATH Lab Exam 1 Deck (58):
1

Where do osteocytes come from? 
 

Once an osteoblast becomes surrounded by matrix, it becomes an osteocyte.

2

 From what cell is the osteoclast derived? 
 

It is derived from a monocyte precursor cell located in the hematopoietic marrow.

3

 Why are vertebrae preferentially affected in osteoporosis? 

 

Loss of bone is most rapid from trabecular bone. Vertebrae have a prominent trabecular component.

4

How does estrogen serve to maintain bone mass? 

Estrogen may maintain bone mass by inhibiting the release of cytokines that stimulate bone resorption (IL-1, TNF) while upregulating the synthesis of other cytokines (TGF-beta) involved in bone formation.

5

 response of bone to fracture

 Osteoblasts arise from pluripotent progenitor cells in the periosteum and granulation tissue. They produce woven bone, resulting in a bony callus that stabilizes the fracture site.

6

What is the significance of the empty lacunae at the ends of the trabecular bone? 

The empty lacunae indicate that the bone is necrotic.

7

Which organ is the preferential site for metastases in patients with osteosarcoma? 
 

The lungs.

8

production of osteoid matrix by the tumor cells

osteosarcomas

9

multiple cells can be found within a single lacuna

Chondrosarcoma

10

 At what age do patients develop chondrosarcoma, and which anatomic sites in the skeleton are affected? 

 

Patients with chondrosarcoma are older than those with primary osteosarcoma; the mean age for chondrosarcoma is 43 years. The most frequent locations are in the pelvis, proximal femur, ribs, sternum, and the shoulder girdle. It is the most common malignant tumor of the scapula and sternum. 

11

What are the most common age and sex of a patient with giant cell tumor of bone? 
 

Giant cell tumors usually arise between the age 25-45, and there is a slight female predominance.

12

Prostatic adenocarcinoma produces __________ foci in the skeleton.

osteoblastic

13

 How does the distribution of affected joints in the RA hand differ from that seen in degenerative joint disease? 

The lesions of degenerative joint disease in the hand are found in the distal interphalangeal joints, are bony, and are not symmetrical.

14

How are joints destroyed in RA?

  • In RA, there is diffuse narrowing of the joint space.
  • The cartilage is destroyed by the release of IL-1 and TNF, which depresses the synthesis of proteoglycans, and by proteases released from neutrophils.
  • As well, proliferation of the synovial membrane leads to pannus formation, which isolates the cartilage from the synovial fluid, its source of nutrients. The severe, extensive damage of RA often leads to ankylosis.
  •  In chronic RA, the periarticular bone is osteoporotic, a change secondary to disuse of the affected limbs, to the stimulation of osteoclasts by corticosteroid therapy, or to the release of RANK-L by activated lymphocytes in the synovium.

15

Which class of lymphocytes predominates in the inflammatory infiltrate in RA?

  • T cells play the pivotal role accounts for the inflammation and joint destruction.
    • CD4+ cells accumulate in affected joints, where they stimulate monocyte-macrophages to release cytokines and recruit B cells, which produce the autoantibody rheumatoid factor.
    • During active inflammation, the synovial tissue generates a plethora of cytokines/growth factors. It is now generally accepted that IL-1 and TNF are key mediators in the cytokine cascade.

16

 List two important histologic changes found in the synovial membrane in joints affected by rheumatoid arthritis. 
 

The synovium is proliferative and is infiltrated by numerous lymphocytes and plasma cells.

17

What is the pannus? 

The pannus consists of the inflamed, hyperplastic synovium that extends over the articular surface.

18

How does RANK-L contribute to the destruction of the joint? 

RANK-L is released from activated lymphocytes in the synovium, stimulating the proliferation of osteoclasts. Osteoclasts rapidly erode the subchondral bone.

19

Where do rheumatoid nodules typically develop? 
 

The nodules typically appear on the extensor surface of the forearm below the elbow, or at sites of local pressure, such as the Achilles tendon. Less commonly, they form in the lungs, spleen, myocardium, and heart valves. The subcutaneous nodules are firm, nontender, and round to oval.

20

 What is the common name of osteophytes that develop at the distal interphalangeal joints of women? 

These osteophytes are called Heberden nodes.

21

 What would be the characteristic feature of joint fluid aspirated from the joint affected with gout? 
 

The fluid would contain large numbers of neutrophils and long, needle-like, sodium urate crystals.

22

Besides joints, what other organ is affected in gout? 

In patients with chronic gout, the kidney can be severely damaged; approximately 20% of patients die of renal failure. Renal lesions are many: precipitation of urates in the medulla forms tophi; uric acid stones may form; and in some cases, there is acute renal failure due to precipitation of urates in the collecting tubes.

23

Which nonmelanocytic disorders of the skin can present as pigmented lesions?

Seborrheic keratoses are very common pigmented lesions, occuring most frequently in middle-aged and older individuals.    Basal cell carcinomas usually present as a pearly papule or nodule with dilated blood vessels (telangiectasias), but they can also occur as an ulcerated, an eczematous, or a pigmented lesion.  Vascular tumors (hemangioma, Kaposi sarcoma) often have a blue-brownish color.

24

What is the relation between this thickness and the prognosis?

The thickness of a melanoma, measured histologically between the granular layer of the epidermis and the deepest melanoma cell, is the most important factor that determines the prognosis of a melanoma. This thickness is called the Breslow thickness.

25

Function of langerhan cells

Dendritic cells, located in the upper layers of the epidermis. They take up antigenic signals and communicate this information to lymphocytes.

26

Describe the morphological differences between melanoma cells and cells of a nevocellular nevus. 
 

Nevus cells lack pleomorphism and mitotic figures and are usually considerably smaller than melanoma cells. Nucleoli are not visible in nevus cells, while melanoma cells often show prominent red nucleoli.

27

 Describe the sentinal node procedure. 
 

The patient is injected at the site of the scar of the malignant melanoma with a blue dye, a radioactive substance, or a combination of both. The sentinel node then absorbs the dye/radioactive substance. The lymph node turns blue and can be identified by color and/or the presence of radioactivity.

28

 What is the risk of developing a malignant melanoma in a dysplastic nevus? 

The risk of developing a malignant melanoma in an isolated dysplastic nevus is low.  However, in members of families prone to develop malignant melanomas, dysplastic nevi can transit into melanomas in a short period of time.

29

What is the diagnosis when a large amount of seborrheic keratosis occurs explosively? 

The occurrence of multiple seborrhoic keratoses over a short period of time is called the Leser-Trelat, a paraneoplastic syndrome, probably caused by the production of transforming growth factor-alpha by malignant cells.

30

Do the cells of a sebborrheic keratosis resemble the cells of an adnexal structure? 

The name seborrheic keratosis may suggest an origin from sebaceous glands, but this is not correct. The term seborrheic is due to the clinical appearance of the lesions. The cells of a seborrheic keratosis most resemble basal cells of the normal epidermis.

31

 What is the difference between real epithelial cysts and the so-called "horn" cysts of seborrheic keratoses? 
 

Epithelial cysts are lesions formed by invagination and cystic expansion of the epidermis or the epithelium forming a hair follicle. The cysts are lined by normal epidermal or follicular epithelium. There is no real epithelial proliferation. In seborrheic keratosis, an epithelial proliferation is present and the small cysts occur by invagination of the hyperkeratotic surface epithelium.

32

 What is the name of multiple, very small, epidermal inclusion cysts, usually occuring on the face of young persons? 

 

Multiple, small, epidermal inclusion cysts are called milia.

33

 Which histological type of epithelial cyst is this? 

This epithelial cyst lined by epithelium resembling normal epidermis and filled with keratin is an epidermal inclusion cyst.

34

Name three other histological types of epidermal cysts. 

  • Pilar or trichilemmal cysts are lined by epithelium resembling follicular epithelium and filled by a homogeneous mixture of keratin and lipids.
  • A cyst lined by epidermal epithelium with adnexal structures is called a dermoid cyst.  
  • A more rare epithelial cyst, lined by sebaceous duct gland epithelium with small sebaceous glands, is the steatocystoma multiplex.

35

 To which group of tumors do syringomas belong? 

Syringomas belong to the group of benign adnexal (appendage) tumors. They are lesions with differentiation towards eccrine sweat glands.

36

When the scalp is covered completely by cylindromas, this is called a ________. 
 

turban tumor

37

What people have an increased risk for developing basal cell carcinomas? 

An increased risk for developing basal cell carcinomas is present in 1) lightly pigmented people with sun-damaged skin; 2) immunosuppressed patients; 3) patients with inherited defects in DNA replication or repair (eg, xeroderma pigmentosum); 4) patients with the basal cell nevus syndrome.

38

What are the large clefts between the tumor nests and the stroma? 

During the tissue fixation procedure, the stroma shrinks away from the epithelial tumor nests, creating artifactual clefts.

39

What is the main clinical differential diagnosis of superficial basal cell carcinomas? 

The main clinical differential diagnosis of superficial basal cell carcinomas is an eczematous dermatitis. Other possibilities are Bowen's disease, dermatomycoses, and, if the lesion is pigmented, even a malignant melanoma.

40

What other factors may induce actinic keratosis? 
 

Not only chronic exposure to sunlight (most important factor), but also ionizing radiation, hydrocarbons, and arsenicals may induce actinic keratosis.

41

What is the name of the in situ carcinoma of the skin? 

In situ carcinomas of the skin are often caused by HPV infection and are called Bowen's disease.

42

 Why are immunosuppressed patients at high risk for developing squamous cell carcinomas of the skin? 

Immunosuppressed patients have decreased protection against human papillomavirus (HPV), a causative agent in many (but not all) squamous cell carcinomas of the skin.

43

What other skin tumor shows well-differentiated, but atypical squamous epithelium and is surrounded by lymphocytic infiltrate? 

Histologically, a keratoacanthoma can be very hard to differentiate from a well-differentiated squamous cell carcinoma. The keratoacanthoma is increasingly considered to be a squamous cell carcinoma with spontaneous regression.

44

 What is the name of the groups of neutrophils lying in the parakeratosis? 

These groups of neutrophils are Munro microabscesses.

45

 What would be the diagnosis if these microabscesses were much larger? 

Pustular psoriasis

46

 Describe the clinical presentation of mucosal lesions in lichen planus. 
 

Mucosal lesions in lichen planus affect the oral mucosa and the genital mucosa, especially the glans penis. The mucosal lesions are clinically different from the purple, polygonal papules seen on the skin. White, reticulated (netlike) lesions can be seen on the oral and genital mucosa.

47

Considering the histology of an active lesion, explain why lichen planus leaves hyperpigmentation. 
 

In active lesions of lichen planus, there is an impressive destruction of the basal layer of the epidermis. In this layer, keratinocytes contain the largest amount of melanin pigment. The pigment is present in the keratinocytes just above the nucleus in order to prevent nuclear damage from UV radiation. As  keratinocytes are destroyed, they become 'incontinent' for the melanin pigment, which they drop into the upper dermis, where it is taken up by macrophages. The melanin-containing macrophages give the clinical appearance of hyperpigmentation.

48

 What are the main complications of pemphigus vulgaris and other blistering diseases? 
 

Blistering diseases can be complicated by secondary infections and extreme loss of fluid.

49

 What is the difference between spongiosis and acantholysis? 

Spongiosis is caused by the presence of fluid within the intercellular spaces of the epidermis. The intercellular attachment sites (desmosomes) are not primarily affected. Only in severe spongiosis can the mechanical pressure on the desmosomes, followed by damage of the desmosomes, cause formation of intraepidermal vesicles.  Acantholysis refers to the loss of attachment between the keratinocytes. This can be caused by autoantibodies against desmosomes, as in pemphigus, or by inherited dysfunction of desmosomal structures.

50

In another clinical and pathological variant of pemphigus, the antibodies react with a more superficial antigen. Which antigen and what variant of pemphigus? 

In the superficial layers of the epidermis, desmoglein 1 is present. Antibodies against desmoglein 1 result in pemphigus foliaceus, which has very superficial blisters with a very thin blister roof. These lesions clinically appear as erythema and erosions; real blisters are hardly ever found, because the thin blister roof is very friable.

51

What is the age of most bullous pemphigoid patients? 

Patients with bullous pemphigoid are generally elderly individuals, 50-70 years old.

52

How can one differentiate between bullous pemphigoid and other causes of eosinophil-rich subepidermal blisters? 

The clinical history is important. Was there an insect sting or insect bite? Does the patient use drugs that can cause bullous eruptions? Finally, the diagnosis has to be made by direct and indirect immunofluorescence, in which bullous pemphigoid will be positive and the insect reaction and the bullous drug eruption will be negative.

53

What is the difference between direct and indirect immunofluorescence? 

Direct immunofluorescence is done on a biopsy specimen of the skin of the patient. The skin is incubated with labeled complement or immunoglobulins.  Indirect immunofluorescence is done with the antibody-containing serum of the patient. Control skin or other control epithelium is incubated with the patient's serum.

54

What is the causative agent in all these verrucous lesions? 

Verruca plantaris, verruca palmaris, verruca vulgaris, and condyloma acuminatum are all caused by infection with human papillomavirus (HPV).

55

Which type of HPV is often detected in dysplastic HPV-induced skin lesions? 
 

16

56

Hydroxyproline in urine

Paget's disease

57

Basal cell carcinoma in people under 20

Gorlin syndrome

58

Gene involved in Gorlin syndrom

PCTH

*Autosomal dominant

Chromosome 9