Slu Path Case Studies

Front 1

What identifies a tumor of the bronchus as SCC?

Back 1

keratin formation and lack of gland formation.

Front 2

What brown pigment can surround neuronal tissue?

Back 2

keratin

Front 3

In a _______, it has been shown the stromal cells are the neoplastic(monoclonal) cells while the surrounding epithelial cells are secondary(non-neoplastic).

Back 3

fibroadenoma(breast)

Front 4

What are some ectodermally derived structures?

Back 4

Hair, sebacious glands, epidermis

Front 5

Name some endodermally derived tissue. Mesodermally derived?

Back 5

respiratory type mucosa with ciliated epithelium and small mucous glands.

Mesodermal - cartilage and fat

Front 6

Differentiate between lymphoma and carcinoma in the lymph.

Back 6

Carcinomas fill subcapsular sinus while lymphomas generally replace entire node.

Front 7

This can indicate adenocarcinoma.

Back 7

cytoplasmic mucin vacuoles.

Front 8

Numerous white tan tumors present on liver? Primary or metastatic?

Back 8

Metastatic. If primary it would have just been one or few nodes.

Front 9

What is notable about pancreatic cancer?

Back 9

Bone metastasis often cause osteoblastic changes as opposed to osteolytic.

Front 10

How would a patient with lung carcinoma metastatic to bone present?

Back 10

bone pain

Front 11

If I have an metastatic adenocarcinoma in the liver, where is a possible point of origin for primary tumor?

Back 11

Pancreas. It could have travelled through portal venous system.

Front 12

What is/causes pseudomyxoma peritonei?

Back 12

It is when the peritoneal cavity fills with mucin/tumor. Can be caused by mucinous colon carcinoma. Sometimes referred to as "jelly belly"

Front 13

How would a benign thyroid follicular adenoma present?

Back 13

rapid enlargement of thyroid

Front 14

Describe thyroid adenomas

Back 14

well formed, uniformly regular shaped, cuboidal follicular epithelial cells with normal polarity.

Front 15

Describe reasons to favor a benign adenomatous polyp vs a carcinoma.

Back 15

size(> 2cm), lack of invasion

abnormal architectural structures would indicate carcinoma

Front 16

Describe a likely characteristic of colon villous adenoma

Back 16

inability to produce mucin

Front 17

Back 17

well differentiated adenocarcinoma retaining ability to make glands

Front 18

How would a carcinoma presenting in the head of the pancreas obstructing the bile duct present?

Back 18

painless jaundice

Front 19

Back 19

Adenocarcinoma of pancreas. Note few but present gland formation identifying adenocarcinoma. Also, vascular invasion is shown.

Front 20

Back 20

perineural invasion by adenocarcinoma cells

Front 21

Back 21

This malignant tumor may be an adenocarcinoma arising from the columnar epithelial lining of the bronchus or a squamous cell carcinoma arising from squamous metaplasia.

Front 22

differentiate adenocarcinoma, SCC and neuroendocrine small cell carcinoma.

Back 22

Differential diagnosis includes adenocarcinoma, squamous cell carcinoma and neuroendocrine small cell carcinoma (oat cell carcinoma). The latter two are typically central (as in this case). Adenocarcinoma is usually peripheral (scar cancer).

Front 23

Back 23

Squamous cell carcinoma (SCCA) of bronchus. Haphazard cords of infiltrating cells. Keratin formation but no glands identify this as SCCA.

Front 24

Intercellular bridges, which indicate desmosomes are a feature of?

Back 24

SCCA

Front 25

Back 25

leiomyoma

Front 26

Back 26

leomyosarcoma

Front 27

Back 27

osteoid produced by osteosarcoma

Front 28

Patients with FAP have a mutation in what gene?

Back 28

APC

Front 29

Patients with NF-1 have a mutation in what gene?

Back 29

neurofibromin.

RAS and GTPase activity that downreglates RAS

Front 30

What determines homing of cancer cells to organs?

Back 30

Anatomic considerations(drainage...lymph/vascularization)

Tumor cells may have receptors for endothelial cells on certain organs

Certain tissues may not favor metastases because the microenvironment may inhibit proteolytic enzymes needed for invasion by tumor cells

Front 31

Back 31

Neurofibroma, spindle cells with features of Schwann cells and fibroblasts in wavy bundles, uniform in shape and size. Nuclei are elongated, curved. There is little pleomorphism or mitotic activity.

Front 32

Back 32

Neurofibrosarcoma. Compared to neurofibroma, it is more hyperchromatic with larger nuclei, more variation in shape, size, higher N:C ratio. Mitoses are present.

Front 33

What route of metastasis is commonly used by sarcomas?

Back 33

Sarcomas spread by invading blood vessels.

Front 34

What factors induce vascularization (angiogenesis) of tumor?

Back 34

Two important ones are basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) produced by tumor cells or by host cells like macrophages that accumulate in tumors).

Front 35

How frequently are mutations in TP53, RAS, and APC seen in other types of malignancies?

Back 35

p53 is most common gene mutated in human cancer, mutated in > 50% of all malignancies.
RAS is most common mutated protooncogene in human cancer, mutated in 15-20% of malignancies.
APC mutation is seen in very few other tumors (eg, gastric, esophageal cancers)

Front 36

What are the functions of p53 and RAS in normal cells?

Back 36

p53 is “guardian of genome”. With DNA damage, normal p53 gene causes cell cycle arrest in G1, providing time for repair of DNA damage. If repair is successful, cells enter cycle again; if not successful, p53 gene causes cell death by apoptosis.
RAS is normally a signal-transduction molecule. When cells receive growth promoting stimulus, RAS-GDP is converted to RAS-GTP which is active form of RAS, and sends growth promoting signals to nucleus. Normally, RAS-GTP is rapidly converted to its inactive form by hydrolysis of GTP to GDP

Front 37

How does genomic instability influence neoplastic transformation?

Back 37

Genomic instability contributes to neoplastic transformation indirectly, by predisposing to mutations in protooncogenes and tumor suppressor genes

Front 38

What is this? What stage? What would consistency of tumor be based on stromal appearance? What is the pink material in between tumor cells?

Back 38

Breast adenocarcinoma

Moderately differentiated

Hard and gritty. Collagen makes it hard or scirrhous.

Collagen

Gland formation can’t be seen readily, because glands are compressed by thick collagenous stroma.

Front 39

How is estrogen receptor expression involved in etiology of this tumor?

Back 39

Estrogen may bind to receptors on tumor cells and promote growth.
Estrogen is not mutagenic, but it is a tumor promoter, not a tumor initiator.

Front 40

Significant of CSF samples in terms of cancer?

Back 40

If signet ring cells are found it indicates that cancer has metastasized a lot(Stage IV)

Front 41

which mutations associated with initation?

Back 41

APC

Front 42

Which mutations associated with tumor progression?

Back 42

p53, RAS, DCC

Front 43

Other than Colon cancer, what else is Colon carcinoembryonic antigen increased in?

Back 43

gastric, pancreas, lung or breast cancer.

also alcoholic cirrhosis, hepatitis, UC, Crohn disease. Healthy smokers

Front 44

What must invasive cells be capable of to perpetuate?

Back 44

Invasive cancer cells must be able to bind to basement membrane and extracellular matrix by laminin receptors and fibronectin receptors.
To degrade ECM, they produce proteolytic enzymes (e.g., collagenase).

Front 45

what is this?

Back 45

metastatic colon adenocarcinoma to liver

Front 46

NF I patients have benign neurofibromas in or attached to nerve trunks. NF I patients have increased risk of _________

Back 46

neurofibrosarcoma (Malignant Peripheral Nerve Sheath Tumor).

Front 47

Back 47

In a neurofibroma, it is likely that both NF1 alleles are inactive. By comparison, normal cells of a NF1 patient have only one inactivated allele. This inactive NF1 is inherited in the germline providing the first hit, according to the two-hit hypothesis of tumor development.

Front 48

Describe Kwashiorkor

Back 48

Kwashiorkor. “Sugar baby” In this form of malnutrition, due to protein deprivation, subcutaneous fat and muscle mass are relatively spared.
There is generalized edema (due to hypoalbuminemia), reflected in puffy eyelids, face and extremities.  

Front 49

Describe Marasmus

Back 49

Marasmus  When dietary protein and calorie deficiencies are proportional, subcutaneous fat and skeletal muscle are catabolized to provide energy, amino acids, initially sparing viscera.

Front 50

Describe what the liver of a malnourished child would look like.

Back 50

Liver of child with kwashiorkor is yellow, fatty, due to reduced serum levels of carrier proteins.
The liver of the child with marasmus is normal, extremities show wasting.

Front 51

What is wrong with this child?

Back 51

Rachitic Rosary  Defective bone mineralization leads to overgrowth at costochondral junctions, producing bead-like expansions (hence designation rosary).
Pigeon-breast deformity also apparent.  

Rickets   - Hypocalcemia due to vitamin D deficiency leads to insufficient mineralization of osteoid matrix, causing weakness of bones.
In a growing, ambulatory child, this weakness causes legs to bow outward, producing a varus deformity.

Front 52

Whats up here?

Back 52

Beriberi, ankle edema. Beriberi is manifestation of thiamine (vitamin B1) deficiency, characterized by high-output congestive heart failure, resulting in peripheral edema, as evident in dependent pitting edema in this patient.
In U.S., alcoholism is a common cause of thiamine deficiency.

Front 53

What's up?

Back 53

Pellagra, dermatitis, before and after treatment
Dermatitis of niacin deficiency has redness, thickening, roughening, scaling of exposed skin, most noticeable on the hands, neck and nose. It can also affect mucous membranes of mouth and vagina.     

Front 54

Why?

Back 54

Zinc deficiency leads to distinctive rash, known as acrodermatitis enteropathica, typically surrounds eyes, nose, mouth, anus, extremities.
Growth retardation, altered immune function, and infertility also occur with zinc deficiency.

Front 55

what?

Back 55

Skin, follicular hemorrhage, vitamin C deficiency
Hemorrhages have affected hair follicles, producing small red dots (petechiae).
Periosteum, joint spaces and central nervous system can also be affected.  

Front 56

Describe lung that has pnuemocystis pneumonia

Back 56

heavy, red, atelectactic

bilateral fluffy infiltrates, prominent at hilum, base.

Front 57

Back 57

normal lung

Front 58

How is response to therapy assessed in AIDS patients?

Back 58

PCR amplification of HIV-1 is currently the method of choice for assessing viral load and response to therapy in patients with AIDS.

Front 59

What other types of specimens are typically collected to detect Pneumocystis?

Back 59

Bronchial washings or sputum samples are collected to diagnose Pneumocystis

Front 60

HIV stratification of categories is based on....

Back 60

CD4 count

>500 ul is low probability of progression
<200 is high probability of progression

Front 61

most common CNS disease in AIDS. What does it look/present like?

Back 61

Primary HIV encephalitis causes progressive decline in cognitive function, with memory loss, withdrawal. Affects deep gray matter, white matter, causes white matter pallor,

Front 62

What stain is used for myelin?

Back 62

Luxol fast blue

Front 63

Can you think of another disease in immunosuppressed patients that may result in demyelination?

Back 63

Progressive multifocal leukoencephalopathy is another disease that may result in demyelination in this patient population.

Front 64

How does HIV-1 meningoencephalitis differ pathologically from HIV-1 aseptic meningitis, which occurs 1 to 2 weeks after seroconversion?

Back 64

HIV-1 aseptic meningitis, although not well studied, typically shows a mild lymphocytic meningitis with some myelin loss. HIV-1 meningoencephalitis is typified by a parenchymal inflammatory reaction that occurs in a scattered and perivascular pattern.

Front 65

What happens to retina in AIDS?

Back 65

CMV infection - hemorrhage, purulent exudate, ulceration, CMV inclusions in retinal cells.

Front 66

What are more common organs involved by CMV infection in immunocompromised host?

Back 66

Most often, CMV is in salivary glands, kidneys, liver, lungs, gut, pancreas, thyroid gland, adrenal, brain (to name a few!).

Front 67

Back 67

CMV

Front 68

Back 68

Microglial nodule with multinucleated giant cell. Oligodendroglia, astrocytes, macrophages proliferate as response to injury, forming microglial nodules.
Specificity for HIV-1 can be demonstrated with immunoperoxidase stain with antibody for HIV p24 antigen.

Front 69

What's wrong?

Back 69

Small bowel, nodular Mycobacterium avium-intracellulare infection

Front 70

What are common pathogens producing diarrhea in patients with AIDS?

Back 70

The common pathogens producing diarrhea in patients with AIDS include Mycobacterium avium-intracellulare, Cryptosporidium or Isosporidium, and cytomegalovirus. In addition, a general rule is that any pathogen that infects the immunocompetent patient may also infect the immunocompromised patient, which would put all the common bacterial and viral pathogens on this list as well

Front 71

How would the MAI picture differ pathologically from cryptosporidiosis?

Back 71

Cryptosporidium is not invasive, they attach to superficial portions intestinal epithelium. MAI are in histiocytes in lamina propria, submucosa.

Front 72

Back 72

Small bowel, Mycobacterium avium-intracellulare infection Mucosa packed with histiocytes. Organisms in histiocytes stain red with acid-fast stain.

Front 73

How do CMV infections differ in immunocompetent vs. immunosuppressed patients?

Back 73

In immunocompetent, acute CMV infection resembles acute infectious mononucleosis.

In immunosuppressed, CMV disease, whether (acquired primarily or by reactivation), can be disseminated, fulminant, lethal with multiorgan involvement.

Front 74

What sort of cells does CMV turn up in?

Back 74

CMV may infect a variety of cell types, including epithelial, endothelial, mesenchymal cells

Front 75

What is this...
Point out where each structure is....
Pseudomembrane
Necrotic mucosa
Residual crypts
Macrophage nucleus
CMV inclusion

Back 75

CMV infection of colon

Front 76

What are the similarities, pathogenetically, between this picture and Clostridium difficile-associated pseudomembranous colitis?

Back 76

Both CMV and Clostridium difficile may produce colitis with pseudomembranes. In CMV disease, the pseudomembranes result from direct epithelial necrosis and, probably more importantly, ischemic necrosis secondary to vascular damage by CMV. In C. difficile-associated pseudomembranous colitis, the pseudomembranes result from toxin-mediated destruction of the epithelium, as well as ischemic necrosis secondary to thrombosis of underlying small vessels.

Front 77

What is important about the image on the left? What caused it?

Back 77

PML is caused by a papovavirus that infects the oligodendroglia directly, causing necrosis. Because the oligodendroglia produce myelin, demyelination occurs in the infected areas, noted in the image on the left. The characteristic histologic feature of PML, seen on the right, is infection of the oligodendroglial nuclei, resulting in a glassy smudged appearance of the chromatin.

Front 78

What is seen that is important in these pictures?

What is this caused by?

Back 78

This shows an area of necrosis infiltrated by reactive, rod-shaped, microglial cells. Such clusters of microglial cells are called microglial nodules. The high-power inset demonstrates a cyst of Toxoplasma organisms containing multiple bradyzoites.

Toxoplasmosis, an opportunistic infection. It affects AIDS and bone marrow transplant

Front 79

What other organs are most commonly involved by Toxoplasma?

Back 79

Toxoplasma causes pneumonitis, lymphadenitis, chorioretinitis, encephalitis.

Front 80

What is important about this?

Back 80

CNS lymphoma cause mass in brain, perivascular lymphomatous infiltrate. Characteristically B-cell neoplasms associated with EBV reactivation in immunosuppressed population. Majority contain EBV genome.
Virus most likely causes prolonged B-cell activation, with superimposed additional genetic alterations, cells become malignant.  

Front 81

What is this from?

Back 81

CSF sample taken from a patient affected with CNS lymphoma due to EBV.

Front 82

What is this?

Back 82

Sample of Kaposi Sarcoma

sarcoma purple-red vascular tumor with plump spindled cells outlining vascular spaces. Extravasated erythrocytes are also common.
KS has been associated with Kaposi sarcoma-associated herpes virus (KSHV) found in virtually all Kaposi sarcomas, both AIDS-associated and non-AIDS associated. The jury is still out on whether virus causes lesion, is cofactor, or is incidental.

Front 83

What is the intestinal manifestation of Kaposi Sarcoma?

Back 83

Patients with Kaposi sarcoma may have life-threatening hemorrhage from intestinal involvement by Kaposi sarcoma