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Pathology 2 Final > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What is toxic granulation and why does it occur?

A

dark course granules in granulocytes (neutrophils) seen in peripheral blood smears in patients with inflammatory conditions. Common in patients with sepsis. thought to be due to impaired cytoplasmic maturation in the effort to rapidly generate large numbers of granulocytes.

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2
Q

In leukocytosis, what does neutrophil predominance suggest?

A

bacterial infections, actue inflammation, necrosis, MI

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3
Q

In leukocytosis, what does lymphocyte predominance suggest?

A

acute viral pinfx (EBV, CMV, viral hepatitis), chronic inflammation (TB, etc.)

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4
Q

In leukocytosis, what does eosinophilia suggest?

A

allergy (drugs, foods, inhalants) and parasitic infx

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5
Q

What is bandemia and what does it suggest?

A

excess of band cells (immature WBCs). signifies infection, sepsis, inflammation

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6
Q

What is mesenteric adenitis and what disease is it often confused with?

A

inflammation of mesenteric lymph nodes in the abdomen. Can be caused by Yersinia enterocolitica. May be confused with acute appendicitis if it occurs in the RLQ (preceeded by a sore throat)

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7
Q

How do you tell the difference between mesenteric adenitis and acute appendicitis?

A

mesenteric adenitis will have concomitant pharyngitis, HA and NO vomiting/rebound tenderness

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8
Q

What are the three areas of the lymph node and what type of cells do they contain in majority?

A

Paracortical areas: T-Cells
Secondary lymphoid follicle: B-Cells
Medullary cords: Macrophages and plasma cells

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9
Q

In an examination of an enlarged LN, you find that swelling is due to follicular hyperplasia. What disease is this associated with? Which immune cells are being activated here?

A

humoral immune response (RA, toxoplasmosis, early HIV infx….). Activated B cells

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10
Q

In an examination of an enlarged LN, you find that swelling is due to paracortical lymphoid hyperplasia. What disease is this associated with? Which immune cells are being activated here?

A

cellular immune response (drugs, acute viral infx, EBV, post vax). Activated T cells

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11
Q

In an examination of an enlarged LN, you find that swelling is due to sinus histiocytosis. What disease is this associated with? Which immune cells are being activated here?

A

distention and prominence of lyphatic sinusoid, nodes draining cancers such as carcinoma of the breast. endothelial and histioctyes are involved.

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12
Q

In regards to WBC neoplasms, what are two types of genetic derangements causing them?

A

lymphoid neoplasms: Hodgkins, non-Hodgkins

myeloid neoplasms: abnormal hematopoietic cell, myelodysplastic syndromes histiocytoses, multiple myeloma…AML, CML

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13
Q

How does the presentation of Hodgkins lymphoma differ from NHL in terms of tenderness and location?

A

HL present as non-tender nodal enlargement
2/3rd of NHL present as non-tender nodal enlargement
1/3 of NHL arise at extranodal sites

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14
Q

Majority of lymphoid neoplasms are from which types of cells?

A

80-85% are B-cell origin

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15
Q

How does Hodgkins Lymphoma spread?

A

lymph node to lymph node/ orderly

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16
Q

Which lymphoma has Reed-Sternberg cells?

A

Hodgkin Lymphoma

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17
Q

Compare/Contrast NHL and HL cellular findings:

A

NHL have mutations in B or T cells

HL is marked by the presence of Reed-Sternberg cells

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18
Q

Compare/Contrast NHL and HL age-ranges:

A

HL generally occurs in younger 15-24 aged patient and patients over 60
NHL is rare in young patients, most dxs made in patients >60

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19
Q

Compare/Contrast NHL and HL Incidence:

A

HL accounts for less that 1% of cancers in the US, about 15% of lymphomas.
NHL accounts for 4% of all cancers in the US, about 85% of lmphomas.
in both cases, men are affected more than women

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20
Q

Compare/Contrast NHL and HL Locations:

A

HL usually starts in the lymph nodes in the neck. however, it can spread to other lymph node groups. NHL can start in a variety of locations depending on the type of cancer and cells affected

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21
Q

Compare/Contrast NHL and HL Progression:

A

HL progresses in an orderly fashion between lymph nodes and is often caught before Stage IV.
NHL are less orderly, sometimes more aggressive and are more likely to be caught in advanced stages

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22
Q

What are the characteristics of ALL?

A

Hyperploidy is most common (>50 chromosomes). Philadelphia chromosome present- t(9;22)

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23
Q

What is the most common leukemia of adults in the western world?

A

CLL

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24
Q

What is the only leukemia not associated with radiation or drug exposure?

A

CLL

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25
Q

In which disease are smudge cells seen?

A

CLL

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26
Q

What are the characteristics of CLL and how does it present?

A

Morphology: BM involvement in all cases. tumor cells usually infiltrate the splenic and hepatic portal tracts. Chromosomal translocations are rare. They have a distinctive immunophenotype
Clinical Presentation: M:F 2:1; >50 yo; medial survival 4-6 years; lymphadenopathy, hepatosplemomegaly
GI infiltrates –> diarrhea, malabsorption, ulceration, megaloblastic anemia
disrupts normal immune function, hypogammaglobulinemia, Abs to RBC (AIHA and thrombocytopenia)
fatigue, wt los, anorexia, DOE, abd fullness, asymptomatic LA

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27
Q

What is the most common form of NHL?

A

follicular lymphoma

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28
Q

What infxs are associated with NHL?

A

EBV, HTLV-1, HepC, Kaposi Sarcoma, H.pylori

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29
Q

What does the genetic translocation leading to follicular lymphoma cause (in terms of product that is produced)?

A

over expression of bcl-2 protein (antagonist of apoptosis) promotes survival of follicular lymphoma cells

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30
Q

What are the 3 categories of Burkitts Lymphoma?

A

African (endemic) Burkitt lymphoma, sporadic (nonendemic), subset of aggressive lymphomas in HIV (highly undifferentiated Bcell lymphoma)

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31
Q

What is the morphology of Burkitss lymphoma?

A

intermediate sized lymphoid cells, “starry sky” pattern in LN, macrophage proliferation with ingested nuclear debris

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32
Q

What are genetic factors of Burkitts lymphoma?

A

c-MYC gene translocations on chromosome 8, latent EBV infection

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33
Q

What is the clinical presentation of Burkitts Lymphoma?

A

children/YA, manifestation at extranodal sites
endemic BL: mass in the mandible and abd viscera
sporadic BL: ileocecum/peritoneum abd mass
BM/Blood involvement is rare
an aggressive cancer that responds well to high-dose, short-term chemotherapy

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34
Q

Compare/Contrast multiple myeloma with Waldenstrom macroglobulinemia

A

MM (plasma cell myeloma): most important and most common monoclonal gammopathy
Waldenstrom macroglobulinemia: blood hyperviscosity due to high IgM, common in adults with lymphoplasmacytic lymphoma

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35
Q

Which infections are common in patients with multiple myeloma?

A

recurrent infxs with (s.pneum/s.aureus/e. coli). Most common cz of death d/t decreased production of Igs

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36
Q

What test is necessary to definitively dx MM?

A

Bone Marrow Biopsy

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37
Q

What 4 complications frequently occur in Waldenstroms macroglobulinemia?

A

Visual impairment (d/t retinal vein distention, retinal hemorrhages and exudate)
Neurological problems (HA/dizziness, deafness, stupod d/t sluggish blood flow)
Bleeding (complexes form)
Cryoglobulinemia (ppt of macroglobulins at low temp, sxsof Raynauds phenomenon and cold urticaria

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38
Q

In which disease are flower cells seen? What is the prognosis of this disease?

A

Adult T-cell leukemia/lymphoma. Dx is rapidly progressing and fatal in months-1 year

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39
Q

Which immune cells cause mycosis fungoides/Sezary Syndrome? and what are the 3 stages of the lesion that occur with those diseases?

A

Tumor of CD4+ helper T Cells, mostly involves with skin

  1. premycotic phase: inflammatory phase
  2. plaque phase: raised, indurated, irregularly outlines, erythematous plaques
  3. tumor phase: multiple, large (up to 10 cm), red-brown nodules correlates to systemic spread.
40
Q

What are the 4 stages of Hodgkins disease?

A

Stage 1: single lymph node/extranodal site
Stage 2: two or more lymph node regions on the same side of the diaphragm alone or limited extranodal sites
Stage 3: LN regions on both sides of the diaphragm/spleen and contiguous extranodal sites
Stage 4: multiple disseminated foci of one or more extranodal organs/tissues

41
Q

Which virus is associated with HL?

A

EBV

42
Q

What is strange about ETOH and HL?

A

In HL, there is pain in involved LN with alcohol consumption

43
Q

What is the difference between arteriosclerosis and atherosclerosis?

A

arteriosclerosis occurs when blood vessels become thick and stiff, restricting blood flow.
atherosclerosis refers to the buildup of fats, cholesterol and other substances in and on your artery walls (plaques) which can restrict blood flow

44
Q

What are the steps on the non-specific vascular wall response to injury?

A

endothelial activation
smooth muscle cell roles
development, growth, remodeling
intimal thickening

45
Q

What are endothelial cell activators? What do the deactivate? what types of products are normally secreted by the endothelium when the system is in balance and health?

A

healthy endothelium secretes: cytokines, GFs, bacterial products, hemodynamic forces, lipid products, viruses, complement (in response to things like cigarette smoke/hypoxia, eg)
activators deactivate the production of ECM (collagen, elastin, proteoglycans

46
Q

Which products of clinical importance are produced by vascular smooth muscle?

A

Make ECM: Collagen, Elastin, Proteoglycans

47
Q

Which vascular smooth muscle products decrease with the normal aging process? What effect does that have?

A

the intima thicken with age from an increase in collagen, and a decrease in elastin. –> hypertension

48
Q

What is an AVM? and why does the vein dilate so much?

A

Arteriovenous malformation: abnormal connection between arteries and veins, bypassing the capillary system. The vascular anomaly is widely known because of its occurence in the central nervous system, but can appear at any location. AVM lack the dampening effect of capillaries on the blood flow, which means that the AVM can get progressively larger over time as the amount of blood flowing through increases. It also causes the surrounding area to be deprived to the functions of capillaries, resulting in a tangle of blood vessels, often called a nidus. Can be extreemely fragile and prone to bleeding.

49
Q

What is the difference between a bruit and a thrill?

A

Bruit: abnormal sound or murmur heard upon auscultation
Thrill: vibration felt by the practitioner during palpation

50
Q

What is a fatty streak, and is it normal?

A

fatty streak is the first grossly visible lesion in the development of atherosclerosis. appears as an irregular yellow-white discoloration on the luminal surface of an artery, consisting of aggregate of foam cells, located beneath the inner, endothelial layer of an artery. Fatty streaks may also include T cells, aggregated platelets, smooth muscle cells. It is the precursor to atheromas that may become plaques. They are not normal but are seen more and more often. THey are a response to early pathology.

51
Q

What are the eight steps in the pathogenesis of atherosclerosis?

A
  1. Chronic endothelial injury
  2. LDL, cholesterol in arterial wall
  3. oxidation of lipoproteins
  4. monocytes migrate to endothelium
  5. platelet adhesion and activation
  6. migration of smooth muscle from media to intima to activate macrophages (foam cells)
  7. proliferation of smooth muscle and ECM
  8. accumulation of lipids in cells and ECM
52
Q

What are the 4 MODIFIABLE risk factors for arteriosclerosis?

A

hyperlipidemia, hypertension, cigarette smoking, diabetes mellitus

53
Q

What was the real value of the Framingham study?

A
  1. finding that decrease blood pressure decreases MI risk.
  2. gave us “risk factors”, gearing medicine towards preventative care.
  3. demonstrated pros/cons of individual tailoring of medicine vs. mass prescribing (some medications were causing stroke)
54
Q

What percentage of hypertension is “essential”?

A

95%

55
Q

What are the two types of histopathological findings in vessel appearance with hypertension?

A
  1. Benign: hyalization of arteriole wall (most difficult to treat)
  2. Malignant: fibrinoid necrosis and “onion skinning” of arteriole wall (hyperplastic)
56
Q

How does the appearance of elastic fibers differ in normal vs aneurysmal changes?

A

Normal arteries have short, tight elastic fibers like rubber bands.
arteries with aneurysmal changes will show disrupted, fragmented elastic fibers

57
Q

What are the potential sequelae of aneurysms (7)?

A

Rupture, obstruction, embolism, compression, ureter, spine, mass effect

58
Q

What are the potential symptoms of thoracic aneurysms (6)?

A

Encroachment, Respiratory difficulties, Hoarseness, Dysphagia, Cough, Pain

59
Q

What are two complications of thoracic aneurysms?

A

aortic valve dilation, aortic valve rupture

60
Q

What is a dissecting aneurysm?

A

aneurysm in which the wall of an artery tears longitudinally. blood surges through the tear, causing inner and middle layers of the artery to separate (dissect).

61
Q

What are the characteristics of vasculitides?

A

chiefly arterial
5% infectious, 95% non infectious
non infectious are generally autoimmune (persistent findings of immune complexes, anti-neutrophil Abs- Wegeners, Temporal-, anti-endothelial cell abs-Kawasaki)
often drug related, especially small blood vessels (hypersensitivity)

62
Q

What is the most feared sequelae of temporal arteritis?

A

blindness

63
Q

Why is Takayasu Arteritis also called pulseless disease?

A

subclavian blockage presents as pulselessness in upper extremities on PE.

64
Q

What are the characteristics of Kawasakis disease?

A

children <4
coronary arteries affected, is the leading cause of acquired heart disease in children in the USA and JAPAN. Fatal in 1%.
Red tongue, adenopathy, anti-endothelial cell Abs, chest pain

65
Q

What is so strange/unique about thromboangiitis Obliterans or Buergers Disease?

A

100% caused by cigarette smoking, M»»F, 30s-40s

66
Q

What organ system must be evaluated in young people with hypertension? What disease are you looking for and which test do you use?

A

Check the Renal system! Looking for renal artery stenosis. poor blood flow to the kidneys because of obstructed lumen. kidney wants to increase blood flow so it produces substances to increase peripheral resistance….Dx with ultrasound. Check anyone under 35 with hypertension

67
Q

Why is the term mycotic aneurysm a misnomer?

A

a “mycotic” aneurysm is any aneurysm that has become secondarily infected, usually by bacteria. hence the name “mycotic” (viral) is a misnomer.

68
Q

Which class of diseases usually have a vasculitis component?

A

most classical systemic auto-immune diseases have an element of vasculitis. Three magnets for ag-ab complexes: GBM, synovia, blood vessels

69
Q

Skin discoloration can be red, white or blue. What type of pathology is associated with each?

A

Red: Hyperemia
White: Pallor
Blue: Cyanosis

70
Q

What are the 5 P’s of arterial occlusion?

A

Pallor, Pain, Paresthesia, Pulselessness, Poikilothermia (polar bear)

71
Q

What is the underlying pathology behind varicose veins and venous stasis ulcers?

A

Variceo veins are related to increased venous pressure, age, valve dysfunction. Thought to arise with dysfunctional backflow, causing increased venous pressure. –> venous HTN, blood cant flow through, veins stretch, allow blood proteins to leak into extracellular space. THis isolates ECM molecules and GFs, preventing them from healing wounds. Fibrinogen leaks, –> deficient fibronolysis, fibrin build-up, preventing tissue oxygenation. WBCs also accumulate, releasing ROS, inflammatory molecules. Contributes to further ischemia

72
Q

Do superficial varicose veins usually cause thrombophlebitis? (DVT)

A

No, 90% of DVTs come from deep veins

73
Q

At what level of the leg are DVTs treated in the hospital with anticoagulation, vs outpatient anticoagulation?

A

General rule: is DVT is the below the knee–> outpatient. if the DVT is above the knee, it is treated in the hospital

74
Q

What is an inferior vena cava interruption filter or greenfield filter?

A

“umbrella” mechanical system put in the IVC, catching the incoming clots. Usually placed in through the femoral vein and is deployed in the IVC. Can only be used in the venous system because it is a low-pressure system (can be placed in the subclavian vein in RARE cases of DVT from upper extremity?

75
Q

What causes lyphedema, what surgery is famous for causing this?

A

any imaginable type of damage to the lymphatics could cause lymphedema. Radical mastectomy is the most famous for causing this.

76
Q

What is a hemangioma?

A

benign blood vessel tumor that is red and can be blanched. Capillary and Cavernous types. (cherry angioma, eg)

77
Q

What is telangiectasia?

A

a condition characterized by dilation of the capillaries, which causes them to appear as small red or purple clusters, often spidery in appearance on the skin or organ surface (spider veins, eg)

78
Q

What is Osler-Weber-Rendu?

A

a rare genetically determined disorder that affects blood vessels througout the body and results in a tendency for bleeding. HHT is an autosomal dominant disorder characterized by vascular dysplasia and hemorrhage. Prognosis is good as long as bleeding is recognized and promptly controlled.

79
Q

What is Nevus Flammeus?

A

Port wine stain, birthmark. vascular anomaly (capillary malformation on the skin)

80
Q

What is angiosarcoma?

A

Rare, have to stain with Ab against VWF, nucleus will be oddly shaped

81
Q

What is Hamartoma?

A

benign focal malformation that resembles a neoplasm. This is not a malignant tumor, and it grows at the same rate as the surrounding tissues. It is composed of tissue elements normally found at the site, but which are growing in a disorganized mass

82
Q

What is the difference between angioplasty, stents and grafts?

A

Angioplasty: plaque fracture, dissection and arterial dilation initially. re-stenosis in about 6 mos
Stent: metallic mesh, permanently placed, often drug coated. used to prevent thrombosis, spasm, delay re-stenosis.
graft: 400,000 CABG grafts per year in the USA. Saphenous v/Internal mammary a/internal thoracic a. 50% patient after 10 years with saphenous v./ 90% after 10 years with mammary a.

83
Q

What is the cause of OCA (oculocutaneous albinism) ? do they have melanocytes?

A

inherited disorders in which melanocytes are present, but melanin production in inadequate.

84
Q

What are the 4 components of acne vulgaris and which bacteria is implicated most often?

A
  1. Keratin plugging blocking outflow of sebum d/t changes in the infundibulum of the follicle.
  2. Hypertrophy of the sebaceous glands, often hormonal
  3. colonization of the follicle by lipase-synthesizing bacteria (Propionibacterium acnes).
  4. inflammation of the follicle, due in part to the breakdown of sebum into pro-inflammatory acids.
85
Q

What is the difference between Erythema Marginatum and Erythema Migrans?

A

Erythema marginatum: cutaneous manifestation of acute rheumatic fever; post-infectious, immune mediated complication of GABHS pharyngitis.
Erythema migrans is a cutaneous manifestation of infection with Borrelia burgdorferi- Lyme disease Vector: Ixodes scapularis- deer tick

86
Q

What virus causes Molluscum contagiosum?

A

poxvirus

87
Q

What are the 3 microbiological cuases of palm/sole rashes?

A

“You drive CARS with palms and soles”
CA- coxsackievirus A (hand, foot and mouth disease)
R- Rickettsia Tickettsii (rocky mountain spotted fever, centrifugal rash)
S- Syphillis (secondar)
(also TSS)

88
Q

What is Virchows Triad?

A

hypercoaguability, stasis, vascular injury (microtrauma)

89
Q

Are melanomas usually painful?

A

no

90
Q

Would a stain for Factor VIII help identify a tumo as being of vascular origin? why/why not?

A

YES. coagulation factor VIII is present in endothelial cells.

91
Q

Is blanching an important test in determining if a tumor is blood vessel in origin?

A

YES

92
Q

Why is the necrosis of Wegener’s not called “caseating”?

A

because by tradition “caseating” is attributed to TB. Wegeners is primarily a disease of upper and lower respiratory tracts, however eye involvement is frequent and may range from mild conjunctivits to dacrocystitis, episcleritis, scleritis, granulomatous sclerouveitis, ciliary vessel vasculitis and retro-orbital mall lesions.

93
Q

Why are arteritides highly liked to autoimmune diseases?

A

there are rarely any known causative external (ie infectious) pathogens and many are associated with autoABs

94
Q

Dissection can be both a cause or an effect of an aneurysm. Would the continued dissection of that acute hemorrhage result in a True or False aneurysm?

A

Neither, it’s a dissection

95
Q

What is a true vs false aneurysm?

A

True aneurysm: involves all three layers of the artery wall

False aneurysm: bleeding contained by outer layers of the artery.

Pathology 2 Final (2 decks)

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