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pathology year 2 term 1 > path fall final > Flashcards

path fall final Flashcards

1
Q
  1. What is toxic granulation and why does it occur (why are their extra structures in the cytoplasm)?
A

neutrophils containing coarse purple granulations in cytoplasm. Occurs during: severe infection and bacterial sepsis

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2
Q
  1. What is bandemia and what does it suggest?
A 
Band cells (immature neutrophils):
• usu a few seen with infxn
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3
Q
  1. What is mesenteric adenitis and what disease is it often confused with? How do you tell the difference between mesenteric adenitis and that disease (in terms of the history you obtain from the patient)?
A

Mesenteric adenitis - mimics acute appendicitis.
A form of lymphadenitis, or enlarged nodes due to microbes, cell debris, foreign matter introduced into wounds It’s seldom serious and clears on its own. Often preceded by a sore throat.

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4
Q
  1. Know the different anatomical structures in the lymph node, and which cells reside in those areas
A 
primary follicle
paracortical area (T cells)
secondary follicle (B cells)
germinal center ( B cells)
medullary cords (macrophages and plasma cells)
medullary sinus (histocytes)
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5
Q
  1. In an examination of an enlarged LN, you find the swelling is due to follicular hyperplasia, what diseases is this associated with? Which immune cells are being activated here?
A

follicular hyperplasia : activation of the humoral immune response caused by :
RA, toxoplasmosis, early stages of HIV infxn.

• Activation of B cell-rich germinal centers, as well as macrophages containing nuclear debris (tingible-body).

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6
Q
  1. In an examination of an enlarged LN, you find the swelling is due to Paracortical lymphoid hyperplasia?what diseases is this associated with? Which immune cells are being activated here?
A

paracortical lymphoid hyperplasia:Form of lymphadenitis
Stimuli that activate cellular immune response
• drugs
• acute viral infxns – esp EBV, post vaccination to certain viral dzs
• Activates T-cell regions of the node.
• macrophages and eosinophils.

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7
Q
  1. In an examination of an enlarged LN, you find the swelling is due to sinus Histiocytosis??what diseases is this associated with? Which immune cells are being activated here?
A

sinus histocytosis (also reticular hyperplasia): Happens with some cancers
• Distention & prominence of lymphatic sinusoids
• nodes draining cancers, such as carcinoma of the breast • Lymph nodes are usually non-tender.

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8
Q
  1. In regards to WBC neoplasms, what are the two types of genetic derangements causing them?
A

Lymphoid and Myeloid Neoplasms. Caused by Chromosomal translocations & oncogenes or Inherited genetic factors

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9
Q
  1. How does the presentation of Hodgkins lymphoma differ from NHL in terms of tenderness? How about with where they arise?
A

Hodgkins: All cases of HL present as non-tender nodal enlargement localized or generalized.

NHL: 2/3 of NHL present as non-tender nodal enlargement,1/3 arise at extranodal sites (skin, stomach, brain, etc)

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10
Q
  1. Majority of lymphoid neoplasms are from which types of cells?
A

Majority of lymphoid neoplasms (80% -85%) have a B-cell origin

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11
Q
  1. How does Hodgkin lymphoma spread?
A

Hodgkin lymphoma spreads in an orderly fashion. Contiguous lymph nodes.

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12
Q
  1. Which lymphoma has Reed-Sternberg cells?
A

Hodgkins

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13
Q
  1. Be able to compare and contrast NHL with HL
A

Hodgkins: Hodgkin lymphoma spreads in an orderly fashion

  • B cell origin
  • Spreads in orderly fashion
  • Etoh consumption causes pain
  • Reed Sternberg cells

Non Hodgkins: Arise at small extranodal sites ( GI tract, bone, skin, oral & nasal pharynx, tonsils, salivary glands, thyroid, testes, breast, & CNS).

  • 80% of pts. have generalized dz making staging difficult
  • lacking Reed-Sternberg cells.
  • 50% more common in males
  • 80-% B cell origin, 20% T cell
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14
Q
  1. What are the characteristics of ALL?
A

acute lymphoblastic leukemia
-predominant precursor B cell tumors
• manifest in childhood with abrubt stormy onset
-Numerical & structural changes in the chromosomes (hyperploidy) of the leukemic cells. (90% of pts)
-Sxs related to depression of marrow (fatigue, pallor, thrombocytopenia, neutropenia)
-bone pain
-CNS involvement
-testicular enlargement
-hepatosplenomegaly, LA
T-cell ALL (male adolescents)

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15
Q
  1. What chromosomal abnormality is associated with ALL?
A

worse prognosis: Presence of Philadelphia chromosome - t(9;22)
better prognosis: Presence of t (12;21)

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16
Q
  1. What is the most common leukemia of adults in the western world?
A

Chronic Lymphocytic Leukemia (CLL)

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17
Q
  1. What is the only leukemia not associated with radiation or drug exposure?
A

CLL–Etiology is based on immunodeficiency states of some

sort.

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18
Q
  1. In which disease are smudge cells seen?
A

CLL – peripheral blood smear –

• “smudge cells” due to the fragility of the cells

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19
Q
  1. What are the characteristics of CLL and how does it present?
A
  • Bone marrow involvement in all cases.
  • Chromosomal translocations are rare distinctive immunophenotype
  • Most pts are > 50, M:F = 2:1
  • Median survival 4-6 yrs
  • Lymphadenopathy & hepatosplenomegaly in 50-60%
  • GI infiltrates (megaloblastic anemia dt decr. folate)
  • disrupts immune functioning (increased infx, AIHA and thrombocytopenia)
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20
Q
  1. What is the most common form of NHL?
A

Follicular Lymphoma:
Painless, generalized LA
• Incurable; indolent waxing & waning course
• 7-9 yr survival
• 30-50% undergo histological transformation to diffuse large B-cell lymphoma with a survival of < 1 yr. (Similar to CLL)

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21
Q
  1. What infections are associated with NHL?
A
  • EBV
  • Human T-cell leukemia virus type 1 (HTLV-1)
  • Hepatitis C virus (HCV)
  • Kaposi sarcoma–associated herpesvirus (KSHV)
  • Helicobacter pylori infection
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22
Q
  1. What does the genetic translocation leading to Follicular Lymphoma cause (in terms of a product that is produced)?
A

Genetic translocation leads to overexpression of BCL2 protein:
• antagonist of apoptosis

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23
Q
  1. Know the categories and morphology of Burkitt Lymphoma as well as the clinical presentation
A

1) African (endemic) Burkitt lymphoma
2) Sporadic (nonendemic) Burkitt lymphoma
3) Subset of aggressive lymphomas in HIV
Intermediate sized lymphoid cells.
• “starry sky” pattern – in LN
translocations of the c-MYC gene on chromosome 8.
-children/YA
-extra nodal sites
- endemic Burkitts in the mandible or abdominal viscera
-Involvement of BM & blood is rare
-responds well to chemo

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24
Q
  1. Compare and contrast multiple myeloma with Waldenstrom macroglobulinemia
A

Plasma cell neoplasms
MM: Most important & most common monoclonal gammopathy (Produces IgG (IgA) or incomplete light or heavy chains)

  • insulin involvement
  • skeletal involvement (destructive bone tumors), can spread to lymph nodes
  • Il-6 cytokine
  • males, african americans, elderly
  • X ray shows “punched out” lesions,pathological fractures
  • Rouleaux formation in PB smear
  • High ESR!
  • Kidney damage due to BENCE-JONES proteins
  • hypercalcemia and recurrent infections (#1 cause of death)

WM: syndrome with blood hyperviscosity due to high levels of IgM.
• Commonly seen in adults with lymphoplasmacytic lymphoma.

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25
Q
  1. Which infections are common in patients with multiple myeloma (MM)?
A

staph aureus, e. coli, strep pneumoniae

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26
Q
  1. What test is necessary to definitively diagnose MM?
A

Bone marrow biopsy

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27
Q
  1. What 4 complications frequently occur in Waldenstrom macroglobulinemia?
A
  • visual impairment
  • neurological problems
  • bleeding
  • Raynaud phenomenon
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28
Q
  1. In which disease are flower cells seen? What is the prognosis of that disease?
A

Adult T-Cell Leukemia/ Lymphoma
tumor cells with multilobulated nuclei called “cloverleaf” or “flower” cells.
–Dz is rapidly progressing and fatal in months –1 year.

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29
Q
  1. 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.

1) Premycotic phase – inflammatory phase.
2) Plaque phase – raised, indurated, irregularly outlined, erythematous plaques.
3) Tumor phase – multiple, large (up to 10 cm or >), red-brown nodules correlates to systemic spread.

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30
Q
  1. Be able to stage Hodgkins based on the distribution of the disease (this is always a board question)
A

I–Involvement of a single lymph node region (I) or involvement of a single extralymphatic organ or site (IE).

II–Involvement of two or more lymph node regions on the same side of the diaphragm alone (II) or with involvement of limited contiguous extralymphatic organ or tissue (IIE).

III–Involvement of lymph node regions on both sides of the diaphragm (III), which may include the spleen (IIIS) and/or limited contiguous extralymphatic organ or site (IIIE, IIIES).

IV–Multiple or disseminated foci of involvement of one or more extralymphatic organs or tissues with or without lymphatic involvement.

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31
Q
  1. Which virus is associated with HL?
A

EBV

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32
Q
  1. What is strange about ETOH and Hodgkin lymphoma?
A

drinking etoh causes pain!

33
Q
  1. What’s the difference between Arteriosclerosis and Atherosclerosis?
A

Arteriosclerosis is a generic term for thickening and loss of elasticity of arterial walls.
Atherosclerosis, the most common pattern (99%), is a chronic inflammatory response of the arterial wall initiated by injury to the endothelium.

34
Q
  1. Know the steps of the non-specific vascular wall response to injury
A
  1. Endothelial “activation”
  2. Smooth muscle cell roles - vasoconstrict/dilate, make ECM, regulated by promotors & inhibitors
  3. Development, growth, remodeling - sum total of all processes
  4. Intimal “thickening” - key feature of non-specific and atherosclerosis
35
Q
  1. What are endothelial cell activators? What do the activators deactivate? (what types of products are normally secreted by the endothelium when the system is in balance and health)
A

cytokines, growth factors, bacteria, hemodynamic forces, viruses, lipid products, complement, hypoxia, cigarette smoke
These activators inhibit normal endothelial secretions - prostacyclin (inhibits platelet activation), thrombomodulin (inhibits thrombin), heparin (anticoagulant), & plasminogen (plasmin prescursor, dissolves fibrin)

36
Q
  1. Which products of clinical importance are produced by vascular smooth muscle?
A

Extracellular matrix, composed of collagen, elastin, and proteoglycans

37
Q
  1. Which of those decrease with the normal aging process? What effect does that have?
A

Elastin

Skin becomes less compliant, decreased turgor, skin feels more brittle, dry, like paper.

38
Q
  1. What is an AVM, and why does the vein dilate so much?
A

ArterioVenous Malformation, or an AV fistula - abnormal communication btw high pressure arteries and low pressure veins; usually congenital, or acquired by trauma or inflammation; the vein dilates in response to the high pressure it is exposed to from the artery; can be surgically clipped if there are 1 or 2, but many will result in a loss of perfusion; common cause of spontaneous brain bleed

39
Q
  1. What is the difference between a bruit and a thrill?
A

Bruits are unusual blood sounds on auscultation from turbulent flow. Thrills are the vibration associated with a murmur, detectible on palpation.

40
Q
  1. What is a fatty streak, and is it normal?
A

Cholesterol clefts - needle shaped washed out spaces in arteries; they are normal, develop in teens.

41
Q
  1. There are about 7 steps in the pathogenesis of atherosclerosis, what are they?
A

Chronic endothelial injury -> LDL/cholesterol in arterial wall -> Oxidation of lipoproteins -> monocytes migrate into endothelium -> platelet adhesion and activation -> migration of smooth muscle from media to intimate to activate macrophages -> proliferation of smooth muscle and ECM -> accumulation of lipids in cells and ECM

42
Q
  1. What are the 4 major MODIFIABLE risk factors for arteriosclerosis?
A

Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes

43
Q
  1. What was the real value of the Framingham study? (Beyond the basic one that if you decrease blood pressure you decrease the risk of having an MI)
A

It identified the major risk factors of atherosclerosis, of which several are modifiable. non-modifiable include increasing age, male gender, and family hx.

44
Q
  1. What percentage of hypertension is “essential”?
A

95% (essential = primary)

45
Q
  1. What are the two types of histopathological findings in vessel appearance with hypertension? (ie onion = hyperplastic etc)
A 
Hyaline = benign HTN, hyalinization of walls
Hyperplastic = malignant HTN, fibrinoid necrosis & onion skin of arteriole wall
46
Q
  1. How does the appearance of elastic fibers differ in normal vs. aneurysmal changes?
A

normal elastic fibers are parallel and overlapping, with very uniform spaces between. Aneurysmal elastic fibers are disrupted and fragmented, with some moved out of parallel arrangement, and with gaps between.

47
Q
  1. What are the potential sequelae of aneurysms?
A 
Rupture
Obstruction
Embolism
Compression (ureter, spine)
Mass effect
48
Q
  1. What are the potential symptoms of thoracic Aneurysms?
A 
Encroachment
Respiratory difficulties
Hoarseness
Dysphagia
Cough
Pain
Aortic valve dilatation
Rupture
49
Q
  1. What is a dissecting aneurysm?
A

Dissection = blood or hemorrhage disruption the wall of a large artery, and can be both a cause or an effect of aneurysm.

50
Q
  1. What is the most feared sequelae of temporal arteritis?
A

Blindness

51
Q
  1. Why is Takayasu Arteritis also called pulseless disease?
A

Because it is an inflammation of the aortic arch and other heavily-elastic arteries (subclavian), resulting in dramatically decreased peripheral pulse due to narrowing and rigidity.

52
Q
  1. What is so strange or unique about Thromboangiitis Obliterans or Buergers disease?
A

It is 100% resultant of cigarette smoking, and can be completely stopped by quitting.
It presents as dry gangrene, so tissue sloughs off and requires no amputation.

53
Q
  1. What organ system must be evaluated in young people with hypertension? What disease are you looking for, and which test do you use?
A

The kidneys. Renal HTN. Tests: CBC, urine dipstick, Ultrasound?

54
Q
  1. Why is the term Mycotic Aneurysm a misnomer?
A

A “mycotic” aneurysm is an aneurysm that has become secondarily infected, usually by bacteria. Hence mycotic (myco - fungus) is a misnomer.

55
Q
  1. Which class of diseseas usually have a vasculitis component?
A

Auto-immune - SLE, RA, etc.

56
Q
  1. Skin discoloration can be red, white or blue…. Which pathology is associated with each color?
A

Red -> hyperemia, hemangioma
White -> pallor, Raynauds
Blue -> cyanosis, Varicose veins, thrombophlebitis

57
Q
  1. What are the 5 P’s of arterial occlusion?
A 
Pain
Parasthesia
Pallor
Pulselessness
Paralysis
58
Q
  1. Do superficial varicose veins usually cause thrombophlebitis (DVT)?
A

90% DEEP veins of the legs, not superficial

59
Q
  1. At what level are DVT’s treated in the hospital with anticoagulation, vs outpatient anticoagulation?
A

Most patients with confirmed proximal vein DVT may be safely treated on an outpatient basis. Exclusion criteria for outpatient management are as follows:

  • Suspected or proven concomitant PE
  • Significant cardiovascular or pulmonary comorbidity
  • Iliofemoral DVT
  • Contraindications to anticoagulation
  • iherited coagulation deficiency/bleeding disorder
  • pregnancy
  • obesity
  • renal failure
60
Q
  1. What is an Inferior Vena Cava Interruption Filter or Greenfield Filter?
A

(medscape) Inferior vena cava (IVC) filter placement is most commonly indicated for deep venous thrombosis (DVT) or pulmonary embolism (PE) when anticoagulation therapy is contraindicated.
* *Inferior vena cava (IVC) filters are designed for their clot-trapping effectiveness and ability to preserve flow in the IVC

61
Q
  1. What causes lymphedema, what surgery is famous for causing this?
A 
Lymphatic channels blocked or scarred or absent. ANY damage to lymphatics can cause this.
Post surgical
 • Post radiation
 • Filaria
• Congenital
• Tumoral (peau d’orange- breast)
62
Q
  1. What is a hemangioma? How about a telangiectasia? Osler-Weber-Rendu? Port wine stain? Angiosarcoma? Hamartoma?
A

hemangioma: Often a generic term for ANY benign blood vessel tumor. Can be “Capillary” or “Cavernous”. Small vs large spaces.
telangiectasia: Spider veins.

Osler-Weber-Rendu: Hereditary Hemorrhagic . HHT is an autosomal dominant disorder characterized by vascular dysplasia and hemorrhage.Telangiectasia in the buccal mucosa!

Port wine stain: Congenital Nevus Flammeus

Angiosarcoma:Malignant and atypical vascular tumor. Early pulmonary metastases.

Hamartoma: Benign vascular tumors. Not a true neoplasm.

63
Q

What is the difference between angioplasty, stents and grafts?

A

Angioplasty -
Stent - permanent metallic mesh installed, patent longer than angioplasty, often drug coated to reduce clotting risk
Graft -

64
Q
  1. What is the cause of OCA? (do they have melanocytes?)
A

Melanocytes are present, but melanin production is inadequate.

65
Q
  1. What are the 4 components of acne vulgaris and which bacteria is implicated most often?
A

Keratin plugging blocking outflow of sebum
Hypertrophy of sebaceous glands
Colonization of follicle by lipase-synthesizing bacteria
*Propionibacterium acnes
Inflammation of the follicle

66
Q
  1. What is the difference between Erythema Marginatum and Erythema Migrans?
A

Marginatum - cutaneous manifestation of ARF, erythema at the margin, normal appearance in center of lesion, move rapidly across the skin (minutes to hours)
Migrans - cutaneous manifestation of Borrelia burgdorferi infection (Lyme dz), red macule or papule that expands, often with central clearing, and may have smaller lesions with indurated centers.

67
Q
  1. What virus causes Molluscum Contagiosum?
A

poxvirus (MCV)

68
Q
  1. What are the 3 microbiological causes of palms/soles rashes?
A

CARSS:
CA - Coxsackievirus A - hand, foot & mouth
R - Rickettsia Rickettsii - Rocky Mtn Spotted Fever
S - Syphilis (secondary)
S - TSS (staph aureus, strep pyogenes)

Other causes of palm/sole rashes exist that are non-microbiological (e.g. Kawasaki’s)

69
Q

vasculitidies: Temporal (Giant cell)arteritis

A
  • older adults
  • mainly arteries of head/temporal region, visible, palpable, surgically accessible
  • granulomatous wall inflammation diagnostic
  • assoc w/ESR elevation
  • anti-neutrophil Ab’s often positive
70
Q

vasculitidies: Takayasu arteritis

A
  • Involves aortic arch and highly-elastic arteries (subclav)
  • most common in young Asian women
  • Females disease
  • Necrosis
71
Q

vasculitidies: Polyarteritis nodosa PAN

A
  • any medium or small artery, often visceral
  • infarcts, aneurysms, ischemia
  • classical auto-immune dz - SLE, RA, SS
  • segmental, transmural, necrotizing inflammation
  • sometimes anti-neutrophil Ab’s, esp smaller vessel dz
72
Q

vasculitidies: Kawasaki Dz

A 
Children <4
• Coronary arteries
• LEADING cause of ACQUIRED heart disease in children
• USA and JAPAN
• Fatal in only 1%
• Red tongue, adenopathy
• Anti-endothelial cell abs
73
Q

vasculitidies: Microscopic polyangiitis hypersensitivity vasculitis/ leukocytoclastic vasculitis

A
  • all types of small vessels (veins, capillaries)
  • fragmented neutrophils
  • most are allergic rxns to allergens (penicillin, strep)
  • dermatologist’s dz
  • nuclear “dust” from neutrophils - leukocyto”clasia”
74
Q

vasculitidies: Wegener Granulomatosis

A
  • M>F, 40s
  • acute necrotizing granulomas of upper+lower resp tract
  • often renal involvement, “crescentic” glomerulonephritis
  • anti-neutrophil-cytoplasmic-Ab’s (anca) usually present
  • mortality improved, recurrence main concern
75
Q

vasculitidies: Thromboangiitis obliterans/ Buerger Dz

A
  • 100% caused by cigarette smoking
  • M»>F, 30s, 40s
  • often arteries 100% obliterated => obliterans
  • Extremeties most often involved
76
Q

In leukocytosis, what does neutrophil predominance indicate?

A 
Neutrophils:
 • bacterial infxns
• acute inflammation
• necrosis
• myocardial infarction (MI)
77
Q

In leukocytosis, what does lymphocyte predominance indicate?

A

lymphocytes

  • acute viral infxn (EBV, CMV)
  • chronic inflammation/ infection (TB)
78
Q

In leukocytosis, what does eosinophil predominance indicate?

A

eosinophils:
• allergy (drugs, foods, inhalants)
• parasitic infxn

pathology year 2 term 1 (1 decks)

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