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Path II Final > Study Guide > Flashcards

Study Guide Flashcards

0
Q

Neutrophilia

A

Bacterial infxns, acute inflammation, necrosis, MI

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1
Q

Toxic granulation

A

Dark coarse granules found in granulocytes (esp neutrophils) dt impaired cytoplasmic maturation because trying to generate large numbers.
Seen in peripheral blood of pts w inflammatory conditions (esp sepsis)

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2
Q

Lymphocyte predominance

A

Acute viral infxn (EBV, CMV, viral hepatitis) and chronic inflammation (TB, etc)

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3
Q

Eosinophilia

A

Allergy (drugs, food, inhalants), parasitic infxn

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4
Q

What is bandemia and what does it suggest?

A

Excess band/immature WBCs released by BM into blood.

Infection, sepsis, inflammation

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5
Q

Mesenteric adenitis

A

Inflammation of mesenteric LNs in abdomen. Bacterium–Yesira entercolitica. If in RLQ can be confused w appendicitis.
Has pharyngitis, HA, NO vomiting, NO rebound tenderness

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6
Q

Cells in paracortical areas of LNs

A

T cells

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7
Q

Cells in secondary lymphoid follicle

A

Mostly B cells

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8
Q

Cells in medullary cords of LNs

A

Macrophages and plasma cells

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9
Q

Enlarged LN dt follicular hyperplasia is assoc w

A

Activated humoral response–RA, toxoplasmosis, early stages of HIV infxn.
Activate B cell rich germinal centers

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10
Q

Enlarged LN dt paracortical lymphoid hyperplasia is assoc w..

A

Distention and prominence of lymphatic sinusoids/nodes draining cancers–carcinoma of breast
Cells involved: endothelial cells and histiocytes

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11
Q

2 types of genetic derangements that cause WBC neoplasms…

A

Chromosome translocation

Oncogenes

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12
Q

How does the presentation of Hodgkin’s lymphoma differ from Non-Hodgkin’s re tenderness and location?

A

All Hodgkin’s: non tender.

2/3 non-Hodgkin’s: non tender. 1/3 extra nodal sites (skin, stomach, brain, etc)

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13
Q

Majority of lymphoid neoplasms…

A

B-cell origin (80-85%)

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14
Q

How does Hodgkin’s lymphoma spread?

A

Orderly, LN to LN

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15
Q

Which lymphoma has reed Sternberg cells?

A

Hodgkin’s

Non-Hodgkin’s has mutated B cells or T cells

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16
Q

Hodgkin’s vs non-Hodgkin’s

A

HL: 15-24 yrs, >60yrs. 1% of cancers/15% lymphomas. Begins in neck lymph nodes.
NHL: >60yrs. 4% of cancers/85% of lymphomas. Can begin anywhere. Less orderly, more aggressive, caught in advanced stages

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17
Q

Characteristics of ALL

A

Predominant precursor B cell tumors and manifests in childhood
T cell ALL: less common, present in adolescent males, thymic involvement.

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18
Q

ALL chromosomal abnormality

A

Hyperploidy (>50 chromosomes), Philadelphia chromosome t(9,22)

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19
Q

Most common leukemia of adults in western world?

A

CLL

*only leukemia not assoc w radiation or drug exposure

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20
Q

In which disease are smudge cells seen?

A

CLL

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21
Q

Morphology of CLL

A

BM involvement. SLL tumor cells usu infiltrate the splenic white and red pulp and hepatic portal tracts. Chromosomal trans locations are rare. Distinct immunophenotype.

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22
Q

Clinical presentation of CLL

A

Average 60yrs, M:F 2:1, survival 4-6 yrs. lymphadenopathy and hepatosplenomegaly.
GI infiltrates–> diarrhea, malabsorption, ulcers, megaloblasric anemia.
Disrupted immune fxn (hypogammaglobulinemia, antibodies to RBCs or platelets)
Fatigue, wt loss, anorexia, DOE, abdominal fullness, LA

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23
Q

Most common form of non-Hodgkin’s lymphoma

A

Follicular lymphoma

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24
Q

What infections assoc w NHL?

A

EBV, human T cell leukemia virus, Hep C virus, H pylori, kaposi sarcoma assoc herpes virus

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25
Q

What does the genetic translocation leading to follicular lymphoma cause

A

Over expression of BCL2 protein, antagonist of apoptosis, promotes survival of follicular lymphoma (expressed 90% of cases)

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26
Q

Burkett Lymphoma categories

A

African (endemic) Burkitt lymphoma
Sporadic (nonendemic) Burkitt lymphoma
Subset of aggressive lymphoma in HIV–highly undiff B cell lymphoma that involves sites other than LNs and RE sys

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27
Q

Burkitt Lymphoma morphology

A

Intermediate sized lymphoid cells. Starry sky pattern in LN. Numerous macrophages w infested nuclear debris surrounded by clear space

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28
Q

Clinical presentation of Burkitt lymphoma

A

Children and young adults in 30% of childhood NHL in US
Extranodal sites.
Endemic: Mass in mandible and abdominal viscera
Sporadic: ileocecum or peritoneum w large abdominal mass
Involvement of BM and blood is rare
Aggressive cancer that responds to high dose, short term chemo

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29
Q

Multiple myeloma vs waldentrom macroglobulinemia

A

MM: plasma cell myeloma. Most import and common monoclonal gammopathu
WM: high IgM–> blood hyperviscosity. Seen in adults w lymphoblastic lymphoma

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30
Q

Infections common in pts w multiple myeloma…

A

Bacteria–S pneumo, S aureus, E. coli–most common cause of death (decreased immunoglobulins)

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31
Q

Test to diagnose MM

A

BM examination

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32
Q

What 4 complications in waldentrom macroglobulinemia?

A

Visual impairment, neurological problems, bleeding, cryoglobulinemia (Raynaud’s and cold urticaria)

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33
Q

In which disease are flower cells seen? What is prognosis?

A

Adult T cell leukemia/lymphoma. Fatal in months-1 year

34
Q

Which immune cells cause mycosis fungoides/ Sezary syndrome? What are three stages of the lesion?

A

Tumor of CD4+ helper T cells. Involves the skin

1) premycotic, 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

35
Q

Be able to stage Hodgkin’s based on distribution of the disease

A

1) single LN or single extranodal organ or site
2) 2+ LNs on same side of diaphragm
3) LNs on both sides of diaphragm or spleen and extranodal site
4) disseminated foci

36
Q

Which virus is assoc w Hodgkin’s lymphoma?

A

EBV

37
Q

What effect does alcohol have on Hodgkin’s?

A

Pain in involved LNs.

38
Q

Arteriosclerosis

A

Blood vessels become thick and stiff, sometimes restricting blood flow to your organs and tissues

39
Q

Atherosclerosis

A

Buildup of cars, cholesterol and other substances in and on artery walls–plaques–which can restrict blood flow

40
Q

Steps of non specific vascular wall response to injury

A

Endothelial activation
Smooth muscle cells
Development, growth, remodeling
Intimal thickening

41
Q

What are endothelial cell activators? What do they deactivate?

A

Cytokines, GFs, bacterial products, hemodynamic forces, lipid products, viruses, complement, hypoxia, cigarette smoke

Deactivate: products of ECM–collagen, elastin, proteoglycans

42
Q

What does vascular smooth muscle produce?

A

ECM–collagen, elastin, proteoglycans

43
Q

Arteriovenous malformation

A

AVM. Abnormal connection between arteries and veins. Well known in CNS but happens anywhere.
Get progressively larger over time as volume of blood flow increases. Can –> nidus, a tangle of blood vessels without capillaries. Extremely fragile, prone to bleeding

44
Q

Bruit

A

Sound or murmur heard upon auscultation.

45
Q

Thrill

A

A vibration felt by the practitioner during palpation

46
Q

What is a fatty streak? Is it normal?

A

first grossly visible leison in atherosclerosis. Irregular yellow-white on lumen of artery, made of foam cells (and maybe T cells, platelets, smooth muscle cells). Precursor of atheromas that may –> plaques.
Not normal. Beginning of pathology. Common.

47
Q

7 (8) steps in 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 SM and ECM
8) accumulation of lipids in cells and ECM

48
Q

4 major MODIFIABLE risk factors for arteriosclerosis

A
  • Hyperlipidemia
  • Hypertension
  • Cigarette Smoking
  • Diabetes Mellitus
49
Q

real value of the Framingham study

A

4 main causes arteriosclerosis.

study gave us “risk factors” and geared medicine on a path of prevention. It also demonstrated the pros and cons of giving medicine specifically tailored to meet the needs of the
individual versus giving medicine that works for most. (i.e. some medications given for heart conditions were causing stroke in some individuals)

50
Q

percentage of hypertension is “essential”?

A

95%

51
Q

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

52
Q

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

A

NORMAL arteries will have short, tight elastic fibers much like rubber bands
Arteries with ANEURYSMAL CHANGES will show DISRUPTED, FRAGMENTED elastic fibers

53
Q

potential sequelae of aneurysms

A
  • Rupture
  • Obstruction
  • Embolism
  • Compression
  • Ureter
  • Spine
  • Mass effect
54
Q

potential symptoms of thoracic Aneurysms

A 
• Encroachment
• Respiratory difficulties
• Hoarseness
• Dysphagia
• Cough
• Pain
Complications?
• Aortic valve dilatation
• Rupture
55
Q

dissecting aneurysm

A

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

56
Q

Characteristics of the various vasculitides

A

Mostly arteries!
• Infectious (5%) vs. Non-infectious (95%)
• NON-infectious are generally “AUTO”-IMMUNE. Why? Persistent findings: Immune
complexes, ANTI-NEUTROPHIL AB’s (Wegener’s, “Temporal”), ANTI-ENDOTHELIAL CELL
AB’s (Kawasaki)
• Often DRUG related (Hypersensitivity, e.g.), especially small blood vessels.
Temporal/giant cell=mostly adults, blindness
Kawasaki=red tongue, children, coronary. USA and Japan.
Takayasu=subclavian blockage
Polyperiarteritis nodosa=small or medium, visceral arteries

57
Q

What is the most feared sequelae of temporal arteritis?

A

blindness

58
Q

Why is Takayasu Arteritis also called pulseless disease?

A

Subclavian blockage present
as pulseless upper extremities (arms, hands, and wrists with weak or absent pulses on
the physical examination).

59
Q

characteristics of Kawasaki Disease?

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, chest pain.

60
Q

unique about Thromboangiitis Obliterans or Buergers disease?

A

100% caused by cigarette smoking, MEN»>F, 30’s, 40’s

61
Q

What organ system must be evaluated in young people with hypertension?

A

Renal system. Renal artery
stenosis. Poor blood flow to the kidneys because of obstructed lumen. Kidney wants
to increase blood flow so it produces all sorts of substances to increase peripheral
resistance and get more blood flow through the glomerulus. Dx with ultrasound,
check anyone under 35 years old with hypertension.

62
Q

Why is the term Mycotic Aneurysm a misnomer?

A

A “mycotic” aneurysm is any
aneurysm that has become secondarily infected, usually by bacteria.
And mycotic means fungus!

63
Q

Which class of diseases usually have a vasculitis component?

A

Most classical systemic auto-immune diseases have an element of vasculitis.
3 magnets for Ag-Ab complexes: GBM, synovia, and blood vessels!!!

64
Q

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

A 
White = PALLOR
Blue = CYANOSIS
Red = HYPEREMIA
65
Q

the 5 P’s of arterial occlusion?

A

Causes skin to turn white: Paresthesia, Pain,

Pallor, Pulselessness, Poikilothermia(Polar)

66
Q

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

A

Varicose veins are related to increased venous pressure, age, valve dysfunction.
Venous stasis ulcers arise when venous valves that exist to prevent
backflow of blood do not function properly, causing the pressure in veins to increase.The body needs the pressure gradient between arteries and veins in order for the heart to pump blood forward through arteries and into veins. When venous
hypertension exists, arteries no longer have significantly higher pressure than veins,
and blood is not pumped as effectively into or out of the area. Venous hypertension
may also stretch veins and allow blood proteins to leak into the extravascular space,
isolating extracellular matrix (ECM) molecules and growth factors, preventing them
from helping to heal the wound. Leakage of fibrinogen from veins as well as
deficiencies in fibrinolysis may also cause fibrin to build up around the vessels,
preventing oxygen and nutrients from reaching cells.Venous insufficiency may also
cause white blood cells (leukocytes) to accumulate in small blood vessels, releasing
inflammatory factors and reactive oxygen species (ROS, free radicals) and further
contributing to chronic wound formation. Build-up of white blood cells in small blood
vessels may also plug the vessels, further contributing to ischemia.

67
Q

Do superficial varicose veins usually cause thrombophlebitis (DVT)?

A

No, 90% of DVTs

come from DEEP veins

68
Q

At what level are DVT’s treated in the hospital with anticoagulation, vs outpatient anticoagulation?

A

DVT is below the knee, treated with anticoagulants outpatient
ABOVE knee, treated in the hospital.

69
Q

What is an Inferior Vena Cava Interruption Filter or Greenfield Filter?

A

“Umbrella”mechanical system put in the IVC, catching the incoming clots in the “umbrella”.
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)

70
Q

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

A

damage to lymphatics, ie surgery, radiation. Mastectomy most famous.

71
Q

hemangioma?

A

Benign blood vessel tumor that is red and can be blanched. CAPILLARY (juvenile, birthmarks, small vascular spaces) and CAVERNOUS (adult, do not regress, LARGE vascular spaces).

72
Q

telangiectasia?

A

dilation of the capillaries, which causes them to appear as small red or purple clusters, often spidery in appearance, on the skin or the surface of an organ.
Osler-Weber-Rendu? a rare genetically disorder that affects blood vessels throughout the body –> a tendency for bleeding. HHT is an autosomal dominant disorder characterized by vascular dysplasia and hemorrhage. The prognosis for patients with
the disease is good as long as bleeding is promptly recognized and adequately controlled.
Port wine stain (Nevus flammeus)? It is almost always a birthmark. It is
caused by a vascular anomaly (a capillary malformation in the skin).

73
Q

angioplasties

A

Balloon. Plaque fracture (crackling sound), Dissection, Arterial dilatation initially, Restenosis ~6 months.

74
Q

Stents

A

Metallic mesh, Permanently placed, Stays patent longer than

angioplasty, OFTEN DRUG COATED, Goals: Prevent thrombosis, Prevent spasm, Delay RE-stenosis.

75
Q

Grafts

A

400,000 CABG grafts per year in USA, take a chunk from Saphenous v., Internal mammary a. (internal thoracic a.)
50% patent after 10 years, for saphenous v., 90% patent after 10 years, for mammary a., Endothelial and smooth muscle migration and
proliferation are key factors for success

76
Q

What is cause of OCA?

A

albinism. Inherited disorders in which

melanocytes are present, but melanin production is inadequate

77
Q

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

A
  1. Keratin plugging blocking the outflow of sebum due to changes in the infundibulum of the follicle
  2. Hypertrophy of the sebaceous glands. Often the result
    of hormonal stimulation
  3. Colonization of follicle by lipase-synthesizing bacteria -
    Propionibacterium acnes
  4. Inflammation of the follicle, due in part to the breakdown
    of the sebum into pro-inflammatory fatty acids.
78
Q

Erythema Marginatum

A

cutaneous manifestation of acute rheumatic fever (ARF); A

post-infectious, immune-mediated complication of GABHS pharyngitis.

79
Q

Erythema migrans

A

Bulls eye. cutaneous manifestation of infection with Borrelia burgdorferi
– Lyme disease. Vector: Ixodes scapualris – deer tick.

80
Q

What virus causes Molluscum Contagiosum

A

A poxvirus skin infection

81
Q

What are the 3 microbiological causes of palms/soles rashes?

A

CARS
• CA- Coxsackievirus A: Coxsackie virus (hand, foot and mouth disease)
• R- Rickettsia Rickettsii: Rocky mountain spotted fever (centrifugal rash)
• S- Syphilis (secondary)
(• TSS is the honorary other one that fits this category)

82
Q

Angiosarcoma?

A

Rare, have to stain with Ab agains Van willibrands factor, nucleus will be oddly shaped

83
Q

Hamartoma?

A

It is a benign, focal malformation that resembles a neoplasm in the
tissue of its origin. 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 that site, but which are growing in a disorganized mass.

Path II Final (3 decks)

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