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Heme 1 > final > Flashcards

final Flashcards

1
Q

B lymphocytes are derived from

A

BM stem cells

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2
Q

B cells mature into

A

plasma cells that secrete IGs

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3
Q

MC IG?

A

IgG

IgA is in the gut

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4
Q

these IGs are seen in hypersensitivity rxns

A

IgD/IgE

two heavy and light chains

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5
Q

what is complement

A

-Lysis of bacteria or blood cells
-opsonize (coat) bacteria/blood cells for phagocytosis
-Immunoglobulins presenting to T-cells
Develops in the spleen, fully developed by 5-6 years of age (we don’t want to remove spleen before this)

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6
Q

AIDS

A
  • RNA virus with 3 groups
    1) group specific Ag
    2) reverse transcriptase and integrase
    3) envelope codes to envelope proteins
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7
Q

when an infected HIV cell goes into replicative phase what is happening?

A

the provirus will produce mRNA and RNA to create new HIV virions

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8
Q

normal CD4+ count vs AIDS count

A

normal-800-1000

AIDS-<400

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9
Q

which cells does HIV infect?

A

CD4 (helper T cells)

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10
Q

how to dx AIDS?

A

ELISA
Western Blot
may nto be positive for 3 months after exposure

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11
Q

how to treat AIDS?

A

HAART (higly active anti-retro viral therapy)

type reverse transcriptase inhibitors and a protease inhibitor

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12
Q 
Diploid
Haploid
Aneuploid
Hyperdiploid
Hypodiploid
Psuedodiploid
A 
Diploid = 46 chromosomes
Haploid = 23 chromosomes
Aneuploid = more or less than 46 chromos.
Hyperdiploid = more than 46 chromosomes
Hyplodiploid = less than 46 chromosomes
Pseudodiploid = 46 with chr rearrangement
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13
Q

tumor suppressor genes inhibit cell division. Loss of one allele may predispose to certain tumors suh as

A

retinoblastoma

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14
Q

Philadelphia Chromosome + in ALL indicates

hyperdiploidy in ALL indicates

A

poor prognosis

favorable prognosis

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15
Q

Blast cells fail to differentiate but divide - result is bone marrow failure

A

acute leukemia

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16
Q

MC form of leukemia in children (3-5)

A

acute lymphoblastic leukemia
-CD 10+ precursor B type is a marker on the cell that shows equal sex distribution
-CD 10- T type is MC in males
If kid keeps get sick every few weeks, then after a while they have swollen lymph nodes/spleen/liver
Blood count smear will be full of blasts, then do a bone marrow (normal person would have 5% blast cells,25-40%)
Liver/spleen can start to make red cells which causes them to get bigger

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17
Q

AML is seen in

A
  • any age group
  • less common in kids than ALL
  • Auer rods seen
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18
Q

M0-M7 classification is used for

A

AML

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19
Q

FAB classification is used for

A

ALL

mediastinal lymph nodes are common with ALL

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20
Q

Breaking tumor cells down releasing all intracellular contents into blood

A

tumor lysis syndrome, give allopurinol

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21
Q

when to perform BMT on ALL vs AML

A

ALL- second remission

AML-first remission

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22
Q

CML is seen in

A
  • middle aged pts
  • Ph +
  • 70% change to ALL/AML (when this happens they are dead within a year)
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23
Q

when do CML pts need a transplant by?

A

age 55

24
Q

CLL is mainly seen in

A

adults
Mikulicz’s Syndrome = salivary & lacrimal inability to produce these fluids
doesn’t transform into acute

25
Q

Reed Sternberg cells are seen in

A

Hodkins disease

26
Q

how does Hodkin’s present?

A

Present with painless, non-tender, asymmetrical enlarged superficial nodes, fever, weight loss, night sweats

27
Q

this histological finding shows the best prognosis for Hodgkin’s

A

lymphocyte predominance

28
Q

stages of Hodkins

A

1-one set of lymph nodes
2-2 sets of lymph nodes on same side of body
3-lymph nodes above and below diaphragm
4-outside involvement
B indicates fever, night sweats, weight loss (10%) - over 6 mos
S indicates splenic involvment

29
Q

hwo to dx hodgkins

A
  • CXR
  • Bone Marrow
  • CT
30
Q

hodgkin’s treatment?

A

stage I and IIa get radiation

stage IIb, III, IV get radiation and chemo

31
Q

NHL is a disease of which cells?

A

B lymphocytes

32
Q

presentation of NDL

A

Anemia, neutropenia (infections), thrombocytopenia (purpura)
Hepatosplenomegaly (organ involvement)
Enlarged mesenteric/retroperitoneal nodes

33
Q

NHL prognosis is based on

A

histology

34
Q

HDL tx?

A

autologous marrow transplant to cure patient if radiation or chemo doesn’t work

35
Q

Burkitt’s

A

B-lymphoblastic lymphoma
Massive jaw lesions, extranodal abdominal & ovarian involvement in African children
“Starry Sky”

36
Q

Multiple Myeloma

A

-Proliferation of BM plasma cells
-Lytic bone lesions (holes in the bone)
-Bence Jones protein/paraprotein
ex-person walking and falls, has a fracture

37
Q

clinical features of MM

A
  • bone pain
  • anemia
  • repeated infections
38
Q

how to dx MM?

A
  • alk phos
  • High BUN (higher the BUN, less life expectancy)
  • renal failure
39
Q

how to tx MM?

A
  • chemo
  • allopurinol
  • BMT for younger
40
Q

polycthemia vera

A
  • increased RBCs

- Becomes sludgy/sticky and plugs up vessels in brain causing HAs, blurry vision, dyspnea

41
Q

secondary polycythemia

A

-compensatory increase in erythropoieten from
-higher altitudes
-cardiac disease
pulmonary disease

42
Q

Kid w/rash on butt down to feet
Vessels break leading to bruises
The kid is fine, make sure to test urine and guaiac for bleeding
Treat with steroids, usually self limiting

A

Henoch-Schoenlein Syndrome
Immune complex hypersensitivity reaction
Usually children following an acute infection

43
Q

hemolytic uremic syndrome is caused by

A
  • E. Coli
  • pt presents with bloody diarrhea
  • treat with plasmapharesis and plasma transfusion
44
Q

ITP

A

Idk why but you have no platelets
Typically follows infection, abs are continued to be made and they attack platelets
Occurs in the spleen, can remove the spleen and this will cure, increases platelet count a SHIT ton
Rash doesn’t blanch
No treatment necessary just follow the platelets, can give steroids and taper, above 30/40k then leave it alone
IV IG in the hospital will cure
Rh+ give rhogam

45
Q

intrinsic pathway activates factor

A

XII—>XI—>IX—->vWF + VIII—–>X

46
Q

extrinsic pathway activates factor

A

VII—–>X

crush injury will activate this

47
Q

factor X becomes….

A

prothrombin which turns into thrombin

fibrinogen which turns into fibrin

48
Q

fibrin degradation product is called

A

d-dimer

49
Q

hemophilia a

A

missing factor VIII

50
Q

how to treat hemophilia A

A

Give the recombinant medication every day via IV for a normal life

51
Q

hemophilia b -christmas disease

A

missing factor IX

52
Q

how to treat hemophilia b?

A

This is blood bank stuff, no manmade med

Given every second or third day

53
Q

VWD

A
  • autosomal dominant
  • MC general hemophilia
  • helps protect factor XIII
  • Platelets don’t function properly, don’t close up the hole
54
Q

From sepsis, meningitis, etc

Clotting everywhere! Put person on heparin

A

DIC

55
Q

DIC triad

A
  • thrombocytopenia, decreased fibrinogen, increased split products (FDP)

Heme 1 (4 decks)

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