Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Path 2 > Block 1 > Flashcards

Block 1 Flashcards

1
Q

Chromosomal mutation alpha thalassemia

A

Chromosome 16

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Chromosome mutation beta thalassemia

A

Chromosome 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Chronic myeloid leukemia mutation

A

t(9;22) - Philadelphia chromosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Myelodysplastic disorder mutation

A

Deletion on chromosome 5 or 7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Myeloproliferative disorders mutation

A

JAK2 (tyrosine kinase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

B cell chronic lymphocytic leukemia has aberrant expression of ___

A

CD5 B cells have two digit markers T cells have single digit markers Plasma cells have triple digit markers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Follicular lymphoma mutation

A

t(14;18) Over expression of Bcl2 behind Ig promoter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mantle cell lymphoma mutation

A

t(11;14)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Burkitt’s lymphoma mutation

A

t(8;14) c-MYC also t(8;22) or t(2;8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Differentiate Hodgkin or non-Hodgkin lymphoma Age > 60 +/- B symptoms Single, generalized, non-contiguous lymphadenopathy B or T cell proliferation Variable prognosis

A

Non-Hodgkin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Differentiate Hodgkin or non-Hodgkin lymphoma Age variable Prominent B symptoms Contiguous, rarely generalized lymphadenopathy Reed-Sternburg, reactive cells Good prognosis

A

Hodgkin lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MC leukemia >60 yo Asymptomatic Lymphocytes, spleen, and LN Autoimmune hemolytic anemia Small, round lymphocytes, diffuse growth, proliferation centers. Smudge cells CD19+, CD20+, CD5+, CD23+ FMC7- Deletions or trisomies Indolent course

A

B cell lymphoma CLL or SLL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Generalized lymphadenopathy +/- B symptoms Follicular growth, mixed small and large cells Bone marrow paratrabaecular lymphoid aggregate CD19+, CD0+, CD10+ Germinal centers are Bcl2+ t(14;18) Bcl2 Indolent course

A

Follicular lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chronic inflammation tissue mass Gastric (H. Pylori), thyroid (Hashimoto’s), eye, lung Epithelial destruction Gastric, diffuse infiltration by lymphocytes CD19+, CD20+ CD5-, CD10- t(11,18), resistant to antibiotics

A

Extranodal Marginal Zone Lymphoma (MALToma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Splenomegaly, bone marrow fibrosis-dry tap, cytopenia Hairy cells Fried egg Myelofibrosis CD19+, CD20+, CD11c+, CD25+, CD103+ Tartrate resistant acid phosphatase (TRAP) BRAF mt Indolent course

A

Hairy cell leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Waldenstrom Macroglobulinemia - IgM monoclonal protein - hyper-viscosity, vision, neuro, bleeding, cryoglobulin (Raynaud’s), lymphadenopathy, splenomegaly Lymphocytes and plasma cells Rouleux RBCs IgM serum protein CD19+ and CD20+ lymphocytes CD138+ plasma cells Indolent course

A

Lymphoplasmacytic lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Enlarging node/mass, B symptoms, de novo or transformation form low grade Common in HIV+, especially in brain Diffuse growth, large cells CD19+, CD20+, CD10 +/- Ki67 proliferation marker Aggressive course

A

Diffuse large B cell lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Enlarging node/mass (terminal ileum) B symptoms Endemic in jaw in Africa, 100% EBV Sporadic HIV+ Diffuse growth Starry sky (apoptosis) Basophilic cytoplasm vacuoles CD19-, CD20+, CD10+ Ki67+ proliferation marker t(8;14) c-MYC Aggressive course

A

Burkitt lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Lymphadenopathy, splenomegaly, GI tract, B symptoms Diffuse growth Cleaved cells CD19+, CD20+, CD5+, FMC7+ CD23- Cyclin D1 + t(11;14) cyclinD1 Promotes progression through the cell cycle Aggressive course

A

Mantle cell lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

CRAB Calcium elevation Renal complications Anemia Bone disease Elderly, 2x blacks Increased infections Urine Bence-Jones protein Amyloidosis- Congo red stain, Apple green birefringence Lyric, punched-out lesions Hyper-viscosity- headaches, fatigue, bruising, GI bleeding, vision abnormalities just as retinopathy IgG >3g/dL (serum M spike) Plasma cells > 20-30% in bone marrow CD19-, CD20- CD138+ Cytoplasmic light chain Translocations, gains or deletions Progressive course

A

Plasma cell myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Asymptomatic, labs negative IgG < 3g/dL Plasma cells < 10% 1% per year —> myeloma

A

Monoclonal gammopathy of unknown significance (MGUS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Leukocytosis, lymphadenopathy, splenomegaly, hypercalcemia, rash HTLV1+ Japan, Caribbean, Africa -mycoses fungoides -Sezary syndrome Lymphocytosis Clover leaf, flower cell CD3+, CD4+ Reverse transcriptase + Aggressive

A

Adult T cell leukemia/lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Abdominal pain, weight loss, diarrhea, obstruction, celiac disease Small intestine, intraepithelial T cells Villous atrophy, ulcer, mass CD3+ Aggressive

A

Enteropathy associated T cell Lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Lymphadenopathy, extranodal sites Adult and children Large pleomorphic cells (hallmark cells) CD30+, ALK+, CD15- t(2;5) Good prognosis unless ALK-

A

Anaplastic large cell lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Destructive mass, commonly nasopharyngeal EBV associated Asia Destruction of blood vessels, necrosis CD3+, CD8+ T cells CD56+ NK cells Aggressive course

A

Extranodal NK/T cell lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cutaneous lesions, patches, plaques, nodules Epidermotropism Pautrier’s microabscesses Cerebriform nuclei CD3+, CD4+ Indolent course Palliative treatment but not curative

A

Mycoses fungoides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Aggressive systemic variant of cutaneous T cell lymphoma Generalized erythroderma Lymphadenopathy Leukocytosis Cerebriform nuclei

A

Sezary syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Unifocal- adults, lytic bone lesion Multifocal- children, multiple lytic lesions, skin, hepatosplenomegaly Oval cells, grooved cells Birbeck granules on electron microscopy CD1a+ S100+

A

Langerhans cell histiocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Differentiate Classical Hodgkin’s (CHL) and Nodular Lymphocyte Predominant Hodgkin (NLPH) Age variable Single or contiguous LN Classical, lacunar, mononuclear cell type CD30+, CD15+ CD20- EBV+/- Good prognosis

A

CHL Includes: Nodular sclerosis Hodgkin lymphoma Mixed cellularity Hodgkin lymphoma Lymphocyte depleted Hodgkin lymphoma Lymphocyte rich Hodgkin lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Differentiate Classical Hodgkin’s (CHL) and Nodular Lymphocyte Predominant Hodgkin (NLPH) Male <35yo Single LN Nodular, RS cell Popcorn cells Background cells- lymphocytes CD20+ CD30-, CD15- EBV- Very good prognosis

A

NLPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

70% of all CHL Young patients Mediastinal +/- B symptoms Broad collagen bands Nodules Classic RS cell, lacunar cells Background cells: eosinophils, neutrophils, lymphocytes CD30+, CD15+ CD20- EBV+

A

Nodular sclerosis Hodgkin lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

CHL Older patients B symptoms No fibrosis Classic RS cells Background cells: eosinophils, neutrophils, lymphocytes CD30+, CD15+ CD20- EBV ++

A

Mixed cellularity Hodgkin lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

CHL Older adults HIV+ Developing countries No fibrosis Classic RS cells Background cells: histiocytes and fibroblasts CD30+, CD15+ CD20- EBV+

A

Lymphocyte depleted Hodgkin lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

CHL rare Young patients usually no B symptoms Nodular growth Classic RS cells Background cells: lymphocytes CD30+, CD15+ CD20- EBV+ infrequent

A

Lymphocyte rich Hodgkin lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Splenectomy increases risk of infection with ___ bacteria

A

Encapsulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Epithelial neoplasm of the thymus Lymphocytes are non neoplastic Adults with SOB and a mediastinal mass Paraneoplastic syndrome Myasthenia gravis Pure red cell aplasia Graves, pernicious anemia, dermatomyositis Tx: resection Invasion decreases outcome

A

Thymoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Identify the disease

A

Iron deficiency anemia

Hypochromic and microcytic RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Identify the disease

A

Anemia of chronic disease

Increased Ferritin

Decreased serum iron

Decreased transferrin

Decreased % saturation

Decreased TIBC

Increased FEP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Identify the disease

A

Sideroblastic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Identify the diseases (2)

A

Target cells

EITHER:

sickle cell anemia (normocytic, extravascular hemolysis)

B thalassemia (microcytic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Identify the diseases (2)

A

Expanded hematopoiesis

EITHER:

sickle cell anemia (normocytic, extravascular hemolysis)

B thalassemia (microcytic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Identify the diseases (2)

A

Megaloblastic anemia

Either: B12 or folate deficiency

Enlarged RBCs and WBCs, including neutrophils which appear as hypersegmented

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Identify the cell type

Appears in ___ anemias

A

Reticulocytes

Normocytic anemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Identify the disease

A

Hereditary spherocytosis

Extravascular hemolysis and normocytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Identify the disease

A

Sickle cell anemia

Extravascular hemolysis and normocytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Identify the disease

A

Hemoglobin C

HbC crystals in RBCs

Extravascular hemolysis and normocytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Identify the substance present in this slide

A

Hemosiderin

Iron storage not readily available

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Identify the disease

A

G6PD

Heinz bodies and Bite cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Identify the disease

A

Immuno hemolytic anemia (IHA)

RBC agglutination, can be due to IgG or IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Identify the disease

A

Microangiopathic hemolytic anemia

Schistocytes and Helmet cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Identify the disease

A

Aplastic anemia

Bone marrow is replaced by fat cells

Normocytic anemia with decreased production of RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Differentiating leukemoid reaction from CML

Leukemoid reaction:

Asymptomatic or symptomatic?

Present/not toxic granulation?

Present/not basophils?

Present/not increased alkaline phosphatase?

Present/not altered genetics?

A

Symptomatic

Present toxic granulation

Absent basophils

High LAP

Normal genetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Identify the disease

A

Leukemoid Reaction

Band cells

high LAP

ABSENT BASOPHILS (CML)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Identify the disease

A

CML

PRESENT BASOPHILS

Increased blast cells (left shift)

Low LAP

t(9;22)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Infectious Mono or B cell lymphoma (CLL/SLL)?

young patient

Fever, pharyngitis, LN and splenomegaly

Acute

Atypical lymphocytes

Positive Monospot/EBV

Normal flow cytometry

Self-limiting

A

Infectious mononucleosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Identify the disease

A

Infectious mononucleosis

Atypical but BENIGN lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Identify the disease

A

B cell lymphoma (CLL/SLL)

small lymphocytes with condensed chromatin and scant cytoplasm

Smudge cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Identify the disease

2:1 kappa:lambda light chain ratio

A

Reactive follicular hyperplasia

Normal light chain ratio, therefore not malignant (malignant shows 1 LC)

59
Q

Identify the disease

A

Polycythemia vera

Giant platelets

Hypochromia as a result of repeated phlebotomy

60
Q

PV or Secondary Polycythemia?

Elevated WBC and platelets

Splenomegaly

Normal o2

low EPO

Bone marrow shows all myeloid cells

Abnormal genetics, JAK2 mt

A

Polycythemia Vera

61
Q

Identify the disease

A

Essential thrombocytosis

Elevated platelets

Increased megakaryocytes

62
Q

Identify the disease

A

Primary Myelofibrosis

Leukoerythroblastic reaction

Tear-drop RBC

Nucleated RBC

Myeloid precursors

(Bone marrow shows fibrosis)

63
Q

Identify the disease

A

Myelodysplastic Syndrome

Peripheral smear shows dysplastic/bilobed neutrophils (Pseudo-Pelger-Huet cells)

Bone marrow is hypercellular with megakaryocytes

Ringed sideroblasts also present

64
Q

Identify the disease

A

AML - acute myeloid leukemia

Myeloblasts with Auer rods, azurophilic granular material

65
Q

Identify the disease

CD34+

TdT+

A

Acute lymphoid leukemia (ALL)

66
Q

Identify disease

A

Follicular lymphoma

Equally sized abnormal follicles

67
Q

Identify the disease

A

MALToma

Invades gastric mucosa

68
Q

Identify the disease

A

Hairy cell leukemia

69
Q

Identify the disease

A

Lymphaplasmacytic lymphoma

70
Q

Identify the disease

Bcl2+

A

Follicular lymphoma

(Follicular hyperplasia shows unevenly sized follicles and Bcl2-)

71
Q

Identify the disease

A

Diffuse large b cell lymphoma (DLBCL)

72
Q

Identify the disease

A

Burkitt lymphoma

Starry sky (apoptosis)

Basophilic cytoplasmic vacuoles

73
Q

Identify the disease

A

Mantle cell lymphoma

Cleaved cells

74
Q

Identify the disease

A

Burkitt’s lymphoma

Starry sky (apoptosis)

75
Q

Identify the disease

Lytic, punched out lesions of __ cel myeloma

A

Plasma cell myeloma

76
Q

Identify the disease

A

Rouleaux cells of Plasma cell Myeloma

77
Q

Identify the disease

A

Clover leaf cells of

Adult T cell lymphoma/leukemia (ATLL)

78
Q

Identify the disease

Large pleomorphic cells of ___?

A

Anaplastic large cell lymphoma

79
Q

Identify the disease

A

Mycoses Fungoides

Pautrier’s microabscesses

Epidermotropism

Cerebriform nuclei

80
Q

___ cells are usually present in ___ Hodgkin Lymphoma

A

Reed-Sternberg cells in Classical Hodgkin’s lymphomas

81
Q

Identify cell type and disease

A

Grooved nuclei of Langerhans cell Histiocytosis

82
Q

Identify structure and disease

A

Birbeck granules of Langerhand cell Histiocytosis

83
Q

___ Hemostasis

Platelet adhesion and activation by binding to exposed subendothelial ECM. Secreted products recruit other platelets to form a temporary hemostatic plug.

A

Primary

84
Q

____ Hemostasis

Activation of the coagulation cascade by the release of tissue factor. Polymerized fibrin and platelet aggregates together form a solid, permanent plug.

A

Secondary

85
Q

Activation of counter-regulatory mechanisms by ___ restricts the hemostatic plug to the site of injury to break down the clot.

A

tissue plasminogen activator (tPA)

86
Q

Platelet (GpIb) to ECM (exposed collagen) adhesion is mediated by _____?

A

vWF

87
Q

Aggregation is reversible and caused by the release of ___ from already adhered platelets.

A

ADP

88
Q

Platelet-to-platelet adhesion is mediated by what platelet protein and what other molecule?

A

GpIIb/IIIa

Fibrinogen

89
Q

Defect in GpIIb/IIIA is called ?

A

Glanzman Thrombasthenia

90
Q

Deficiency of GpIb is called ?

A

Bernard-Soulier syndrome

91
Q

Deficiency of platelet adhesion to exposed collagen is called ?

A

vWF disease

92
Q

The fibrinolytic system is mediated mainly by ___ which acts primarily on fibrin to cleave clots. Also activates complement system by cleaving C3 into C3a and C3b.

Broad-spectrum endopeptidase

fibrin –> TPA and FSPs

Elevated breakdown products in thrombotic states such as DIC

A

Plasmin

93
Q

Alpha-2 antiplasmin and alpha-2 macroglobulin are ____ inhibitors, which prevent the cleavage of clots (decreased fibrinolysis).

A

plasmin

94
Q

___ is an inhibitor of clotting factors II, IX, X, and XII, thrombin, proteins C and S, plasmin, and kallikrein

Potentiated by heparin

A

Antithrombin-III

95
Q

___ inhibits Vit-K dependent clotting factors II, VII, IX, and X

A

Coumadin (Warfarin)

96
Q

(2)

Vit K dependent protease inhibitors

First activated by thrombin-thrombomodulin complex and inhibits factors V and VIII in the presence of its cofactor (2)

A

Proteins C and S

97
Q

Defects in ___ hemostasis typically present as petechiae, whereas defects in ____ hemostasis present as bleeding into joints and soft tissue.

A

Primary

Secondary

98
Q

Disease?

An autoimmune disorder associated with IgG or other processes

Platelet phagocytosis by splenic macrophages, but normal sized spleen

Prolonged bleeding

Normal PT, PTT

Increased megakaryocytes in bone marrow

Tx: glucocorticoids in chronic disease

A

Immune Thrombocytopenic Purpura (ITP)

99
Q

Disease?

Formation of abnormal Ab that activate platelets after treatment with clot inhibitor

Leads to thrombocytopenia and arterial thrombosis (life threatening)

A

Heparin-induced Thrombocytopenia (HIT)

100
Q

Disease?

Impaired platelet production and increased destruction lead to thrombocytopenia

CD4 and CXCR4 on megakaryocytes allow these cells to be infected. Then they are prone to apoptosis and their ability to produce platelets is impaired.

A

HIV Associated Thrombocytopenia

101
Q

Disease?

Excessive activation of platelets, which deposit as thrombi in small vessels

Can cause microangiopathic hemolytic anemia and widespread organ dysfunction.

Consumption of platelets leads to thrombocytopenia

Deficiency in platelet enzyme ADAMTS13 (vWF metalloprotease), normally degrades vWF

Neuro symptoms

A

Thrombotic Thrombocytopenic Purpura (TTP)

102
Q

ITP or TTP?

Ig attack platelets

Acute and Chronic

No thrombosis

Hemorrhage

Large immature platelets

Steroids or splenectomy

A

ITP - Immune thrombocytopenic purpura

103
Q

ITP or TTP?

Microangiopathic hemolytic anemia

Schistocytes (helmet cells)

Thrombosis

Hemorrhage

Neuro symptoms

ADAMTS13 deficiency

A

TTP - thrombotic thrombocytopenic purpura

104
Q

Disease?

Childhood onset

Verotoxin-producing E. coli O157:H7

Absorbed in gastric mucosa where it alters endothelial cell function and results in platelet activation and aggregation

Bloody diarrhea

Petechiae

Increased renal failure

A

Hemolytic Uremic Syndrome (HUS)

105
Q

___ irreversibly inhibits COX and can suppress the synthesis of TXA2, necessary for platelet aggregation.

A

Aspirin

106
Q

Disease?

MC inherited bleeding disorder

spontaneous bleeding from mucous membranes, menorrhagia

plasma levels measured as Ristocetin cofactor activity, which is reduced

Increased bleeding time

Normal platelet count

A

von Willebrand Disease

107
Q

Disease?

Factor VIII deficiency

X-linked recessive; inversion of X abolishes synthesis of Factor VIII

MC hereditary disease associated with life-threatening bleeding

massive, spontaneous hemorrhage

Prolonged PTT

Normal PT

A

Hemophilia A

108
Q

Disease?

Factor IX deficiency

X-linked recessive

A

Hemophilia B

Christmas Disease

109
Q

Disease?

acute or chronic activation of the coagulation cascade

consumption of coagulation factors

Widespread microthrombi and microangiopathic hemolytic anemia

Thrombi in all organs

2 major mechanisms trigger this disease: release of tissue factor or other procoagulants into circulation OR widespread endothelial injury

Schistiocytes and helmet cells

Disease secondary to malignancy, obstetrics, sepsis, trauma, uncontrolled bleeding, surgery, etc.

Decreased platelet count and fibrinogen

Increased bleeding time, PT, and PTT

Increased fibrin split products and D dimer

A

DIC - Disseminated intravascular coagulation

110
Q

Disease?

post-transfusion fever and chills within 6 hours

Attributed to release of donor leukocyte inflammatory mediators

Responds to antipyretics

Increased incidence with increased blood storage time

A

Febrile nonhemolytic reaction

111
Q

Spontaneous abortion is most commonly caused by what?

A

Chromosomal abnormalities (MC trisomies)

Others include: infection, endocrine abnormality, uterine abnormality, immunologic dysfunction, or teratogenic causes

112
Q

___ abortion

Uterine bleeding without cervical dilation, 50% will abort

Tx: bed rest

A

Threatened

113
Q

____ abortion

Uterine bleeding with cervical dilation

100% will abort

Tx: curettage

A

Inevitable

114
Q

___ abortion

Some products of conception remain in the uterus

Tx: curettage

A

Incomplete

115
Q

___ abortion

Intrauterine fetal death without onset of labor

tc: curettage

A

Missed

116
Q

____ abortion

3+ consecutive spontaneous abortions

A

Habitual

117
Q

____ abortion

infection of products of conception along with infection of upper genital tract

Tx: antibiotic and evacuation

A

Septic

118
Q

Pregnancy outside the uterine cavity, most commonly the fallopian tube ampulla.

Risk: PID, previous incidence, adhesions, endometriosis, previous surgery, IUD, in vitro fertilization

Classic triad: unilateral pelvic or lower abdominal pain, vaginal bleeding, tender adnexal mass following 2-6 weeks of amenorrhea

Abrupt onset of excruciating abdominal pain with rapid progression to shock, indicative of tubal rupture.

Dx: serum bHCG, ultrasound, laparoscopy/biopsy. Presence of chorionic villi is essential

A

ectopic pregnancy

119
Q

What trimester is this placenta currently in?

A

First trimester

Chorionic villi composed of a delicate mesh of central stroma surrounded by two discrete layers of epithelium

outer = syncytiotrophoblast

inner = cytotrophoblast

120
Q

What trimester is this placenta currently in?

A

Third trimester

Chorionic villi composed of stroma with a dense network of dilated capillaries surrounded by markedly thinned-out syncytiotrophoblast and cytotrophoblast layers, which appear as one layer.

121
Q

Disease?

Low lying placenta, especially one that covers the cervical os.

Severe hemorrhage can result in cervical dilation and early delivery

Painless vaginal bleeding without any warning after 28 weeks

Complete, partial, or marginal

Intrauterine fetal growth retardation

Can also be complicated by placenta accreta

A

Placenta previa

122
Q

Disease?

Lack of formation of the decidual plate, thus, chorionic villi extend into myometirum. The placenta cannot separate normally following delivery.

Results in severe hemorrhage

A

Placenta accreta

123
Q

Disease?

Premature separation of the placenta prior to delivery with the formation of a retroplacental blood clot. Blood supply, therefore oxygen and nutrients, to the fetus is compromised.

Risk: HTN, prior incident, maternal age, multiparty, cocaine, cigarettes, trauma

Painful vaginal bleeding, uterine tenderness, fetal distress, shock, DIC

After 30 weeks (third trimester)

A

Abruptio placenta

124
Q

Disease?

Umbilical cord inserted into the sides of the membrane, rather than the central part of the placental tissue

A

Velamentous placenta

125
Q

Disease?

Separate placental lobes

A

Succenturiate lobes

126
Q

Disease?

Expansion of maternal surface centrally unto the fetal surface

A

Circumvellate placenta

127
Q

___ placenta

A

Bipartite (almost two)

128
Q

MCC postpartum hemorrhage

A

Uterine atony

129
Q

Disease?

In monochorionic twins, the donor twin sometimes becomes anemic and the recipient becomes plethoric

A

Twin-twin transfusion syndrome

130
Q

Disease?

Infection of fetal membranes, amnion and chorion

Usually ascending infection from the genital tract

E. coli, group B strep, and gonorrhea

Premature rupture of membrane and early delivery

A

Acute chorioamnionitis

131
Q

Disease?

A dense band-like inflammatory exudate on the amniotic surface

Acute inflammatory cells

A

Acute chorioamnionitis

132
Q

Disease?

Acute inflammation of the placental cord

A

Acute funisitis

133
Q

Disease?

Infection of chorionic villi

A

Villitis (placentitis)

134
Q

Disease?

HTN, edema and proteinuria in pregnancy

Usually nulliparous

Severe disease can cause headaches, dizziness, and visual disturbances

HELLP: hemolytic anemia, elevated liver enzymes, low platelets

A

Pre-eclampsia

135
Q

Disease?

HTN, edema, and proteinuria in pregnancy that progress to seizures and DIC

A

Eclampsia

136
Q

Tx for grand mal seizure control

(used in eclampsia)

A

MgSO4

137
Q

Disease?

A

Placental infarct

138
Q

Disease?

Maternal vascular lesion observed in pre-eclampsia and idiopathic intrauterine growth retardation

Characterized by fibrinoid necrosis of the vessel wall, an accumulation of lipid-laden macrophages, and a mononuclear perivascular infiltrate

A

Acute atherosis

139
Q

Disease?

No fetal parts or normal chorionic villi

Entire uterus is filled with edematous, avascular villi with the appearance of a bunch of grapes. Trophoblastic proliferation of both syncytio- and cytotrophoblasts with atypia.

46XX or 46XY

Empty ovum fertilized by either (more commonly) one sperm (with subsequent chromosome duplication) or two sperm without duplication

Increased bHCG

Ultrasound: snowstorm pattern

Increases risk of choriocarcinoma

A

Complete hydatidiform mole

140
Q

Disease?

Villous enlargement, edema, and trophoblastic proliferation of both syncytio- and cytotrophoblasts with atypia.

A

Complete hydatidiform mole

141
Q

Disease?

Only part of the placenta shows changes.

Fetal parts along with normal placental structures in the unaffected portion

69 XXY triploidy

one or two sperm fertilize a NORMAL egg

does not usually increase the risk of choriocarcinoma

A

Partial hydatidiform mole

142
Q

Disease?

Only part of the placenta shows changes.

Fetal parts along with normal placental structures in the unaffected portion

69 XXY triploidy

one or two sperm fertilize a NORMAL egg

does not usually increase the risk of choriocarcinoma

A

Partial hydatidiform mole

143
Q

Disease?

Malignant cytotrophoblasts and syncytiotrophoblasts

Uterine bleeding

Elevated bHCG

Widespread metastases are common

Risk: molar pregnancy, spontaneous abortion, 25% normal pregnancy

A

Choriocarcinoma

144
Q

Disease?

Malignant cytotrophoblasts and syncytiotrophoblasts

Uterine bleeding

Elevated bHCG

Widespread metastases are common

Risk: molar pregnancy, spontaneous abortion, 25% normal pregnancy

A

Choriocarcinoma

Path 2 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions