Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Skin, Lymph, Blood > Dr. Singh - Hematopathology : WBC, LN, Spleen, Thymus > Flashcards

Dr. Singh - Hematopathology : WBC, LN, Spleen, Thymus Flashcards

1
Q

Leukocyte common Ag marker

A

CD45 (Basophils, N ,Eosinophil, Tcells, Bcells, NK cells, Moocytes)

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

Early myeloblast marker

A

CD34

E, N, B

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

Early Lymphblast marker

A

Tdt (T-cells, B-cells, NK cells)

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

lymphocyte markers

A

CD19, CD20, Pax-5 (T-cell, B-cell)

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

Natural Killer cell markers

A

CD56, CD16

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

Helper T cells markers

CTL cells markers

A

CD4+

CD8+

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

High myeloblast count can be a sign of

A

Acute Leukemia type

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

Leukopenia
What
Most common

A

Low WBC

Neutropenia (extreme neutropenia = agranulocytosis)

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

Absolute neutropenia is found how
WBC : 6.0x10^3
N : 4%
Bands : 2%

A

Absolute N Count = .06(6000) = 360

** anything under 500 is very serious

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

what can cause neutropenia

A
  1. Toxic drugs for chemotherapy destroying bone marrow
  2. Aplastic anemia
  3. Megaloblastic anemia
  4. Ab mediated destruction
  5. Hypersplenism (spleen sequesters and destroys blood cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can happen when you have neutropenia

And how to TX

A
  1. Bacterial and Fungal infection

2. G-CSF (to recolonization)+ Abs

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

Leukocytosis

A

Too much N

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

Increased N marrow production caused by

A

Chronic infection or cancer

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

Increased release of N form marrow stores

A

Acute inflammation

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

Decreased Margination

A

Exercise (N unstick from vessels and enter circulation)

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

Decreased extraversion into tissues

A

Glucocorticoids

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

High N
High Lyphocytes
High E
High B

A

Acute bacterial infection, MI
Viral infection
Asthma, parasite, drug reactions
CML

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

Germinal centers + medullary sinuses expand

A

During infection

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

Acute supportive lymphadenitis

A

Painful puss filled LN usually from pyogenic infection, high neutrophils, abscess forms in LNs

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

Follicular hyperplasia

A

Lymphadenitis
Many follicular areas that swell
The lymphocytes expand in the germinal center usually viral

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

Organization in the LN

A

Germinal area or center and mantel area around it

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

Sinus histocytosis

A

M are increased in the LN sinuses and seen usually in malignancy or drainage of foreign material - tattoo ink (they are histiocytes)

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

Lymphoid neoplasia involves

A

B,T, NK, plasma cells

Hodgkin

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

Myeloid neoplasia involves

A

AML
Myelodysplasia
Myeloproliferative neoplasia

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

Histiocytic neoplasia involves

A

Langerhans Cell Histiocytosis

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

3 things usually causing WBC neoplasia

A
  • viral infection (HTLV, EBV, HHV-8)
  • Chronic infection (H Pylori)
  • Genetic mutation that’s acquired
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Acute Lymphoblastic Leukemia/lymphoma

SX

A

Fever - no Neutrophils so easy opportunistic infection
Fatigue - anemic
Bleeding and bruising - no platelets
Pain - expansion of BM from leukemic cells
N,V,Headache - meningis in brain can also have leukemic cells pack in there

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

ALL what happens

A

The lymphoid stem cell divide excessively into blasts and dont become mature WBCs (maturation arrest)
- BM is packed with myeloblast leukemia cells and can be hard to even draws out a BM sample

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

ALL under the microscope

A

Large purple cells that are lymphoblastic ($x size of RBCs)

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

How to DX ALL on peripheral smear looking at the cell markers

A
  1. If there is TdT (prolymphocyte marker) = myeloid cells SEEN
  2. If there is CD19, 20, 10, Pax-5 = B-cells involved SEEN
  3. If there is CD 1-5, 7, 8 = T-cells are involved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How to TX ALL

A

Chemotherapy in CSF
Is usually very successful (age 2-10)
(12:21 transposition)

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

B-cell non-Hodgkin leukemia EXs

A
  1. CLL
  2. Follicular lymphoma
  3. Diffuse large B-cell lymphoma (DLBCL)
  4. Burkitt lymphoma
  5. Mantel cell lymphoma
  6. Marginal Zone lymphoma
  7. Hairy Cell Leukemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

CLL/SLL

Sx and blood smear

A 
None really (usually older adults) however you can run a CBC and see some clone mature lymphocytes that are small (size of RBCs since they are mature)
They are delicate and can smudge (smudge cells seen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

CLL/SLL markers seen

A
  1. CD19, CD5 (B-cells)
    CD20
  2. Look at light chains that are all the same
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

CLL/SLL prognosis

A

Usually fine, however can become aggressive Richter Transformation (from MYC or TP53 mutation)

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

Follicular lymphoma DX

A

It looks the same as Follicular Hyperplasia so you look at the cells
1. 14:18 translocation (IgH next to BCL-2)

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

Follicular Lymphoma SX

A

Painless B-cell proliferation and generalized lymphadenopathy

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

How to stain and see difference in Follicular lymphoma and Follicular hyperplasia

A

Follicular Lymphoma : granular center is stained all brown (+ stain)
Follicular hyperplasia : granular center is stained brown in marginal area only granular center is white

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

Follicular lymphoma grading scale

A

Grade 1 : smaller cells (more mature cells)
Grade 2 : some larger cells
Grade 3 : all larger cells (mostly immature cells)

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

DLBCL is what

A

LARGE Masses in LN or other organ like the spleen

Aggressive and fast growing

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

DLBCL special types

A
  1. Immunodeficiency - related LCL (HIV, post-transplant, or something linked to EBV)
  2. Primary effusion lymphoma (HHV-8)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

DLBCL DX how

A

Cells muted in BCL-6 = over expressed B cells

You see all other B- cell markers

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

Burkitt lymphoma
Looks like
And happens how

A

Starry sky pattern, 99% are dividing constantly
B-cells + MANY tingible (stainable) Ms = to eat a bunch of cells and debri
(Seen with the Ki-67 stain)

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

Burkitt lymphoma from what translocation

A

8: 14 (IgH next to MYC)

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

3 types of Burkitt Lymphomas

A
  1. EBV associated (Endemic in Africa, causing mandibular growth)
  2. Sporadic
  3. HIV-related
    = can be TX well if diagnosed early
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Mantel Cell Lymphoma is what looks like what

A

B- cells resembling mantle cell layer

Small, mature, and fast dividing and aggressive

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

Mantel Cell Lymphoma TX

A

Aggressively and BM transplant

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

Mantel Cell Lymphoma can cause

A

GI mucosal involvement

Polyps (made of lymphocytes not intestinal mucosa = lymphomatoid polyposis)

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

Mantel Cell Lymphoma translocation

A

11: 14 (IgH next to Cyclin D1)

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

Marginal Zone Lymphoma looks like and where

A

In LN or extranodal sites (MALT-oma, GI, bronchial, thyroid) ——> chronic inflammation (H PYLORi INFECTION)

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

Marginal Zone Lymphoma can be seen in what organs

A

CHRONIC INFLAMMATION SITES :

  1. Gastric MALToma (from H- pylori) - Tx the infection and can cause it to go away
  2. Hashimoto’s thyroiditis can lead to MZL
  3. Chronic Sialadenitis can cause Salivary gland MZL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Hairy Cell Leukemia looks like what

A

NEoplastic B-cells that are about 2X as big as RBCs with projections that look hairy on them (very few of them)

53
Q

How to DX HCL

A

Drawing out BM you usually dont get anything due to the BM fibrosis
On blood smear you see some distance between each close packed cell due to hairy cytoplasm

54
Q

HCL can cause what SX

A

Fatigue
Splenomegaly (to start make cells BM cant)
Pancytopenia (very low number of cells and hard to see a hairy cell in the blood)
Anemic (no WBCs, due to hairy BM cells)

55
Q

HCL TX

A

Very good with chemotherapy

56
Q

HCL markers involved

A

CD 25 and CD11c

57
Q

How to DX any B -cell lymphoma

A

Run a flow cytometry

58
Q

Plasma Cell Neoplasia

3 kinds of it

A
  1. Myeloma
  2. Monoclonal gammopathy of uncertain significance (Mgus)
  3. Waldenström macroglubulinemia
59
Q

Plasma cells look like

A

Central dark purple nucleus, light blue cytoplasm, and dark blue Perinuclear Hoff around the cytoplasm

60
Q

Myeloma causes what things

A

Tumor in the BM

  • Lytic Ben lesions
  • Hypercalcemia
  • Renal failure
  • Immune abnormalities
61
Q

Monoclonal gammopathy + myeloma is can be seen on a graph as what and is what

A

Too much gamma seen on electrophoresis
Gamma includes many immunoglobulins
** on looking at serum levels, there is a narrow spike in gamma region and Alb region, normal results would show only a spike at Alb = M SPIKE

62
Q

In gammaopathy + myeloma which immunoglobulins are usually involved in excess

A

IgG and IgA (with K or L light chains)

63
Q

How do we know if something is myeloma or Mgus

A
  1. More then 60% plasmacytosis in BM = Multiple Myeloma DONE

2. if over 10% = you need more information (CRAB Criteria)

64
Q

CRAB criteria

A

C : Calcium elevated
R : Impaired REnal function
A : Anemia
B : Bone Lesions

65
Q

Elevated Calcium presents as and due to what

A

Due to osteolysis (from many plasma cells in the BM)

  • altered mental status
  • seizures
  • cardiac rhythmic disturbances (Short QT)
  • N,V, C
66
Q

Renal Insufficiency presents as and due to what

A
  1. From immunoglobulins that are being filtered through (Ig attach to glycoproteins Tamm Horsfall = BENCE JONES PROTEINS* in tubules) = clog tubules + damage
  2. Proteinuria + light chain in urine
  3. Amyloidosis : Congo red stain + apple green in glomerulus = AL amyloid in myeloma
67
Q

Anemia presents as and due to what

A

From plasma cells in BM not able to make WBC

  • also from IL-6 production = suppression cytokines
  • renal disease = low erythropoietin made
68
Q

Bone Lesions presents as and due to what

A

Can break bone and spontaneous fracture or holes in bone like skull

69
Q

When is hyperviscosity seen

A

Hen you have too much immunoglobulins

70
Q

Where can you see hyperviscosisty

A

Myeloma , Mgus = high IgG (monomer) or IgA (diner)= viscous

Waldenström macroglubulinemia = high IgM a pentomer = extremely viscous

71
Q

Hyperviscosity can cause what

And what does it look like

A

Thromboembolic complications due to sticky blood

Looks like Rouleaux formation (RBCs are sticking like coins)

72
Q

What is another name for Waldenström macroglubulinemia

A

Lymphoplamacytic Lymphoma , due to this disease involves mature B cells that are wanting to differentiate to plasma cells

73
Q

Waldenström macroglubulinemia an cause what

A
  1. Hyperviscosity = visual impairments, stroke, embolic conditions, Cryoglobulinemia (ischemia to fingers)
  2. High IgM
  3. Reynolds phenomenal + Reaulux formation
74
Q

Hodgkin lymphoma vs non-Hodgkin lymphoma

A

H : localized not really spreading,

NH : many different nodes, Waldeyer ring + mesenteric nodes involved, Extranodal presentation

75
Q

Classic Hodgkin Lymphoma you see and markers in it

A
  1. Reed- Sternberg cells (owl eye cells) = CD 15, CD30, Pax-5 + IgH rearrangement
76
Q

How does Classical Hodgkin lymphoma present

A

Localized in one area one LN and then later can spread to another area

  1. Nodular sclerosis : had nodules and fibrosis around it in the LN
  2. Multicellulaity : has many different cells in the LN
77
Q

Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLP HL)

SX

A

Similar to HL however histologically extremely different

78
Q

Nodular LP HL histologically looks like and markers

A

Lymphohistocytic HL cells = Popcorn cells

  • YES CD20
  • NO CD15, CD30
79
Q

NLP HL can transform to

80
Q

How to DX HL

A

You have to stain and look at the cells because the Reed- Stanberg cells are very dilute and very few in the many colonal B- cells
+ CD15 and + CD30
OR
+ Popcorn cells + CD20

81
Q

Peripheral NK/T-cell lymphomas : Anaplastic Large Cell Lymphoma

A

Aggressive T cell tumor form ALK tyrosine kinase gene translocation *

  • usually younger patients (ALK + and good prognosis)
  • some are ALK negative and older (worse prognosis)
82
Q

Peripheral NK/T-cell lymphomas : Adult T- cell leukemia/lymphoma

A

Aggressive CD4+ tumor from a HTLV-1 infection

- Cloverleaf cells in blood **, usually seen on skin as lesions and nodules

83
Q

Peripheral NK/T-cell lymphomas : Large granular lymphocytic leukemia

A

CTL T cell tumor or NK cell tumor associated with a STAT3 TF mutation + cytopenias + autoimmune phenomena

84
Q

Peripheral NK/T-cell lymphomas : Extranodal NK/T cell lymphoma

A

Aggressive tumor from NK cells and linked to EBV infection

85
Q

EBV is liked to

A
  1. Burkitt lymphoma
  2. DLBCL
  3. Extra nodular NK/T cell lymphoma
86
Q

Peripheral NK/T-cell lymphomas : Mycosis Fungoides

A

T-cell lymphoma presenting with skin plaque lesions that are saddle and if biopsied can be mistaken as inflammation, however is t-cell clones
NO HTLV-1 association

87
Q

Peripheral NK/T-cell lymphomas : Sézary Syndrome

A

T-cell lymphoma with erythroderma (Red all over body skin rash, red man syndrome) and leukemia in blood (cerebraform cells in blood)
NO HTLV-1 association

88
Q

Myeloid neoplasms 3 types

A

AML
Myelodysplastic syndromes
Myeloproliferative neoplasms

89
Q

AML

A

Leukemic stem cell which makes only a bunch of blasts and prevents maturation of cells = a bunch of myeloblasts

90
Q

AML is DX how

A
  1. Having 20% or more BLASTS (any WBC) in the BM**
  2. You can see granules in the cytoplasm at times in the blasts
  3. Fever, fatigue, bleeding, bruising, PANCYOPENIA (no blasts in peripheral blood)**
91
Q

AML with genetic aberrations

A

Translocation of 8:21 or 15:17

Good prognosis

92
Q

AML with MDS like features

A

First the patient has myeloid dysplasia and it becomes AML

Poor prognosis

93
Q

AML therapy related

A

Getting AML from therapy such as chemotherapy

Poor prognosis

94
Q

AML not otherwise specified

A

Other types of differentiated blasts like erythroid blasts, Megakaryocytic blasts, Monocytic blast

95
Q

AML 8:21

What happens

A

Usually younger patients
CBF makes mature cells however in this type of translocation a ETO protein + RUNX1-RUNX1T1 blocks the CBF and there is no maturation of the myoblasts

96
Q

AML with 15:17

A

Is also called Acute Promelocytic Leukemia ***8

YOU SEE AUER RODS

97
Q

AML with 15:17 happens how

A

Usually RAR bind to RA and = allows differentiation to N

In this RAR is bound by a PML protein and makes it not want RA, no differentiation to Ns

98
Q

AML 15:17 TX

A

Gleevec or ALL TRANS RA which overrides the PML protein bound to the RXR

99
Q

AML 15: 17 SX and Why when you dont have leukocytosis and panocytopenia sx

A
  • NO leukocytosis, panocytosis at times
  • YOU see HYPERCOAGABILITY (bruising and bleeding and coagulation of blood due to the myloblasts having Annexin = plasminogen -> plasmin AND activated and TF to make F10a)
100
Q

Other unusual AML SX not involving hypercoagability or leukemia or panocytopenia

A
  1. Extra nodular involvement of gingiva (black and red infiltration of myloblasts), and Leukemia cutis (myloblasts to skin)
  2. Soft tissue masses stained +CD34 (in any part of the body)
101
Q

Myelodysplastic Syndrome

A

Clonal disorder in many cell types (not one identical clone)
Usually from therapy
Can come before AML

102
Q

Myelodysplastic Syndrome SX

A

Cytopenia (anemia usually)

103
Q

Myelodysplastic Syndrome DX how

A
  1. Which lineages are effected
  2. Chromosomal translocation
  3. Blast count : increased a bit (are higher risk for AML transformation)
  4. You can see Dyserythropoiesis (multinucleated RBCs), Ring sideroblasts (Fe deposits), Pseudo Pelger-Huet cells (Bilobed N), Dysmegakaryopoiesis (small MK with separate lobes)
104
Q

Looking for excess blasts in Myelodysplastic Syndrome

A

More then 20% = AML

If above 10% : RAEB 2 (refractory anemia excess blast 2) , higher RAEB are more likely to become AML

105
Q

Myelodysplastic Syndrome happen from what mutations

A
  1. Epigenetic mutations
  2. RNA splicing factor mutation
  3. TF mutation
106
Q

Myeloproliferative neoplasms mutation is what

A

Any kinase = proliferation

107
Q

Myeloproliferative neoplasms SX

A

BM proliferated with something
The cells travel to extramedullary areas
AML or ALL can happen

108
Q

CML SX

A
  1. peripheral leukocytosis of mature myeloid cells high number of cells in BM
  2. Splenomegaly (extrameduallary hematopoiesis)
  3. Higher Buffy coat
    4.
109
Q

CML translocation

A

Philadelphia chr (9:22) = activated a kinase BCR-ABL

110
Q

What can you see when testing for CML

A

** Increased buff coat in blood that is centrifuged (higher WBCs)

111
Q

Higher Buffy coat in blood means

112
Q

Wha happens to CML over time

A

If there is a lot of leukocytosis then viscosity can increase and mutations can happen and cause increased blasts = AML or ALL

113
Q

4 types of Myeloproliferative neoplasms

A
  1. CML : WBCs
  2. Polycythemia Vera : RBCs
  3. Essential thrombocythemia : platelets
  4. Primary myelofibrosis : stroma fibroblasts
    2-4 are increased in JAK2 Kinase**
114
Q

What happens during myelofibrosis

A

Can happen as the end stage of Myeloproliferative neoplasms 2-4
- low BM elements due to fibrosis
= SPLENOMEGALY (JAKofy)

115
Q

Langerhans cell histocytosis 3 types

A

Multi focal multisystem
Unisystem
Pulmonary (smokers

116
Q

Langerhans cell histocytosis SX

A

The Langerhans cells (dendritic cells) eat away the bone = lytic lesions

  1. Cleaved nuclei many of them
  2. ** electronmicroscopy showed Birbeck granules (tennis-racket shaped)
  3. ** many E like being there in the blood smears
117
Q

Birbeck granules are found when

A

For Langerhans cell histocytosis (tennis racket shaped)

When looking at electronmicroscopy

118
Q

How to stain for Langerhans cell histocytosis

A
  1. CD1a and S100 (Langerhans cells)

2. Many eosinophils as well

119
Q

Important anatomy of spleen

A
  1. Splenic A goes to it and 1 single splenic vein drains it
  2. Blood opens up to the open circulation pockets
  3. Germinal center (white pulp) = lymphocytes
120
Q

Spleen function

A
  1. Phagocytosis
  2. Sequester RBCs
  3. Ab production
  4. Fetal and adult (if condition) hematopoiesis
121
Q

Splenomegally what and how

A
  1. Follicular hyperplasia in the germinal center = expands Spleen
    - usually from viral infection
  2. Congestive Splenomegaly from hepatic dysfunction (the 1 splenic V is blocked as it goes to the liver)
122
Q

Hypersplenism what and how

A

Enlargement of spleen due to cytopenia
(Blood or spleen problem)
- Hereditary spherocytosis (stiff RBCs)
- Sickle Cell
- Idiopathic thrombocytopenia purpura : platelets are covered by opsonizing Abs
- splenomegally can cause that type of spleen dysfunction to take more RBCs

123
Q

Splenic rupture from what and how

A

ABD trauma
Rapid splenomegaly (Infections Mononucleosis)
- causes Hypotension

124
Q

Splenic Neoplasia

A

Usually vessel neoplasm

Other leukemia’s can involve the spleen make nodules

125
Q

Splenic infarcts

A

It grows so fast it outgrows its vascular supple it needs

Clogged Spenic A (Sickle Cell)

126
Q

Thymus

A

Very cellular in babies

Adults is mostly fat (some squamous Hassle Corpuscle cells)

127
Q

Thymus Hyperplasia

A

Increased cells start to proliferate in the thymus as an adult
Can cause MG

128
Q

Thymoma

A

A tumor is in the thymus as a clonal neoplasm

  • obstruct airway or esophagus is possible
  • MYASTHERNIA GRAVIS
129
Q

Myasthenia Gravis (MG)

A

AutoAbs from thymine hyperplasia or thyoma

AB——> post-synaptic R for ACH = progressive weakness especially as the day goes on , SOB

Skin, Lymph, Blood (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions