Hematology 1

Front 1

What differs anemia and anemic syndrome?

Back 1

Anaemia= less than the normal quantity of hemoglobin in the blood
Anaemic syndrome =clinical syndrome caused by tissue hypoxia

Front 2

Normal value of HB and HTK?

Back 2

HB 136-176 men (120-170 women)
HTK 0,38-0,48

Front 3

What do they stand for?
RBC
MCV
MCH
MCHC

Back 3

RBC= no. of ery
MCV= Volume of ery
MCH= Mass of HB in ery
MCHC= HB cooncentration in ery

Front 4

What are the symptoms of anic syndrome?
Primary, compensation ans secondary?

Back 4

Primary: Tissue hypoxia: pallor, fatigue, weakness, dyspnea

Compensation and adaptation:
Hypercinetic circulation, palpitations, tinnitus

Secondary :
Cardiovascular symptoms – decompensation of ischemic heart disease, AP, IM, claudications

Front 5

Progress and severity of AS depends on:

Back 5

1. Absolute value of Hb
Hgb 70-80 g/l = most of patients suffer from symptoms

2. Speed of onset

3. Age and overall performance of the patient

Front 6

ANAEMIA - CLASSIFICATION
acc. to MCV

Back 6

Morfologic criteria:
According to MCV: (80 – 95 fl)
microcytic, normocytic, macrocytic

Front 7

ANAEMIA - CLASSIFICATION
acc. to MCH

Back 7

According to MCH: (27-32 pg)
normochrome, hypochrome

Front 8

MICROCYTIC ANAEMIA
4 examples

Back 8

MICROCYTIC ANAEMIA
Iron deficiency anaemia
Chronic disease anaemia
Thalasemia, sideroblastic anaemia

Front 9

MACROCYTIC ANAEMIA
2 types + reason

Back 9

MACROCYTIC ANAEMIA
Megaloblaste anaemia(lack of B12, folic acid, MDS)
Macrocytic non-megaloblaste anaemia (usually secondary

Front 10

NORMOCYTIC ANAEMIA
Primary imparement

Back 10

Primar impairment of blood marrow: aplastic anaemia, MDS, PNH,
myelofibrosis.

Front 11

NORMOCYTIC ANAEMIA
Secondary impairmen

Back 11

Secondary impairment of blood marrow :(infiltration, infection,
endocrinological and systemic diseases, ACD)

Front 12

. ANAEMIA WITH RETICULOSIS

Back 12

Haemolytic aneamia corpuscular
Haemolytic anaemia extracorpuscular –
imunne and non-immune based

Front 13

Pathofysiological classification of anemia

Back 13

Proliferation and differentiation disorder
Increased destruction of RBC
Blood loss
Combined etiology

Front 14

Where does iron defic. and ACD affect hb synth?

Back 14

Front 15

Where does sideroblastic anemia affect Hb synth?

Back 15

Front 16

Where does thalasemia affect hb synth?

Back 16

Front 17

Where is B12, folic acid and epoxide an importnant factor in hb synth?

Back 17

DNA synth

Front 18

Which anemia is the most common? (80%)

Back 18

Iron deficiency

Front 19

Sideropenia=?
Happens in how many fertile women?

Back 19

Iron deficiency
35-58% of fertile women

Front 20

What does iron defic. affect except for blood count? (6)

Back 20

DNA synthesis impairement
Tissue fosforylation impairement
Purine metabolism impairement
Colagen synthesis impairement
Granulocyte function impairement
Neurotransmiter function impairement

Front 21

How is iron stored in the body? How many %, where?

Back 21

Hb: 70%
Ferritin: 25%
Myoglobin:4%
Enzymes: 1%

Front 22

What is the interesting thing with iron excretion?

Back 22

There is no physiological excretion mechanism!

Front 23

How much iron do we absorb every day? (and excrete)
And how much does the diet contain?

Back 23

1-2 mg is absorbed even if the diet contains 10-20 mg.

Front 24

Where does most of the iron absorbtion occur?

Back 24

Duodenum and upper part of jejunum

Front 25

How much iron supply do we have in the organism?

Back 25

3000-5000 mg

Front 26

What is hepicidin?
Come from, stimulatet by?
What does it do?

Back 26

Hepcidine

Acute phase reactant
Source: hepatic cells, heart,
Iron stimulates Hepcidine
Hepcidine inhibits iron absorption in the intestine, iron release from macrophages and iron transport via placenta
ACD, hereditary hemochromatosis

Front 27

How much iron is absorbed if you compare meat and vegetables?

Back 27

Meat: 25-30% of iron is absorbed
- Vegetables: 5% of iron is absorbed
So vegetariaans are in risk for iron defic.

Front 28

What happens with 65% of pat with stomach resection?

Back 28

They get aabsorbtion disorders. Can lead to iron defic.

Front 29

How much iron do you lose during menses?

Back 29

ca 3mg/day

Front 30

When is there an increased need for iron?

Back 30

Gravidity
Brest-feeding
Growth

Front 31

Symptoms of iron defic.
What do they mean?

Back 31

Anemic syndrome
Cefalea, paresthesia, fatigue
Tongue burning, angulitis
Odyno-(painful), dysfagia
Sy Kelly-Patterson (hair, nails)
Brittle hair, nails
(Pica, pagofagia)

Front 32

Physical examination findings when iron defic.

Back 32

Pallor – skin, mucous membrane
Blue sclerae
Ulcers/ angulitis
Smooth tongue
Straight/(spoon-shaped) nails
Achlorhydria (low production of hcl), atrophic gastritis

Front 33

Laboratory findings in iron def. 1

Back 33

RDW (rbc distribution): high
Trombocytosis (over 50% of patients)
BM –staining for iron
- lack of Fe in siderophages
- sideroblasts lower then 10%

Front 34

Laboratory findings in iron def. 2
MCV
MCH
MCHC
TRanferrin
S-transferrin
transferrin satur.
S-sTfr

Back 34

MCV under 80fl
MCH under 25ug
MCHC – late symptom
Transferrin -increased
S-ferritin <20ug/l
Transferrin satur. – under15 % (N: 20-40%)
VKFe (TIBC): increased
S-sTfR > 8g/l

Front 35

Diff. diagnose microcytic anemia:
IRON INSUFF.

Fe
TIBC
satTRF
ferritin
TRF receptor

Back 35

Front 36

Diff. diagnose microcytic anemia:
ACD

Fe
TIBC
satTRF
ferritin
TRF receptor

Back 36

Front 37

Diff. diagnose microcytic anemia:
THALASEMIA.

Fe
TIBC
satTRF
ferritin
TRF receptor

Back 37

Front 38

What is ferritin?

Back 38

Acute phase reactant
Nespecific tumorous marker
Level increases with age
(75ug/l in old people = ? = iron defficiency

Front 39

3 types of Iron defficiency:

Back 39

Prelatent
Latent
Manifest - SA

Front 40

Treatment of IDA

Back 40

Treatment of the cause of iron loss
+ iron supply

Front 41

Ferrotherapy

Back 41

150-200mg Fe / day
Until enough supply is formed (ferritin 50ug/l)
Use on an empty stomach
CAVE: polyphenols, milk, egg yolk
Dyspepsia
Parenteral forms (CAVE: anaphylaxis; x new forms are safer - karboxymaltose)

Front 42

If P.o iron treatment is insuff agains iron defic...?

Back 42

Ineffective treatment:
1. Diagnosis checking :BM examination, GIT examination aso…. Cave self-harming
2Switch to i.v. therapy

Front 43

What is Thalassemia and which types are there? Which one is worse?

Back 43

Inherited disorder of Hb structure:
α –thalasemia = α disorder
β – thalasemia = β disorder
β – thalasemia is worse

Can also be devided into minor (usually no symptoms), intermedia (only in Beta) and major (from both parents) depending on ammount of inheritence.

MICROCYTIC ANEMIA

Front 44

What is a typical skull manifistation in a anemic disease?

Back 44

Diploetic fibers from the skull in thalassemia.

Front 45

Lack of B12of folic acid, 2 reasons:

Back 45

Lack of B12of folic acid:
1. Pernicious anaemia - B12 absorption in the distal intestine disorder due to lack of intrinsic factor (produced by parietal cells of gastric mucosa)


2. Dihydrofolat reductase inhibitors (MTX, ARA-C)

Front 46

MEGALOBLASTIC ANAEMIA -CAUSES

Back 46

Insufficient intake of B12 of folic

Absorption impairement:
Increased demand

Increased loss (hepatic laesions, bleeding)

dihydrofolat reductase inhibitors (MTX,pyrimethamin)

Transport disorders because of lack of transkobalamin I. and II

Front 47

Megaloblastic anemia
Blood count:

Back 47

macrocytes (↑MCV, ↑MCH, normal MCHC),
↓RTC,
megalocytes,
megaloblasts,
leukocytosis with left shift,
thrombocytopenia

Front 48

Megaloblastic anemia
Bone marrow

Back 48

hyperplasia of erytropoiesis, megaloblasts

Front 49

Megaloblastic anemia
Biochem

Back 49

↓ B12, ↓folic acid, ↑direct and indirect
bilirubin,
Normal iron!

Front 50

Where is B12 absorbed?

Back 50

B12 absorption in ileum, binding to specific receptor (cubilin)

Front 51

TRANSCOBALAMIN I's role in B12 mtb

Back 51

Binds B12 in plasma,binds to B12 in stomach before binding to intrinsic factor, produced by neutrofiles and cells with exocrine secretion, his lack leads to low serum B12 levels

Front 52

TRANSCOBALAMIN II's role in b12 mtb

Back 52

Enables B12 absorption by cells, receptor on all type of cells, produced by endotelial cells, fibroblasts, ileum cells.., his lack leads to severe B12 deficiency in cells

Front 53

What 3 factors does b12 absorbtion need?

Back 53

1. intrisic factor
2. Transcobalamin I
3. Transcobalamin II

Front 54

What is this?

Back 54

Pernicious anaemia

Front 55

Anaemia with increased no of reticulocytes + subtype

Back 55

HEMOLYTIC ANAEMIA
- corpuscular
- estracorspuscular
bleeding - acute

Front 56

Corpuscular Haemolytic anaemias, pathogenesis

Back 56

Lack of and defects in membrane proteins (ankyrin, spectrin, etc.)
leading to extravascular hemolysis (spleen)

Front 57

Herediatry spheracytisos is what?
Treatment?

Back 57

ongenital spherocytic anemia is a disorder of the surface layer (membrane) of red blood cells. It leads to red blood cells that are shaped like spheres, and premature breakdown of red blood cells

Treatment: Spleenectomy

Front 58

ERYTROCYTE ENZYMOPATHY
Diff. reasons?
Type of anemia?

Back 58

CORPUSCULAR HEMOLYTIC ANEMIA
Defects in enzymes of anaerobe glykolysi (anemia with Heinz bodies)

Defect in enzymes of pentos cycle

Front 59

GLUCOSE-6-PHOSPHATE DEHYDROGENASE defficiency
Results in what?
How do we treat it?

Back 59

Results in: lack of NADPH …. Increased sensitivity to oxydating agents
Treatment:
Prevention of exposure to oxydative agents (medication: antimalarics, sulfonamides,. Food: vicia fava etc.) , splenectomy, stem cell transplant

Front 60

sicle cell anemia – HbS, Thalassemia methHb and so on are example of?

Back 60

Hemoglobinopathies

Front 61

What is this?

Back 61

Sickel cell anemia

Front 62

Sicle cell anemia:
Pathogenesis

Back 62

Substitution glutamate valin on 6. position 
chain: Hb polymerisation, deformation of erythrocyte, Shape=sickle cell.

Front 63

Sickle cell anemia:
Inheritance:

Back 63

Autosomal dominant type
homozygotic form – both B chains impaired

heterozygotic form – one B chain impaired
25-50% HbS – sickle cell trait

Front 64

Sickel cell anemia:
What does it lead to?

Back 64

Hemolysis extravascular + intravascular (small vessel obstruction)

Front 65

Sickle cell anemia:
Clinical picture
treatment

Back 65

Hemolytic + aplastic crisis, splenomegaly


Treatment:
Crisis prevention, transfusions, SCT

Front 66

Pathogenesis of AIHA:

Back 66

Cooperation disorder among supresor T helper T lymphocytes and B lymphocytes responsible for immunity control

Dysregulation of this system leads to insufficient supression of antibody formation against own antigens

Front 67

HEAT ANTIBODIES
(AIHA)

Back 67

IgG character – optimal at 370C
Catch up of erythrocytes with binded antibody by spleen macrophages
EXTRAVASCULAR HEMOLYSIS

Activation of complement by high antibody titre
INTRAVACULAR HEMOLYSIS

Front 68

COLD ANTIBODIES
(AIHA)

Back 68

IgM character – optimál at 40C
Bound to erytrocytes in colder acral parts, possibility of complement activation, ery aglutination

INTRAVASCULAR HEMOLYSIS

EXTRAVASCULAR HEMOLYSIS

Front 69

AIHA –laboratory parameters
Blood count
Biochem
Special test
Proof of intravascular hemolysis?

Back 69

makrocytic anaemia with reticulocytosis
Biochemistry:
 direct and indirect bilirubin,
 urobilinogen in urine
Special tests:
Direct and indirect antiglobuline test (Coombs
test)

INTRAVASCULAR HEMOLYSIS PROOF:
 free Hb in plasma,
 levels of haptoglobin and hemopexin in serum,
hemoglobinuria

Front 70

AIHA treatment

Light form ( Hb > 80 g/l ):

SEVERE form ( Hb < 80 g/l ):

Back 70

Prednisone until Coombs test negative.

When therapy is ineffective:
CYCLOPHOSPHAMIDE

Severe: Both above combined + transfusion.

Front 71

What are the two main functions of the spleen?

Other functions?

Back 71

Filters blood to remove damaged/old RBC- red pulp
Serves as secondary lymphoid tissue by removing infectious agents and using them to activate lymphocytes- white pulp


Other: A significant reservoir for T lymphocytes
Plays an active role in the production of IgM antibodies and complement
Has significant role in the functional maturation of antibodies

Front 72

Back 72

1. Vascular sinusoinds
2. Red pulp
3. follicle
4. Marginal zone
5. Periarterial lymphatic sheet (PALS)
6. White pulp

Front 73

Function of White pulp?

Back 73

The white pulp is circular in
structure and is made up mainly
of lymphocytes. It functions in a
way similar to the nodules of the
lymph node.

Front 74

Function of Red pulp?

Back 74

The red pulp surrounds the white
pulp and contains mainly red blood
cells and macrophages. The main
function of the red pulp is to
phagocytize old red blood cells

Front 75

When is it splenaomegaly (significant)?

Back 75

When Palpable = significant, clear, usually clinically important. Usually after 1,5-2x increase in size.

Front 76

Infections that cause splenomegaly?

Back 76

Bacterial: Typhoid fever, endocarditis, septicemia, abscess
Viral:E-B virus, CMV, and others
Protozoal: Malaria, toxoplasmosis

Front 77

Hematology benign disorders
that cause splenomegaly?

Back 77

Hemolytic anemia
Extramedullary hematopoiesis: thalassemia, osteopetrosis, (myelofibrosis

Front 78

Metabolic diseases that cause splenomegaly?

Back 78

Lipidosis: Niemann-Pick, Gaucher disease
Mucopolysaccharidosis infiltration: Histiocytosis

Front 79

Other randoms that can cause splenomegaly?

Back 79

Congestion (eg right heart failure, thrombosis of v. lienalis)
Cirrhosis
Cysts + abscesses

Front 80

Causes of splenomegaly in malignant haematology (5)

Back 80

Myeloprolipherative diseases (MPD)
2. leukemia
3. Lymphoma
4. Histocytic disease
5. Systemic mastocytosis

Front 81

Hypersplenism

Back 81

Refers to a variety of ill effects resulting from increased splenic function that may be improved by splenectomy


Hypersplenism can be categorized as primary or secondary

Front 82

The criteria for diagnosis of hypersplenism included:

Back 82

The criteria for diagnosis included:
Anemia, leukopenia, thrombocytopenia or a combination of the three
Compensatory bone marrow hyperplasia
Splenomegaly

Front 83

Felty’s Syndrome

Back 83

Is a syndrome consisting of severe rheumatoid arthritis, granulocytopenia and splenomegaly
It usually occurs in patients with a long history of rheumatoid arthritis
Severe, persistent and recurrent infections are characteristic
Moderate splenomegaly is common
Splenectomy is effective in most patients

Front 84

Infectious Mononucleosis in realation to splenomegaly

Back 84

A disease characterized by fever, sore throat, lymphadenopathy and atypical lymphocytes
Most patients are young
Clinical symptoms are similar to those of a severe upper respiratory tract infection
The spleen is enlarged and palpable in over 50% of patients
Splenic rupture may occur

Front 85

Diagnosis of splenomegaly
(Methods)

Back 85

Palpable vs non palpable
US and/or CT scan (PET) (to decide if homegenous or not)
Crucial point: cause of splenomegaly

Front 86

Gaucher’s Disease

Back 86

Is a disorder of lipid metabolism that may result in massive splenomegaly and hypersplenism
Commonly found in the Jewish population
Diagnosis is made by finding the typical Gaucher’s cells in biopsy tissue
Massive splenomegaly is usually the most common form of presentation
The adult form is the most common form
Splenectomy (subtotal) shows great benefits

Front 87

Blood Compositional Changes in the Asplenic or Hyposplenic Patient

Back 87

The absence of functional splenic tissue results in characteristic changes in the circulating blood
Some of these are predictable and desirable results
These changes are considered a measure of its success when splenectomy is performed for a hematologic disease
Howell-Jolly bodies (nuclear remnants) and thrombocytosis (desired result)
Other findings include: target cells, acanthocytes (spur cells), Heinz bodies (denatured hemoglobin) and stippled red cells

Front 88

Back 88

Howell Jolly bodies

Howell-Jolly bodies are round, purple staining nuclear fragments of DNA in the red blood cell

Front 89

Complications of splenectomy

Back 89

Long life OPSI risk

Earleir onset of atherosclerosis

Front 90

Postsplenectomy Sepsis (OPSI)

Back 90

Asplenic patients have an increased susceptibility to the development of overwhelming infection caused by encapsulated microorganisms.
The risk of sepsis is approximately 60 times greater than normal after splenectomy

Front 91

Postsplenectomy Sepsis
The most common bacteria:

Back 91

The most common bacteria: Streptococcus pneumoniae, Neisseria meningitidis or Haemophilus influenzae

Front 92

What is a Differential count?

Back 92

Seperation and counting the leukocytes

Front 93

How many leu is there in peripheral blood/L?

Back 93

4,0 – 10,0 x109/l

Front 94

in which ''pools'' can we find the netruphils + their %?

Back 94

Marrow pool: 90% neutrophils
Blood pool: 3%
Tissue pool: 7% (eg mucosa)

Front 95

Where are Granulocytes & monocyte formed?

Back 95

Granulocytes & monocytes are formed only in bone marrow

Front 96

Lymphocytes are produced in?

Back 96

Lymphocytes are produced in MB + in various lymphoid tissues (thymus, lymphnodes, splen, etc)

Front 97

Granulocyte life span

Back 97

Granulocytes:
after released from bone marrow, 4-8 hours circulate in blood
& another 4-5 days in the tissues.
Survive only for few hours in serious infection

Front 98

Monocytes lifespan:

Back 98

10-20 hrs in blood.
Once in tissue they get much larger size to become tissue macrophage → life span month(s)

Front 99

Life span lymphocytes:

Back 99

Life span for week or years depending on body’s need.
They continually circulate in blood & move from blood to tissues & from tissues to blood and again blood to tissues.

Front 100

How are the lobes in the neu connacted?

Back 100

By chromatin

Front 101

Arneth count

Back 101

Arneth count: More the no. of lobes, the more mature is the neutrophil. More the no. of mature cells, Arneth count shifts to right (Vit. B12 or folate deficiency).
More the younger cells → shift to left (infection).

Front 102

Back 102

Neutrophil

Front 103

Neutrophil's granules:

Back 103

neutrally
stained granules

1. Primary/ lysosomal granules: less in no. containing acid hydrolases
2. Secondary granules: more numerous. Contain
Lactoferin,

Front 104

Neutrophil function

Back 104

Phagocytosis: 1st line of defence, ingest & destroy a bacteria.

Pyrogens & inflammatory cytokines: endogenous pyrogen which is an important mediator of febrile response to bacteria + other regulation and inflam. defense reaction

Front 105

Reactive neutrophilia example:
Physiological (6)
Pathological (3)

Back 105

B. Pathological 1)Acute pyogenic (pus forming) infections, 2)Following tissue destruction

Front 106

Neutropenia
Examples of reasons: (6)

Back 106

In children, 2) Typhoid, paratyphoid fever, 3) Viral infection, 4) Malaria, 5) Aplasia of bone marrow,
6) Bone marrow supprepression (failure).

Front 107

Leukemoid reaction

Back 107

Non malignant excesive increase in leukocytes (in most cases neutrophils) in reaction to mostly inflammatory noxas.
WBC can increase up to 40-60 x 109/l , if neutrophilia significant left shift in differential is apparent.

In most cases: sepsis (diffuse peritonitis, acute cholecystitis, acute pyelonephritis, etc.)

Front 108

Back 108

Eosinophil
Nucleus:
Usually (85%) cells ‘bilobed

Cytoplasm:
Acidophilic, appears light pink in colour after staining 2. Granular

Front 109

Eosinopenia
Causes (3)

Back 109

Causes are:- 1) ACTH & steroid therapy, 2) Stressful conditions, & 3) Acute pyogenic infections

Front 110

Back 110

Basophil

Nucleus:
irregular bilobed, often ‘S’
shaped & its boundary is not
clear because of overcrowding
with coarse granules.

Cytoplasm:
Is slightly basophilic & appear blue, it is full of granules.

Front 111

Mast cells

Back 111

Large tissue cells resembling basophils. Present in bone marrow & immediately outside the capillaries in the skin.
These do not enter the blood circulation (normally).
Functions: Mast cells play role in allergic reactions similar to the basophis.

Front 112

Monocyte granules:

Back 112

Azur granules

Front 113

CD56,CD57

Back 113

NK cells

Front 114

CD3

Back 114

T cell rec

Front 115

CD4

Back 115

Thelper 0,1,2

Front 116

CD8

Back 116

Cytotoxic T cell

Front 117

CD19,CD20

Back 117

B lymphocyte

Front 118

Pelger Huët´s

Back 118

Pelger Huët´s abnormal leukocyte morphology:
autosomal dominant inher. disease: hyposegmentation of the nucleus

Front 119

May-Hegglin´s

Back 119

May-Hegglin´s leukocyte abnormality: inherited together leukopenia + Döhle´s inclusions in neutrophils + thrombocytopenia with giant platelets.

Front 120

Leukocyte adhesion defect (LAD):

Back 120

autos. Recessive membrane defect due to lack of CD18 molecule. Defect in chemotaxis, aggregability and phagocytosis. Clinicaly: necrotic skin infections, pneumonits, otitis etc. Therapy: aloSCT.

Front 121

autos. Recessive membrane defect due to lack of CD18 molecule. Defect in chemotaxis, aggregability and phagocytosis. Clinicaly: necrotic skin infections, pneumonits, otitis etc. Therapy: aloSCT.

Back 121

autom. recessive disease with impaired migration and degranulaction of granulocytes. Comes with albinism, nystagmus, photophobia, mental retardation, frequent bacterial infections, peripheral neuropathy. Therapy: aloSCT

Front 122

When do we see Döhle´s inclusions?

Back 122

May-Hegglin's abnormality in neutrophils

Front 123

How many healthy adults have palpable lymphnodes?

Back 123

56%

Front 124

In palpable LN, benign vs. malignant, percentage in individuals below 30 and above 50?

Back 124

In individuals < 30 years: 80% benign etiology

In individuals > 50: 60% malignant etiology

Front 125

Assessing adenopathy: History

Back 125

Age
Tumor or TBC in the history
Allergy
Drugs/medication
Duration of adenopathy
Associated complains (symptoms): fever, night swetting, malaise, weight loss, artralgy, sore throat, fatigue etc.
Smoking
Travels

Front 126

What to look for when doing phsyical examination when lymphadenopathy?

Back 126

Location
Size
Sensitivity
consistency
reaction of surrounding area

Front 127

Autoimmune disorders causing lymphadenopathy: (5)

Back 127

RA, SLE, dermatomyositis, MCTD, Sjögren´s

Front 128

Frequent causes of adenopathy according to the location

Inguinal (or axillar) adenopathy  1cm:

Back 128

Inguinal (or axillar) adenopathy  1cm: usually benign

Front 129

Frequent causes of adenopathy according to the location

Cervical adenopathy:

Back 129

Cervical adenopathy: infections, carcinomas (consistency), lymphomas. Sialoadenitis (pseudolymphadenopathy)

Front 130

Frequent causes of adenopathy according to the location:
Mediastinal adenopathy:

Back 130

Mediastinal adenopathy: lymphomas (mediastinum anterior), sarcoidosis, metastatic cancer

Front 131

Frequent causes of adenopathy according to the location
Isolated axillar adenopathy:

Back 131

Isolated axillar adenopathy: infection, breast Ca, lymphoma

Front 132

Frequent causes of adenopathy according to the location
Isolated inguinal adenopathy

Back 132

Isolated inguinal adenopathy (significant): infection (also veneral), lymphoma, metastatic Ca (consistency)

Front 133

Frequent causes of adenopathy according to the location
Generalized adenopathy:

Back 133

Generalized adenopathy: infection (EBV, HIV, etc.), malignant lymphomas, CLL

Front 134

Tender Vs. painless LN

Back 134

lymph nodes that are tender are more likely to be due to an infectious process,
whereas painless adenopathy raises the concern of malignancy.

Front 135

Lymph node consistency
Lymphoma, ca, infectious?

Back 135

lymph nodes containing metastatic carcinoma are rock hard,
lymph nodes containing lymphoma are firm and rubbery,
lymph nodes enlarged in response to an infectious process are soft.

Front 136

INdication for LN biopsy?

Back 136

Constitutional symptoms (weight loss, fever, night sweats) otherwise unexplained
Persistent adenopathy > 4 - 6 weeks, otherwise unexplained
Increasing size of the lymph node for several weeks
Appearence of additional lymph nodes
Abnormal blood test results (anemia, elevetad ESR, LDH, liver chemistries), otherwise unexplained
Abnormal chest radiograph (e.g. mediastinal adenopathy)

Front 137

LN biopsy comments:

Back 137

Excision of the whole lymh node strongly
preferred

Reasonably experienced surgeon preferred

Fine needle biopsy must be avoided