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Clinical Medicine Internal Medicine Blood System
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Clinical Medicine Internal Medicine Blood System
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- Outline
Blood system 10‘
content
Red series
RBC decrease
anemia
Overview
iron deficiency
Extreme poverty
aplastic disease
dissolve poverty
fine grain
leukocytosis
tumor
MDS
AL/CL
leukemia
L
Lymphoma
MM
Megakaryon
pltreduce
ITP
Anemia Overview
Anemia Overview
Hb (hemoglobin/hemoglobin)
content
adult male
<120g/L
adult women
<110g/L
pregnant woman
<100g/L
composition
globin
heme
Classification
According to the shape of red blood cells
macrocytic anemia
MCV mean red blood cell volume
>100
MCH mean corpuscular hemoglobin
>34
MCHC mean corpuscular hemoglobin concentration
320~360(32~36)
represents disease
Extreme poverty
cannot be divided
MDS myelodysplastic syndrome
It won’t work anymore
Liver disease
vitB12
folic acid
normocytic anemia
MCV mean red blood cell volume
80～100
MCH mean corpuscular hemoglobin
27～34
MCHC mean corpuscular hemoglobin concentration
320~360(32~36)
represents disease
aplastic anemia
It's still good to make it
Acute blood loss leading to anemia
Spleen rupture
microcytic hypochromic anemia
MCV mean red blood cell volume
<80
MCH mean corpuscular hemoglobin
<27
MCHC mean corpuscular hemoglobin concentration
<320(32)
represents disease
iron deficiency
Tie Shao
sideroblastic anemia
Decreased iron utilization
anemia of chronic disease
chronic infection
TGF-b
IFN-r
TNF
hepcidin
Liver synthesis and secretion
reduce red blood cells
Thalassemia (thalassemia)
The older child had nothing to do, so he took the slow Pleasant Goat subway and fell down and suffered acute blood loss.
According to hemoglobin concentration
Mild
>90
Moderate
60~90
Severe
30~60
Extremely severe
<30
According to pathogenesis/cause
Less sources
Decreased red blood cell production (reduced source)
Hematopoietic stem/progenitor cell abnormalities
aplastic anemia
Hematopoietic stem cell failure
There’s nothing wrong with what you’ve made.
MDS myelodysplastic syndrome
Hematopoietic stem cells cannot be used
malignant clonal disease
Hematopoietic dysregulation
Renal anemia reduces EPO
Anemia of chronic disease (increased hepcidin)
Myelopathic anemia (fibrosis, sclerosis)
Insufficient/impaired utilization of hematopoietic raw materials
iron deficiency
Extreme poverty
Small iron particles
More ways to go
Increased red blood cell destruction = hemolytic anemia (life span 120 days, destroyed early)
RBC membrane abnormalities
hereditary
hereditary xx polycythemia
spherical
Oval
Surface/body decline
Acquisition
Paroxysmal nocturnal hemoglobinuria PNH
The expression of CD55/CD59 is significantly reduced and is easily attacked by antibody complement in the body.
Abnormal Hb in RBC (globin abnormality)
Abnormal amount of globin
Thalassemia (thalassemia)
microcytic anemia
globin structural abnormalities
hereditary hemoglobinopathies
hereditary
RBC enzyme abnormalities
Lack of G6PD
Fava disease (hereditary) - all oxidized glutathione, no reduced form
pentose phosphate pathway
pyruvate kinase
Glycolysis
ATP decreases - Na pump decreases - unable to maintain shape
red blood cell factors
extra-erythrocyte factors
Autoantibodies: Autoimmune hemolytic anemia
Hypersplenism (cirrhosis)
Increased loss of red blood cells
acute/chronic blood loss
male
Hemorrhoids/ulcers
female
Menorrhagia
elderly
Tumors (digestive system)
Iron deficiency anemia - most common
Cause
Mainly caused by chronic blood loss
adult male
hemorrhoid
adult women
Menorrhagia
Gynecological diseases
ITP
elderly
gastrointestinal bleeding
tumor
iron metabolism
Iron status in vivo
functional iron
store iron
Ferritin
all cells
serum
hemosiderin
liver
spleen
marrow
food
plant iron
Mainly Fe3
animal iron
Mainly Fe2
Absorption form
Absorption in the upper small intestine,
Heme--biliverdin--bilirubin (excessive jaundice)--bilinogen--bilibin
Cholesterol - bile salts; heme - bile
bile pigment
biliverdin
Bilirubin
cholinogen
Bile hormone
clinical manifestations
Primary disease manifestations
adult male
Hemorrhoids/PU
Middle-aged and elderly people
Melena/feces OB
Adult women (menorrhagia) ITP
Menorrhagia
Bleeding of skin and mucous membranes
vs
General symptoms of anemia
Essence: hypoxia
Dizziness, fatigue, palpitations
Tissue iron deficiency manifestations (specific manifestations)
Essence: Decreased synthesis of iron-containing enzymes
Abnormal behavior
Pica
Abnormal mental growth and intelligence
Iron deficiency dysphagia (plummer-vinson sign
Spoon-shaped nail (anti-nail)
Glossitis
Keratosis of the lips
Auxiliary inspection
Peripheral blood picture (blood Rt)
Microcytic hypochromic anemia (the most common type of microcytic hypochromic anemia)
MCV<80fl
MCH<27fl
MCHC<32pg (320g/L)
peripheral blood smear
RBC central light stain area expands
Hb decrease
Reticulocytes (Ret)
Ret rises or normal
Compensation is possible
Tips on the effectiveness of iron supplementation and judgment on its efficacy
WBC and PLT can be normal (all three systems are reduced in severe cases), and some patients have increased PLT reactivity.
compensatory increase in plt
special case
ITP increased menstruation leads to iron deficiency anemia
plt decreased, WBC normal
RBC (Hb) decrease
In severe cases, two lines are reduced (usually no three lines are reduced)
However, ITP and iron deficiency are generally not reduced by default! ! ! !
iron metabolism
Serum - iron deficiency triathlon
Serum iron SI
decline
Serum ferritin SF
decline
Transferrin saturation TS
decline
1/3--1/10
S all dropped
vs total iron binding capacity TIBC (the amount of iron that transferrin can bind)
rise
Elevated transferrin (TRF/TF)
Elevated unsaturated transferrin (UIBC)
Transferrin receptor (TfR) becomes larger
Serum soluble transferrin receptor (sTfR)
Best indicator of iron deficiency RBC production
Free protoporphyrin (FEP) increases in RBCs
Increased zinc protoporphyrin (FEP) in RBC
RPBF all rises
bone marrow
Active proliferation, mainly erythroid proliferation (compensation)
Compensatory proliferation of the erythroid system, mainly middle and late erythrocytes
nuclear old plasma young
vs nuclear young plasma old giant young
Fine-grained/megakaryocytic system is normal
Bone marrow aspiration (gold standard, most meaningful)
Look at the bone marrow image
See above
Bone puncture is the gold standard for all hematological diseases except anemia/lymphoma
iron stain
intracellular iron
Decreased sideroblasts
extracellular iron
Decreased hemosiderin iron
Decreased bone marrow granules
Dyeable iron disappears
most reliable
First choice besides anemia and lymphoma
Differential diagnosis: microcytic hypochromic anemia
iron deficiency
Cause/pathogenesis
Depletion of iron stores for various reasons
Serum iron SI
decline
Serum ferritin SF
decline
Transferrin saturation TS
decline
Total iron binding capacity TIBC
rise
bone marrow sideroblasts
Decline, <15%
sideroblastic anemia
Cause/pathogenesis
iron utilization disorders
No iron deficiency
Serum iron SI
rise
Serum ferritin SF
rise
Transferrin saturation TS
rise
Total iron binding capacity TIBC
decline
The ninth edition does not fall
bone marrow sideroblasts
rise, ring sideroblasts appear
treat
Primary disease treatment
Eliminate the cause
Iron supplement treatment
Way
Oral administration (preferred) vitC (reducing agent)
intravenous iron supplementation
Great stimulation
iron supplement
Inorganic iron
Ferrous sulfate FeSO4
Small intestinal absorption of ferrous iron
Severe gastrointestinal reaction
Organic iron-little gastrointestinal reaction
Ferrous succinate
Commonly used, oral
1#tidpo
iron dextran
Use sparingly, intramuscular injection, easy to cause allergies
iron sucrose
For intravenous use
time course
Iron supplementation is effective (top-to-bottom process)
Peripheral blood Ret rises (earliest)
5～10 days
Hb rises
2 weeks
Hb returns to normal
February
Supplement functional iron
Continue taking ferrous succinate for 4 to 6 months
Replenish iron stores
Extreme poverty
Cause
vitB12 and/or folate deficiency
One carbon unit reduced
DNA/RNA reduction
cells cannot divide
MCV>100fl
macrocytic anemia
MCV mean red blood cell volume
>100
MCH mean corpuscular hemoglobin
>34
MCHC mean corpuscular hemoglobin concentration
320~360(32~36)
represents disease
Extreme poverty
MDS
Liver disease
People prone to hair loss
vegetarian
elderly
Type A gastritis
After gastrectomy
achlorhydria
diagnosis
Whole blood cells (decrease of three lines) MCV>100fl Gastrointestinal reactions (nausea/anorexia) Vegetarianism Dizziness/fatigue/paleness/palpitations
physical signs
beef tongue
Tongue surface is smooth
Atrophy of tongue papilla
Manifestations of anemia
Dizziness
Weakness
poor income
Palpitations
pale
Auxiliary inspection
Blood
Pancytopenia (Ret)
Decreased blood vitB12/folate
bone marrow
Young nucleus and old plasma
treat
Primary disease treatment
Supplement vitB12/folic acid
Aplastic anemia (AA)
Cause
Chloramphenicol
bone marrow hematopoietic failure
Decreased whole blood cells (three lines)
Decreased reticulocytes
subtopic
granulocytopenia
Leukopenia
Infection (fever, pneumonia)
Reduction of megakaryotype
Decreased megakaryocytes
pltdecline
Bleeding
bone marrow megakaryocytes
meet occasionally
Rare
lack
vsITP
The two series decreased
Auxiliary inspection
Blood
Normocytic normochromic anemia, pancytopenia
Types
Non-severe aplastic anemia
Severe aplastic anemia SAA=requires rescue
Ret
<0.5% and absolute value <15x10^9/L
WBC
<2x10^9/L
Normal (4～10)x10^9/L
Nneutrophils<0.5x10^9/L
Grain deficiency
Normal (2～3)x10^9
plt
<20x10^9/L
Normal 100～300x10^9
No Hb
bone marrow
Multiple site bone marrow aspiration
gold standard
Removal of bone marrow (cytology)
Recommendation--hematology laboratory/laboratory
result
The bone marrow hyperplasia in many parts of the body was severely reduced, the erythroid, granulocytic and megakaryocytic systems were reduced, and the morphology was normal!
Megakaryocytes occasionally/rarely/deficient
Normal morphology, with a significantly increased ratio of lymphocytes/other non-hematopoietic cells
empty bone marrow
bone marrow biopsy
Removing bone tissue (histology)
Pathology Department, universally unselected answers
diagnosis
Decreased whole blood cells (three lines)
anemia, infection, bleeding
Retfall
Decreased megakaryocyte count
No hepatosplenomegaly and lymphadenopathy
treat
Symptomatic and supportive treatment
correct anemia
control infection
Stop bleeding
Prevention/Treatment
immunosuppressive therapy
cyclosporine
Applies to all AA
hematopoietic growth factor
Elevated RBC
EPO
Elevated WBC
G-CSF
elevated plt
TPO
Androgens (for all AA)
Promotes erythroid hematopoiesis, usually takes effect 2 to 3 months after use
Commonly used
Stanozolol (stanozolol)
Testosterone
Testosterone Undecanoate
Testosterone Propionate
Danazol
Hematopoietic stem cell transplantation
No infections or other complications
Age<40
Suitable donor available
Indications
Heavy relapse
Hemolytic anemia = shortened lifespan of red blood cells = premature destruction
Classification
By onset (condition)
acute hemolysis
chronic hemolysis
Press the hemolysis site
extravascular hemolysis
Spleen (mostly)
Hereditary spherical/oval RBC hyperplasia
Warm body type autoimmune anemia
IgG
Thalassemia
Inherited reduction in the number of globin proteins
Hemoglobinopathies
Inherited globin structural abnormalities
viscosity
pyruvate kinase deficiency
Bethune overseas makes people feel warm
Bone marrow (a few)
Spleen removal is ineffective
Bone marrow/in situ hemolysis
Mega-child poverty/MDS
macrocytic anemia
intravascular hemolysis
intravascular
Paroxysmal nocturnal hemoglobinuria PNH
Cold antibody type autoimmune anemia
IgM
Acute hemolysis caused by blood group incompatibility
G6PD deficiency (favismosis) (most)
Rarely, extravascular
According to the cause
RBC itself problem
RBC membrane abnormalities
hereditary
hereditary xx polycythemia
spherical
Oval
Acquisition
Paroxysmal nocturnal hemoglobinuria PNH
The expression of CD55/CD59 is significantly reduced and is easily attacked by antibody complement in the body.
Abnormal Hb in RBC (globin abnormality)
Abnormal amount of globin
Thalassemia (thalassemia)
Structural abnormality
Hemoglobinopathies
hereditary
RBC enzyme abnormalities
pentose phosphate pathway
Issues outside RBC
Autoantibodies: Autoimmune hemolytic anemia
Hypersplenism (cirrhosis)
Differential Diagnosis - Hemolysis = Anemia Jaundice (increased bilirubin)
extravascular hemolysis
Cause
Mostly hereditary
hereditary spherocytosis
Course of disease
Long/chronic hemolysis
clinical manifestations
Anemia Jaundice (severe/obvious)
Splenomegaly
Three Nothings
Ahemoglobinaemia
Swallowed by the spleen
or a small amount of Hb, decreased haptoglobin
Hb-free urine
Ahemosiderinuria
Urine test negative
intravascular hemolysis
Cause
Mostly acquired
PNH
Fava bean disease is hereditary
Course of disease
short/acute hemolysis
clinical manifestations
Anemia Jaundice (mild/none)
Usually asplenomegaly, pain in lower back and limbs
have
Hbemia, decreased haptoglobin (almost 0)
However, it is not possible to differentiate between internal and external based on haptoglobin.
Hb urine (soy sauce color urine)/overflow proteinuria
Hb blocks the renal tubules, causing kidney necrosis
Small phagocytosis of renal tubular epithelium produces hemosiderinuria
Positive urine Rous test
Bilirubin metabolism
The essence of urobilinogen is fecobilinogen
Jaundice problem
hemolytic jaundice
Cause
hemolytic anemia
Blood bilirubin status
IBIL
significantly increased
DBil
rise
but does not exceed the renal threshold
TBil
rise
BloodDBil/TBil
<0.2
Urine
Urinary bilirubin DBil
-
Free bilirubin is fat-soluble and does not appear in urine when elevated.
Urine/fecalbilinogen
Urinary/fecal bile hormone
Dark color of urine and stool (golden)
hepatocellular jaundice
Cause
Cirrhosis
viral hepatitis
Blood bilirubin status
IBIL
significantly increased
DBil
significantly increased
TBil
rise
BloodDBil/TBil
0.2~0.5
Urine
Urinary bilirubin DBil
rise
Urine/fecalbilinogen
Urinary/fecal bile hormone
uncertain
Early days
rise
The ability of liver cells is not bad and can convert bilirubin into bilibinogen.
Late stage
decline
Liver cells are incapable of converting bilirubin into bilibinogen
Obstructive jaundice (obstructive jaundice)
Cause
bile duct obstruction
pancreatic head cancer
Blood bilirubin status
IBIL
rise
DBil
significantly increased
exceeds threshold
TBil
rise
BloodDBil/TBil
>0.5
Urine
Urinary bilirubin DBil
Strong brown color
Urine/fecalbilinogen
Urinary/fecal bile hormone
-
Clay color
Auxiliary inspection
RBC destruction, releasing hemoglobin
Blood Hb
Urinary Hb
Elevated urinary hemosiderin (positive Rous test)
Increased globin (decreased haptoglobin) Heme
biliverdin
Bilirubin
cholinogen
Bile hormone
Indicates increased red blood cell destruction
Indicators of bilirubin metabolism
biliverdin
Bilirubin
cholinogen
Bile hormone
Hemoglobin metabolism
peripheral blood smear
Broken and malformed red blood cells
RBC life measurement
shorten
Indicates erythroid compensatory hyperplasia
Blood
Retrise
internet celebrity
peripheral blood smear
Visible nucleated red blood cells
marrow
The bone marrow proliferates actively, and the proportion of erythroid cells increases, mainly middle and late immature red blood cells.
Granulocyte/erythrocyte inversion
Normal 2～4/1
Some RBCs have nuclear fragments
Cabot ring
Howell-Jolly bodies
special inspection
Antiglobulin test (Coombs test)
Warm body type autoimmune anemia
Acidified serum hemolysis test (Ham test)
Paroxysmal nocturnal hemoglobinuria PNH
Yawn (Ham) and go to sleep
Flow cytometry to detect the expression rate of CD55 and CD59 on cell surface
PNH
Gold standard (normally above 99%)
Methemoglobin reduction test
Fava bean disease
Ferrous Hb (red) is oxidized by nitrite to methemoglobin (purple brown)
Visible cyanosis
Red blood cell osmotic fragility test
Lost ball
Peripheral blood smear shows a large number of spheroidal red blood cells
Lost ball
vs small amount: avoid poverty
treat
Lost ball
Splenectomy
The first choice and most effective examination
avoid poverty
Warm antibody type 80~90%IgG
Glucocorticoids of choice
First line, 90%
Splenectomy
second line
5% of warm antibody types are secondary and have common causes.
Lymphoproliferative disease
Lymphoma
leukemia
autoimmune disease
SLE
Infect
especially viral infections
drug
penicillin
Cephalosporins
Cold antibody type 10~20%IgM
Heat treatment
Thalassemia/PNH
Symptomatic treatment
First choice
Myelodysplastic SyndromeMDS
definition
Hematopoiesis due to diseased blood cells
Key features
High risk for transformation to acute myeloid leukemia (AML) characterized
Differential diagnosis
1
MDS
duplicity
Nature
Hematopoietic stem cell diseased hematopoiesis
Peripheral blood picture
pancytopenia
bone marrow
Active proliferation
Ret
Can be lowered
ever-changing
spleen
Can be big
karyotype
abnormal
aplastic anemiaAA
Same inside and outside
Nature
Hematopoietic stem cell failure
Peripheral blood picture
pancytopenia
bone marrow
Obvious reduction
Ret
decline
spleen
Not big
karyotype
normal
2
MDS
Obvious pathological hematopoiesis
giant baby
Unobvious pathological hematopoiesis
common
macrocytic anemia
in situ hemolysis
direct damage to bone marrow
jaundice
Reduction in three series
Types
FAB typing
primitive cells
<30%
MDS
≥30%
AML
Classification
RA
Peripheral image
<1%
bone marrow
<5%, ring sideroblasts <15%
RAS
Peripheral image
<1%
bone marrow
<5%, ring sideroblasts>15%
RAEB
Peripheral image
<5%
bone marrow
5~20%
RAEB-t
Peripheral image
≥5%
bone marrow
20%～30%
Auer bodies (rod-shaped bodies) appear in myelocytes
CMML
Peripheral image
<5%
bone marrow
5~20%
WHO classification
primitive cells
<20%
MDS
≥20%
AML
laboratory tests
Bone marrow biopsy
gold standard
or bone marrow biopsy
Cytological examination
Original cells<30%(FAB)or<20%(WHO)
karyotyping
mostly missing changes
8
-5/5q-
-7/7q-
20q-
treat
Symptomatic treatment
anemia
blood transfusion
EPO
androgens
Bleeding
Stop bleeding
Infect
Anti-infective
Type treatment
RA
RAS
Mainly anemia, transformed into acute myeloid leukemia AML5% ~ 15% (low), mainly symptomatic treatment
RAEB
RAEB-t
Mainly with a decrease in whole blood cells, converted to AML>40%/60%, mainly combined with chemotherapy
leukemia
Types
FAB typing
≥30% - acute leukemia
<30%——MDS
L
AL acute leukemia
ALL acute lymphoblastic leukemia
AML acute non-lymphocytic leukemia/acute myeloid/acute myeloid
M0～M7 type eight
CL chronic leukemia
CLL chronic lymphocytic leukemia
CML chronic non-lymphocytic leukemia (chronic myeloid/chronic myeloid)
clinical manifestations
Normal bone marrow hematopoietic function is suppressed
Rapid malignant proliferation of leukemia cells (tumor cells)
RBC decrease
anemia
WBC decrease
Infect
fever
pneumonia
pltreduce
Bleeding
bleeding mechanism
A large number of leukemia cells stasis in blood vessels and infiltrate them
pltreduce
Coagulation abnormalities
Infect
Bleeding is more common in the form of skin petechiae, epistaxis/gum bleeding, menorrhagia, and intracranial hemorrhage.
Acute promyelocytic leukemia (M3) is prone to be complicated by DIC and cause widespread bleeding throughout the body
Leukemia cell proliferation and infiltration manifestations
Key words
Big/swelling/tumor/pain/proliferation
list
Enlarged lymph nodes LN
ALL is common
Lymphoma vs cervical lymphadenopathy
Mediastinal lymph nodes: TcALL
Hepatosplenomegaly
giant spleen
CML
Lower sternum tenderness (frequent)
vs lymphoma usually no
Granulocytic sarcoma (chloroma)
true tumor
AML is common, most common in the orbital region
gum hyperplasia and swelling
vs bleeding gums
Central Nervous System/Testicular Leukemia
Compared
central nervous system leukemia
mechanism
blood brain barrier
It is difficult for chemotherapy drugs to pass through (leukemia cell sanctuary, both seen in remission of ALL)
good hair
child
The most common site of extramedullary recurrence
clinical manifestations
increased intracranial pressure
Headache
Vomit
papilledema
treat
Intrathecal methotrexate MTX
Central injection of methamine
male reproductive system leukemia
mechanism
blood-testis barrier
It is difficult for chemotherapy drugs to pass through (leukemia cell sanctuary, both seen in remission of ALL)
good hair
Toddlers and Youth
The next most common extramedullary recurrence site
clinical manifestations
Painless swelling of one testicle, but infiltration on both sides
treat
Bilateral testicular irradiation
radiotherapy
Affects normal cells, causing men to have no reproductive function
Auxiliary inspection
Bone marrow biopsy
The main basis, the gold standard, must be done
FAB: original cells ≥30%
AML classification M0～M7
M0
Primitive cells>30%
M1
Myeloblasts>90%
M2
Myeloid blasts>30~89%
M3 (APL acute promyelocytic leukemia)
Early grain >30%
M4 (grain-single)
Granules ≥ 20%, mononuclear c ≥ 20%
M5 (single)
Mononuclear cells ≥30%
M6 (red)
M7 (giant)
Cytochemical staining
acute shower ALL
Glycogen staining (PAS)
Strong positive, lumpy
Auer body (rod-shaped body)
-
Neutrophil alkaline phosphatase (NAP)
normal or rising
Acute grain AML (M3)
Peroxidase (MPO/POX)
Strong positive
Auer body (rod-shaped body)
Neutrophil alkaline phosphatase (NAP)
Declining or unchanged
Urgent order AML-M5
Non-specific esterase (NSE)
Strong positive
NaF inhibition ≥50%
Auer body (rod-shaped body)
Neutrophil alkaline phosphatase (NAP)
normal or rising
Immunophenotyping
Lymphocytes
Bc
CD10, 19, 20
Tc
CD2, 3, 4, 7, 8
CD5 is found on lymphoid follicle mantle cells
NKc
CD16,56
Granulocytes
AML
Can have CD13, 14, 15
Common to all AMLs
CD13,33
M3
CD13, 33, 117
Does not express HLA-DR and CD34
Chromosome testing (translocation/translocation, t)
AML
M1
t(9;22)
M2
t(8;21)
M3
t(15;17)
Pathogenesis of M3 (promyelocytic leukemia)
M4
t(16;16)
Prognosis is better
M5
t(9;11)
CML
t(9;22)
Pathogenesis of CML (chronic myeloid)
treat
combination chemotherapy
Tips: Use VP for acute lymphadenitis, Hada for acute granules, M3 retinoic acid, central nervous system
ALL
VP protocol (V: vincristine, P: prednisone)
D (daunorubicin: sad)--DVP protocol
L (L-asparaginase: only for ALL, not for AML): DVLP regimen
AML
Hada plan
HA
homoharringtonine
DA
Daunorubicin
IA
Nordaunorubicin
A (cytarabine)
special type
M3
All-trans retinoic acid
First choice
Common side effects of chemotherapy drugs
vincristine
peripheral neuritis
vs isoniazid
Prednisone
Glucocorticoid side effects
Anthracyclines (daunorubicin)
Cardiotoxicity
L-asparaginase
liver damage
allergic reaction
pancreatitis
High dose MTX
Catarrhitis
Cyclophosphamide (CTX)
hemorrhagic cystitis
Monographs
Slow-grain CML
Chronic phase CP--accelerated phase AP--blast phase BC
Lasts 1 to 4 years
Features
Significant increase in white blood cells
leukostasis
Often>20x10^9
marrow
Myeloid hyperplasia is active, blast cells <10%
Splenomegaly (the most prominent sign, giant spleen)
NAP significantly reduced
Significantly reduced, negative, 0
BCR-ABL fusion gene
phchromosome
treat
imatinib mesylate
Gleevec
Tinib-TKI: Inhibits tyrosine kinase
Lymphoma - Bc, Tc, NKc
Classification/Clinical Characteristics
Hodgkin lymphoma HL
Cell source
Bc (almost 100%)
vs skeletal muscle calcium ion source 100% sarcoplasmic reticulum, cardiac muscle cells 80 to 90%
Incidence
10% rare
Predisposing age
two peaks
15～30 years old
>55 years old
Predisposed gender
Male>Female
lymph node dissemination
progressive transfer
Clinical features
Compression/infiltration is rare
systemic symptoms
Common
Fever, night sweats, itching
May be the only systemic symptom
Unique symptoms
Lymph node pain after drinking alcohol
Shingles
Non-Hodgkin LymphomaNHL
Cell source
Bc（80%～90%）
Incidence
90% more common
Predisposing age
any age
Predisposed gender
Male>Female
lymph node dissemination
jump transfer
vs gastric signet ring cell carcinoma: jump metastasis, young women - Wei
Clinical features
Compression/infiltration is common
Chest
Hilar/mediastinal involvement is more common
CNS
Involving the meninges and spinal cord
gastrointestinal tract
Most common in ileum
bone damage
Most common in thoracolumbar spine
systemic symptoms
Rare
Similarity
Painless progressive enlargement of cervical/supraclavicular lymph nodes
vs ALL
Monographs
Hodgkin lymphoma
Cause
HL with symptoms of persistent fever of unknown origin
Slightly older, more male, the disease is more diffuse, often involving retroperitoneal lymph nodes
HL presenting with periodic fever (P-E fever)
There are more female patients, and most of them have itchy skin.
stage
Clinical stage
1
1 on the same side is one issue
2
2 on the same side is phase 2
3
both sides
Spleen involvement
4
liver
under the ribs
Hepatomegaly
lung
Pleural effusion
marrow
Just one location
Group
Group A
Asymptomatic
Group B
Symptomatic
body temperature
Fever>38
Night sweats
Interference: itching
weight
Weight loss >10% within half a year (<6 months)
Auxiliary inspection (special)
First choice for diagnosis
lymph node biopsy
Get more tissue
Organizational form
Immunohistochemistry
chromosome
Common distractions
lymph node puncture
Less tissue is obtained, and the positive rate of diagnosis is low.
Bone marrow aspiration (biopsy)
used for staging
Blood RT
Three lines are normal in the early stage
AnemiaHb
Only mechanism of anemia: secondary autoimmune anemia (warm antibody type)
pancytopenia
Mechanism of pancytopenia: lymphoma cell infiltration in bone marrow
treat
Combined chemotherapy (mainly systemic therapy) supplemented by radiotherapy (auxiliary local therapy)
HL
ABVD preferred
A
Doxorubicin (doxorubicin)
B
Bleomycin
V
Vinblastine
D
methamphetamine
PreviousMOPP
Has been eliminated, affecting fertility function
NHL
Preferred CHOP solution
C
cyclophosphamide
H
doxorubicin
O
vincristine
P
Prednisone
R-CHOP solution
Bc logo CD20
Whether Hodgkin or non-Hodgkin, the CD20-targeting drug rituximab (rituximab) should be added
Multiple myelomaMM
Pathogenesis
Malignant proliferative disease characterized by massive proliferation of monoclonal plasma cells in the bone marrow
Bc--a large increase in plasma cells--antibody (immunoglobulin) = r-globulin
IgA
IgD
IgG
Most common
IgE
IgM
Features: Monoclonal immunoglobulin Ig (M protein)
Light chain rises
Protein of the week: Overflow proteinuria
heavy chain rise
Clinical manifestations - "Crab symptoms" - lumbar spine (low back pain is the first manifestation)
C——Hypercalcemia
R - renal impairment: high serum creatinine
mechanism
B-J protein (BJ protein) damages renal tubules
Hypercalcemia damages renal tubules
Uric acid damages renal tubules
renal amyloidosis
hyperviscosity syndrome
myeloma cell infiltration
A——Anemia
B——Bone damage——most common in lumbosacral area
Auxiliary inspection
Blood
Normocytic normochromic anemia, red blood cells appear beaded/wired in blood smear
Bone marrow biopsy
Preferred diagnostic method
The bone marrow image shows a large amount of abnormal hyperplasia c
myeloma cells
CD38, 56
vsNKc
CD16,56
vsPNH
CD55,59
Immunoglobulin fixed electrophoresis
Classification Diagnosis
Find the M protein
Serum b2 microglobulin (derived from lymphocytes)
Large tumor burden
for clinical staging
diagnosis
Bone pain (lumbosacral region) Crab manifestations RBC beaded = MM disease
installment
D-S staging
1
Hb
>100
Bone X-ray
No abnormality
2
Hb
85～100
Bone X-ray
1 to 3 osteolytic lesions
3
Hb
<85
Bone X-ray
Osteolytic lesions>3
Serum b2 microglobulin (mg/L)
1
<3.5
2
3.5~5.5
3
≥5.5
Group
A
Serum creatinine <177
B
Serum creatinine>177
Treatment: Combination chemotherapy
Newly treated cases
MPT plan
Melphalan
Prednisone
thalidomide
Targeted therapy
Bortezomib (Velcade)
bleeding disorders
Cause classification/diagnosis
Physiological hemostasis
vasoconstriction
vascular disease
Henoch-Schonlein purpura (more common in women, bleeding of skin and mucous membranes)
Platelet hemostatic plug
platelet disease
ITP (more common in women, dual manifestations)
Menorrhagia
Bleeding of skin and mucous membranes
blood clotting
coagulopathy
Hemophilia (more common in males, adolescents)
Types
First
F8
Second
F9
C
F11
Bleeding site
Deep (muscle hematoma)
joint bleeding
Coagulation/anticoagulation/fibrinolysis process
Physiology
laboratory tests
bleeding index
BT bleeding time
response plt level
BT increases during ITP
coagulation index
PT
APTT
CT
TT
plasminogen
ReactionF
Abnormalities in blood vessel walls
vW
Abnormal anticoagulation
antithrombin
PC
P.S.
thrombin regulatory protein
ThrombomodulinTM
Abnormal fibrinolysis
D-dimer
The simplest FDP: formed by cross-linking of two D segments (normally <0.5mg/L)
FDP assay, plasminogen, t-PA assay
3P test (plasma protamine secondary coagulation test)
Reaction FDP exists
Treatment – Classification of Hemostatic Drugs
Constrict blood vessels/increase capillary density/reduce capillary permeability
represent
Kabaklo
Troxerutin
Pituitaryin
vitamin c
Glucocorticoids
Reduce capillary permeability
Fiscal austerity, DINK has no descendants
Drugs required to synthesize coagulation-related components
vitK
antifibrinolytic drugs
aminocaproic acid
benzoic acid
Drugs that promote the release of hemostatic factors
Desmopressin
primary immune thrombocytopenic purpura
definition
acquired autoimmune disease
Pathogenesis
immune mechanism
Humoral immunity
Antibody
complement
cellular immunity
Tc
Influence
peripheral blood
plt excessive damage
marrow
Megakaryocyte maturation disorder
plt generation reduced
clinical manifestations
More common in women, dual presentation
Bleeding of skin and mucous membranes
Petechiae/spots
Nosebleeds
Bleeding gums
Menorrhagia
iron deficiency
intracranial hemorrhage
Important causes of death
Aura manifestations
Oral and buccal mucosal blood blisters
Blurred vision
Extensive bleeding in multiple parts of the body
Often without splenomegaly
laboratory tests
Bone marrow biopsy
First choice for diagnosis
Increased megakaryocytes
immature megakaryocytes
Granular megakaryocytes
Increased immature megakaryocytes
vsAA: massive reduction of megakaryocytes (occasionally/rarely/absent)
lamellar megakaryocytes
Reduced ripening
Plasma antiplatelet antibodies (Ig) and complement
second choice
PA Ig platelet-associated antibody
Mainly IgG
warm body type
MM disease
Rh blood type
SLE
IgM
Cold antibody type
ABO
RA:RF
PA C3
Blood picture (blood Rt)
pltdecline
Bleeding (heavy menstruation)
RBC (Hb) decrease
WBC is normal
No pancytopenia (neither autoimmune anemia)
coagulation test
BT rises
PT/APTT/CT/TT normal
Differential diagnosis
ITP
platelet disease
double performance
Bleeding of skin and mucous membranes
Menorrhagia
More common in women
beam arm experiment
plateletsplt
Significantly reduced
asymmetric purpura
allergic purpura
Increased fragility of blood vessel walls
single expression
Bleeding of skin and mucous membranes
More common in women
beam arm experiment
pltnormal
symmetrical purpura
treat
If plt>30x10^9
The risk of bleeding is small, observation is the first choice
If platelets <20x10^9
Stay in bed strictly to avoid trauma
first line treatment
Glucocorticoids
First choice, 80% effective
Prednisone
Dexamethasone
DXM
effect
Reduce the production of autoantibodies and reduce antigen-antibody reactions
Inhibit the destruction of platelets by the monocyte-macrophage system
Improve capillary permeability
Stimulates bone marrow hematopoiesis and platelet release into peripheral blood
Reduce platelet consumption
intravenous gamma globulin
second line treatment
TPO
immunosuppressant
vincristine
Most common
vs nephrotic syndrome, nitrogen mustard is the first, cyclophosphamide is the most commonly used
Splenectomy
Ineffective for GC, the disease persists for >6 months
vs warm antibody type autoimmune anemia: glucocorticoid first, splenectomy not possible
Platelets<10x10^9/L
emergency treatment
platelet transfusion
First choice
intravenous gamma globulin
Large dose GC granules treatment
TPO
Plasma exchange (removal of antibody complement)
Old version of textbooks
Summarize
spleen
big
tumor
MDS
leukemia
Lymphoma
MM
blood
infective endocarditis
Cirrhosis
Rheumatoid Arthritis
Extravascular hemolysis with splenic destruction
Not big
Extreme poverty
Re-disability
ITP
blood
rheumatic fever
pancytopenia
none
ITP
Iron deficiency products
avoid poverty
have
PNH
Extreme poverty
AA
tumor
MDS
leukemia
Lymphoma
Only in the 4th period did the three series decrease
MM
Fanconi anemia
Evans syndrome
Summary: Commonly used molecular targeted drugs
lung adenocarcinoma
EGFR
Gefitinib
CML/GIST
TPK(PTK)
Imatinib
NHL/HL
CD20
Rituximab
colorectal cancer
EGFR
Cetuximab
breast cancer
HER-2
Trastuzumab (Herceptin)
Summarize
Hematological chemotherapy regimen
MDS
RA,RAS
Symptomatic treatment
RAEB, RAEB-t
combination chemotherapy
leukemia
AL
ALL
VP (DVP, DLVP)
central lymphocytic leukemia
Intrathecal MTX
testicular lymphocytic leukemia
Bilateral irradiation
AML
HA/DA/IA
M3
All-trans retinoic acid
CL
CML
imatinib
Lymphoma
HL
ABV
NHL
CHOP
CD20 Rituximab
MM disease
MPT plan
Frequent examination of lymphoma immunophenotype and chromosomal translocation (internal medicine, pathology)
Overview
Precursors (naive, lymphoid) B and T
TdT (terminal deoxynucleotidyl transferase)
T cells
CD2, 3, 4, 7, 8
B cells
CD19,20,79a
set of cell markers
CD5
Germinal center (including b)
CD10, BCL-6
NK cells
CD16,56
t(14;18)——BCL-2;t(11;14)——CyclinD1
Commonly tested immune phenotypes
non-hodgkin lymphoma
from lymphoid follicle germinal center
follicular lymphoma
CD19, CD20, CD79a
Bc
CD10, BCL-6
germinal center
BCL-2
t(14;18)
Diffuse large B lymphoma
CD19, CD20, CD79a
Bc
CD10, BCL-6
germinal center
BCL-2
t(14;18)
Burkitt lymphoma
CD19, CD20, CD79a
Bc
CD10, BCL-6
germinal center
BCL-2-
t(8;14)
Internal Medicine
CD22
From the mantle/marginal zone surrounding the germinal center of lymphoid follicles
mantle cell lymphoma
CD20, CD10-, CD23-
CD5, CyclinD1
t(11;14)
marginal zone lymphoma
CD20, CD10-, CD23-
CD5-, CyclinD1-
t(11;18)
Common phenotypes of Hodgkin lymphoma HL
Nodular lymphocyte predominant type
CD20, CD79a, CD15-, CD30- or weak expression
CD30, CD15, CD20-, CD45-
TC
anaplastic large cell lymphoma
t(2;5)
Mycosis fungoides/Sezary syndrome
twisted core
Big S twisted around on the catwalk
Summarize
Awer's body (rod-shaped body)
Severe shower-
other
Quick grain
urgent grain list
Erythroleukemia
subtopic
ph chromosome (Philadelphia chromosome negative)
Slow shower-
other
slow grain
Most common
Quick grain
acute shower
PML-RARA
M3 (APL)
t(15;17)
BCR-ABL
Slow-grain CML
t(9;22)
Neutrophil alkaline phosphatase NAP (didn’t understand)
rise
Leukemia-like reaction (significantly increased), acute lymphadenitis, acute monotonia, aplastic anemia, acute purulent infection
decline
Acute myeloid, chronic myeloid (significantly decreased), PNH, simple viral infection
Screenshot 2023-03-07 11.08.09
Summarize
1
Splenomegaly
MDS
leukemia
Lymphoma
MM disease
infective endocarditis
Cirrhosis
Risk-like
felty syndrome
Small spleen
Re-disability
ITP
Extreme poverty
rheumatic fever
2
No whole blood (reduced three lines)
avoid poverty
ITP (plt--RBC reduced, WBC normal)
Have whole blood (three lines reduced)
severe iron deficiency anemia
Extreme poverty
AA
MDS
leukemia
MM
Lymphoma
Stage IV
PNH
ITP iron deficiency
Reduced plt, bleeding leads to loss of red blood cell hemoglobin
White blood cells are usually normal