Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PANRE > hematology > Flashcards

hematology Flashcards

(66 cards)

Start Studying
1
Q

Heme component

A

FE is part of heme- functions to bind and release oxygen as needed

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

globin component

A

5 subunits- in adult hemoglobin- 2 alpha and 2 beta chains- make up the ADULT hemoglobin

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

cheleation therapy

A

patients who receive frequent transfusion to remove excess FE

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

Transferrin and total iron binding capacity (TIBC)

A

Transferrin binds to free Fe —> transferring trasnports FE throughout the body-
TIBC is indirect way of measuring transferring level:
INCREASED transferring and TIBC : Fe deficiency
Decreased Transferrin and TIBC: Anemia of chronic disease

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

Ferritin

A

decreased in FE deficiency
Increased in anemia of chronic disease
Iron is stored in the ferritin protein molecule- IRON IN STORAGE!

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

Hemolytic anemia (intrinsic)- inherited disorders)

A

sickle cell anemia, Thalassemia, G6pd deficiency, Hereditary spherocytosis

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

Extrinsic hemolytic anemia (aquired)

A

autoimmune hemolytic anemia, DIC, TTP, HUS, hypersplenism

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

LDH

A

enzyme found in RBC- too much rbc destruction leads to increase in serum LDH

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

indirect bili

A

if too much rbc distruction - causes jaundice

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

direct bilirubin

A

dark urine production

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

sickle cell anemia

A

hgb S on hemoglobin electrophoresis

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

Thalassemia

A

microcytic anemia with normal or increased iron - no tx response to Fe tx.
alpha thalassemia: hgbA, A2 and F- normal hemoglobin ratios
beta thalassemia: hemoglobin electrophoresis shows decreased A, increased A2 and Increased F

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

G6pd deficiency

A

episodic- sulfa drugs, fava beans, infections- hemolytic anemia

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

hereditary spherocytosis

A

coombs negative and +osmotic fragility test

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

autoimmune hemolytic anemia

A

coombs POSITIVE!- microspherocytes

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

TT{ and HUS: both normal coags

A

TTP: thrombocytopenia, hemolytic anemia, kidney damage ++++++++ neurological symptoms and fever

HUS: TRIAD!= thromboycotpenia, hemolytic anemia and kidney damage- seen in children- kidney inovelemnt higher than in TTP.

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

DIC

A

prolonged PT and PTT

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

rouleaux formation

A

stack of coins- multiple myeloma

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

auto agglutination

A

clumping of RBC- cold agglutinin autoimmune hemolytic anemia

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

howell jolly bodies

A

decreased splenic function !!!

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

hemolytic cells

A

bite cells, schistocytes, keratocytes

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

basophilic stippling

A

SIDEROBLASTIC ANEMIA, THALASSEMIAS, heavy metal poisioning

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

target cells

A

sick cell, thalassemia

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

hypersegemented neutrophils

A

B12 and folate deficiencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Auer rods
Acute myelogenous leukemia
26
reed sternberg cells
hodkin lymphoma
27
b12 deficiency
animal food is main source. b12 binds to IF - absorbed in terminal ileium -b12 def causs abnormal synthesis of DNA pernicious anemia- loss of gastric parietal cells- these secrete IF strict vegans ETOH neuro: paresthesia, gait abnormalities, memory loss, dementia, anorexia, diarrhea, glossitis increase serum omocysteine and methylonic acid IM b12 repplacement
28
folate deficiency
needed for DNA syntehsis- no neuro symptoms. | replace folate
29
iron defi anemia
mc due to bleeding chronic blood loss- colon cancer or hookworm pregnancy crave ice, pica, angular cheilitis, koilonychia (nail spoon)- decreasedferritin, increased TIBC, decreased iron, decreased transferrin sat give iron, vitamin C increases FE absoroption
30
plummer vinson sndreom
dysphagia, esophageal webs, atropic glossitis and fe deficiency
31
lead poisoining
abd pain with constip, neurologic symptoms, basophilic stippling cheleation therapy
32
thalassemia
decreased production of globin chains after 6 months of age- adult HGB is predominant produced adult: hgb A: 2 alphas, 2 betas A2: 2 alphas, 2 DELTAS fetal: 2 alphas: 2 gamma (tracE)- looks like yY
33
alpha thalassemia
MC in SE asians target cells decreased alpha globin chain production- 4 genes determine it mild: no treatment blood transfusion, iron chelating agents
34
beta thalassemia
decreased production of beta globins chains--->excess alpha chains minor- 1/2 major: 2/2 minor- no symptoms cooley's : major: become symptomatic at 6 monthshepatosplenomagly, severe hemolytic anamie,a jaundice TARGET CELLS! increased hgba2 and hgbF periodic blood transfusions, vitamin C, folate, iron chelating agents.
35
chronic disease anemia
increased ferritin- iron storage due to acute phase reactant, decreased TIBC, decreased serum Fe
36
G6pd def
affects mostly males- african american males- heiz bodies- g6pd usually protects rbc enzyme against oxidative stress- without it- hgb becomes methemoglobin- which does not carry oxygen well. --->these denatured hgb are destructed by splenic macrophages: episodic hemolytic anemia EPISODIC: splenomegaly- infections, FAV bbeans, SULFA drugs, antimalarials avoid offending food and drugs iron/folic acid supp, blood transfusions if needed
37
sickle cell disease
micro thrombsois- due to rbc sickling because when someone is hypoxic, decreased solubility- so it causes throbosis- sickeld cells then destroyed by the spleen infections: osteomyelitis: salmonella- aplastic crisis associated with parvovirus! h shaped ventrebra, splenic sequestration, painful occlusive crisis (acute chest syndrome, back, abd , bone pain)- priapism common howell jolly- functional asplenia- due to splenic infarction!
38
TX for sickle cell
IV hydration and OXYGEN!- pain crisis hydroxyurea: reduces frequency of pain crses folic acid immunized for s. neumo, h flu, and n.gonrrhea STEM CELL TRANSPLANT: cure
39
hereditary spherocytosis
+osmotic fragility test, hypercrhomic microcytosis, coombs neg, sphre shaped RBC Tx: folic acid for mild` splenectomy for severe disease
40
autoimmune hemolytic anemia
+direct coombs test: distinguishes from hereditary spherocytosis warm agglutininis: autoimmune- SLE cold: at colder temp- mycoplasma, EBV warm: cortico cold: avoid cold
41
hemostasis
vascular injury causes platelet aggregatin | activation of that: ADP and thromboxane A2- forms platelet plug
42
clotting factors- secondary hemostasis
FIBRIN stands- strengthens the platelet plug Disease: hemophillia, DIC and von willebrand disease extrinsic path( prolongs PT), intrinsic path (prolongs PTT)
43
PTT
heparin, DIC, vwD, hemophilia A and B | factors 1,2,5,8,9, 11 and 12
44
heparin overdose treatment
protamine sulfate
45
PT
extrinsic pathway: warfarin, vitamin K deficiency, DIC | 2, 5,7,10
46
ttp
thromboycopenia- petechiae, mucocutaenous bleeding- skin, oral,nose bleed, 2. MICROANGIOPATHIC hemolytic anemi +neurological symptoms and FEVER! decreased ADAMTS13- vwf cleaving protese: vwf is not cleaved- so it stays there blocking - small vessel thrombosis- RBC become damaged when they circulate in the occluded small vessels- hemolytic anemia normal coag splenomeg
47
TX for TTP
plasmapheriesis- TOC- removes antibodies vs.. ADaMTS13 | CORTICOSTEROIDS, cylclophosphamide
48
HUS
hemolytic uremic syndrome no fever, or neuro symptoms preceded by E.coli- shigella or salmonella gastroenteritis platelet activation by exotoxins: hemolytic anemia, thrombocytopenia OBSERVATION MOSTLY TX: plasmapheresis NO ABX
49
DIC
bleed and coag infections!: gram neg sepsis most common reasons, malignancy, or obstetric thrombosis and widespread hemorrhage decrease thrombin, decreased fibrinogen, increased PTT/PT/INR- severe thrombocytopenia, increased fibrinolysis, increased D dimer TReat underlying....FFP if severe bleed- replaces coag factors
50
ITP
``` autoimmune thrombocytopenia- mc in children after a viral infection -mucocutaneous bleed- no splenomegally normal COAG TESTS! children: observation, IVIG adults: cortico +IVIG ```
51
hemophilia A
only in males- x linked affects intrinsic of clotting +HEMARTHROSIS, +excessive hermorrhage in trauma or surgery, prolonged PTT!!- normal platelet levels TX: factor 8 infusion desmopressin - increases factor 8 and vwf
52
factor 9-deficiency- christmas disases
prolonged PTT- deep tissue bleeding, demopressing IS NOT SUEFUL!! GIVE FACTOR 9 infusion
53
Von willebrand disease
ineffective platelet adhesion- - MOST COMMON HEREDITARY bleeding disorder it is needed for initial platelet adhesions and prevents factor 8 degradation. mucocutaenous bleed- menorrhagia, epistaxis, easy bruising- PETECHIAe common in VWF prolonged PTT, bleeding time and ptt prolongation worse with aspirin mild: no treatment severe:DEsmopressin
54
hodgekin's
bimodal- peaks at 20 and then 50: upper body lymph nodes affected- neck, axilla, sholuder, abdomen Epstein barr virus painless lympadenopathy, night sweats weight loss and fever- if advanced reed-sternberg cells!- mediastinal lymphadenopathy
55
non-hodgkin's lymphoma
painless lymphadenopathy extranodal sites common: GI, skin, CNS MC!! PERIPHERAL LYMPH NODES MOST COMMON!
56
multiple myeloma
plasma cells, african american men, bone pain, recurrent infections, elevated calcium, anemia, kidney failure monoclonal M rotein spike, bence jones proteins, rouleaux formation, punched out lytic lesions STEM CELL TRANSPLANT!- curative
57
ALL
C childhood malignancy FEVER MC symptoms CNS symptoms too hepatosplenomegaly, lymphadenopathy!!! bone marrow: hypercellular with more than 20% blasts!!!, anemia, thrombocytopenia, wbc: 5-100,000 oral chemo: hydroxyurea, stem cell trasnplant
58
CLL
B cell clonal malignancy MC leukemia in ADULTS overall fatigue, lymphadenopathy, hepatosplenomeg DIFERNTIATED lymphocytes with scattered "SMUDGE cells", lymphocytosis more than 20k pancytopenia: thryombocytopenia, anemia chemo: fludarabine
59
AML
MC acute form of leukemia in adults splenomegaly, gingival hyperplasia, LEUKOSTASIS: wBC is more than 100k AUER RODS!!!! more than 20% blasts!
60
CML
philadelphia chromosome: splenomegaly!! more than 100k wbc more than 30 % blasts
61
primary erythrocytosis- polycythemia vera
jak 2 mutation no hypoxia, incresed hemotaocrit- hyperviscosity, pruritis, splenomeg, flushed face phlebotomy is management of choice
62
secondary erythrocytosis
hypoxia - pulmonary disease- COPD, high altitude, cyanotic heart disease- reactive!- normal WBC/platelets distinguishes 2nd from 1st.
63
factor V leidan
MC inheritied cause of hypercoagulability, | - resistant to breakdwon of factor V by cativated protein C- ypecoag- dvt and pe in young patients.
64
protein c deficiency
vitamin K dependent anticoagulant- stimulates fibrinolysis and clot lysis. recurrent DVT and pulm emobilism tx: heparin- anti coag for LIFE
65
antithrombin III def
venous thrombosis!! recurrent DVT or pulmonary emoboli. high dose IV heparin! can lead to heparin resistance because it is activated by heparin
66
chloromphenicol
chemo tx | SIDE EFFECT: APLASTIC ANEMIA

PANRE (18 decks)

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