Heamatology Flashcards
Around which time, the amount of γ and β is the same in a newborn’s blood?
4-6 months postnatally.
When should we administer Anti-IgG to a pregnant woman to prevent hemolytic disease of newborn.
It is needed, in the third trimester of pregnancy and early postpartum—> Rh ⊝ mother; Rh ⊕ fetus. (So obviously, treatment to mother is only NEEDED if she is NEGATIVE–> mnemonic type, no logic in this sentence)
Injecting Anti-IgG to mother will prevent her from making her own, because the ones she makes on her own will cross the placenta and kill the baby!
Pathogenesis of ABO hemolytic disease of the newborn,
The mother is Type O, (O mother) and she already has antibodies against A and B, if she has a fetus of AB type–> Her antibodies are going to cross the placenta and damage the baby’s blood.
How do you differentiate between Rh hemolytic disease and ABO hemolytic disease of newborn?
ABO hemolytic disease of newborn–> occurs in the very first newborn, Rh occurs after the first one!
ABO is not that severe!
A left shift is seen due to increase in ________ cells.
It is seen in two conditions?
Band cells!
Bacterial infections, CML
Rate limiting reaction of HMP shunt?
Glucose-6-Phosphate being converted into 6-PHOSPHOGLUCONATE (asked in uworld)
Catalysed by G6PD (Glucose 6 phosphate dehydrogenase)
What does transketolase do?
Part of HMP-shunt pathway-that occurs in the cytoplasm. (Obviously, occurs in RBCS which have no nucleus so will occur in the cytosol hee naa)
an enzyme of the pentose phosphate pathway that helps convert ribulose 5-P (derived from glucose) to glycolysis intermediates (eg, glyceraldehyde 3-P)
(With trans—> remember 5 into 3–> odd numbers, and trans means 3 genders)
Granules in platelets contain what?
DENSE GRANULES—> Ca2+,
ADP, Serotonin, Histamine;
(CASH)
α granules (vWF, fibrinogen, fibronectin, platelet
factor 4)–> alFa (so everything has F)
_________ from bacterial LPS binds ______ on
macrophages to initiate septic shock.
(HIGHESTT-YIELD–> Have seen so many questions on it)
Lipid A from bacterial LPS binds CD14 on
macrophages to initiate septic shock.
Macrophages are activated by _________
Activated by γ-interferon
What are macrophages of Connective tissue and skin called?
histiocytes inconnective tissue, Langerhans cells in skin.
Basophilia is uncommon, but can be a sign of ________.
CML
So, now we know that CAMAAL BAND is basic!–> CML presents with left shift as well as basophilia
Which cells in the blood contain heparin?
BASOPHILSSSS!
Which cell can bind the Fc portion of IgE to
its membrane?
Mast cells. (High yield)
Which prevents mast cell
degranulation>
Cromolyn sodium prevents mast cell
degranulation.
Vancomycin, opioids, and radiocontrast dye cause rash because they can elicit __________________?
(SO HIGH YIELD)
IgE-independent mast cell degranulation
Location of B-lymphocytes in LN and Spleen?
Follicles of LN,( Follicles are found in the cortex of LN)
White pulp of spleen
Helper T cells vs Cytotoxic T cells, There receptors and what MHC class do they recognize?
Helper T cells--> Helpers even up things---> so CD4+, and recognize MHC class 2. Cytotoxic T cells--> toxic log ziaada hotay hein and they don't even up things--> CD8+, recognize MHC class 1
B ney baeth jaana hota hai? What does it remind you of?
B-cells go reside in the follicles of LN (in the cortex of LN which is in the periphery) and white pulp of spleen (white pulp of spleen is right in the middle). Whereas T-cells circulate in the blood. (80% of circulating lymphocytes are T cells)
B cells which release insulin of pancreas are located in the MIDDLE of the pancreas.
What should you remember about Plasma cells?
Found in bone marrow and normally do not circulate in peripheral blood
Why are HbS and HbC more positively charged than HbA?
HbS has–> Valine (sickling walon ka kaam hai)–neutral
HbC—> has LYSINE (Lies-seen)- positively charged.
The normal Hb has glutamic acid and it is negatively charged, so it goes the farthest from a negative cathode on Hb electrophoresis.
Target cells are seen in?
HALT said hunter to the target.
H- HbC
A- Asplenia (With no spleen, noone removes the extra RBC membrane and hence the cells have excessive surface area to volume ratio resulting in target cells)
-Liver disease (in obstructive liver disease–> there’s increased cholesterol to phospholipid ratio that is why target cells are formed)
T- thalassemia (B thallassemia specially needs to be remembered)
Schistocytes are seen in?
MAHAs (eg, DIC, TTP/HUS, SLE HELLP syndrome, severe HTN due to hyperplastic arteriosclerosis),
Macroangiopathic hemolytic anemia/Mechanical hemolysis(eg, heart valve prosthesis, aortic stenosis)
INTRAVASCULAR HEMOLYSIS CAUSES SCHISTOCYTES/HELMET CELLS (HIGH YIELD)
Acanthocytes vs Echinocytes?
Acantho-cytes/spur cells–> CANTHA BAII–> Projections of varying size at irregular intervals. Seen in ABETALIPOROTEINEMIA.
(Cantha baii spurrs a lot, is irregular and ay-beta ay-beta buhat kertiin hein)
Echinocytes/Burr cells–> Liver disease, ESRD, pyruvate kinase deficiency
Mutation in genes encoding RBC membrane protein _________ causes heriditary elleptocytosis.
Mutations
Which RBC inclusions need supravital stain to be visualized?
Supravital/ crystal violet stain is used to visualize Hein bodies.
Heinz Bodies are seen in G6PD–> When removed in the spleen, RBCS become—> Degma cells/Bite cells.
(Owais used Heinz ketchup and thought of himself as SUPER, was a dog and dogs bite)
3 important findings of Siderblastic anemia:
In Bone Marrow—> Ringed sideroblasts–> perinuclear MITOCHONDRIA visualized via prussian blue stain.
in Peripheral Blood Smear:
1. Basophilic stippling–> BLUE DOTS bharr rahay hein RBCs ko –> basophilic RIBOSOMAL PROTEINS.( Don’t contain iron)—>Ribosomal proteins are accumulated because there’s inhibited rRNA degradation!!
- Pappenheimer bodies—>Basophilic granules (contain iron)–> hammer is made up of iron.
Buhat barra DLA–>???
Macrocytic anemia seen in a non-megaloblastic anemia:
>Diamond-Blackfan anemia
>Liver disease
>Alcoholism
How will 3 deletions of alpha gene and 4 deletions of alpha gene manifest as?
3 deletions mean: (– –/– α)—–> HbH will be seen, excess β-globin forms β4
4 deletions mean: (– –/– –)—> Hemoglobin Barts seen which is γ4
(Barts is gamer!)
Hemoglobin electropheris result differences in β-thalassemia minor and β-thalassemia major?
β-thalassemia minor: increased HbA2 (more than 3.5%)
β-thalassemia major: increased HbF (α2γ2) and increased HbA2 .
Mechanism of action of dimercaprol and where is it used?
MOA is–> SH groups bind to heavy metals and form sulfhydril group.
>used to treat wrist and foot drop in lead poisoning—> Dimercaprol and EDTA are 1st line of treatment
>Given in wilson’s disease where copper is accumulated in a patient’s tissues.
>Arsenic, mercury and lead poisoning.
Another name for dimercaprol is?
British anti-Lewisite/BAL.
Which drugs cause sideroblastic anemia?
Isoniazid, linezolid (HighYield)
Isoniazid inhibits pyridoxine phosphokinase/pyridoxal 5 phosphate/ IN SHORT VITAMIN B6.
Remember, Sideroblastic anemia is due to problem with ALA synthase, and ALA SYNTHASE NEEDS B6 as a co-factor.
(SIDRA, ALA SYNTHASE, SIX)
Extravascular hemolysis specifically occurs in?
Cords of Billroth of red pulp of the spleen.
So if they have described a scenario of extravascular hemolysis–> and shown a histology–> it will be of splenic sinuses/cords in the red pulp!!
Iron and TIBC, are related and what are you supposed to know about it related to different anemia?
IDA—> ↓ iron,↑ TIBC,
Sideroblastic Anemia, hemochromatosis: ↑iron, ↓ TIBC
Iron and TIBC always go opposite to each other, except in Anemia of Chronic disease they go in the same direction.
Anemia of Chronic Disease: ↓ iron, ↓ TIBC
(Ferritin is ALWAYS going to be opposite to TIBC)
AIHA,
Causes of warm and cold AIHA
AIHA–> Type 2 HSR.
Warm AIHA–> Occurs due to IgG. IgG attaches to RBCs. (This IgG is mostly against the Rh antigen of the RBC). These RBCs are eaten by splenic macrophages in the red pulp of spleen. This is called extravascular hemolysis.
Occurs in SLE, CLL, drug induced AIHA due to Cephalosporins, Pencillin, alpha-methyldopa.
Cold AIHA–> Due to IgM against RBCs ( IgM is a pentamer which looks like a snowflake!)–> This activates complement system to destroy RBCs inside the vessel–> Hence, this is INTRAVASCULAR hemolysis.
This is the phenomenon that occurs in infectious mononucleosis (EBV, CMV), CLL, B-cell lymphoma, Mycoplasmapneumoniae infections (High-yield!!!)
Treatment for warm and cold AIHA?
For warm, we can give steroids (prednisone), rituximab, and splenectomy (because spleen is eating up all those tagged RBCs)
For cold, avoid cold exposure and rituximab.
Important presentation related facts of AIHA?
Sudden drop in Hemoglobin, ELEVATED retic count (because BM is workingg)
Coombs tests will be POSITIVE.
Peripheral Blood Smear will show SPHEROCYTES!
