Heamatology Flashcards
(97 cards)
1
Q
Around which time, the amount of γ and β is the same in a newborn’s blood?
A
4-6 months postnatally.
2
Q
When should we administer Anti-IgG to a pregnant woman to prevent hemolytic disease of newborn.
A
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!
3
Q
Pathogenesis of ABO hemolytic disease of the newborn,
A
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.
4
Q
How do you differentiate between Rh hemolytic disease and ABO hemolytic disease of newborn?
A
ABO hemolytic disease of newborn–> occurs in the very first newborn, Rh occurs after the first one!
ABO is not that severe!
5
Q
A left shift is seen due to increase in ________ cells.
It is seen in two conditions?
A
Band cells!
Bacterial infections, CML
6
Q
Rate limiting reaction of HMP shunt?
A
Glucose-6-Phosphate being converted into 6-PHOSPHOGLUCONATE (asked in uworld)
Catalysed by G6PD (Glucose 6 phosphate dehydrogenase)
7
Q
What does transketolase do?
A
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)
8
Q
Granules in platelets contain what?
A
DENSE GRANULES—> Ca2+,
ADP, Serotonin, Histamine;
(CASH)
α granules (vWF, fibrinogen, fibronectin, platelet
factor 4)–> alFa (so everything has F)
9
Q
_________ from bacterial LPS binds ______ on
macrophages to initiate septic shock.
(HIGHESTT-YIELD–> Have seen so many questions on it)
A
Lipid A from bacterial LPS binds CD14 on
macrophages to initiate septic shock.
10
Q
Macrophages are activated by _________
A
Activated by γ-interferon
11
Q
What are macrophages of Connective tissue and skin called?
A
histiocytes inconnective tissue, Langerhans cells in skin.
12
Q
Basophilia is uncommon, but can be a sign of ________.
A
CML
So, now we know that CAMAAL BAND is basic!–> CML presents with left shift as well as basophilia
13
Q
Which cells in the blood contain heparin?
A
BASOPHILSSSS!
14
Q
Which cell can bind the Fc portion of IgE to
its membrane?
A
Mast cells. (High yield)
15
Q
Which prevents mast cell
degranulation>
A
Cromolyn sodium prevents mast cell
degranulation.
16
Q
Vancomycin, opioids, and radiocontrast dye cause rash because they can elicit __________________?
(SO HIGH YIELD)
A
IgE-independent mast cell degranulation
17
Q
Location of B-lymphocytes in LN and Spleen?
A
Follicles of LN,( Follicles are found in the cortex of LN)
White pulp of spleen
18
Q
Helper T cells vs Cytotoxic T cells, There receptors and what MHC class do they recognize?
A
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
19
Q
B ney baeth jaana hota hai? What does it remind you of?
A
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.
20
Q
What should you remember about Plasma cells?
A
Found in bone marrow and normally do not circulate in peripheral blood
21
Q
Why are HbS and HbC more positively charged than HbA?
A
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.
22
Q
Target cells are seen in?
A
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)
23
Q
Schistocytes are seen in?
A
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)
24
Q
Acanthocytes vs Echinocytes?
A
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
25
Mutation in genes encoding RBC membrane protein _________ causes heriditary elleptocytosis.
Mutations
26
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)
27
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!!
2. Pappenheimer bodies--->Basophilic granules (contain iron)--> hammer is made up of iron.
28
Buhat barra DLA-->???
Macrocytic anemia seen in a non-megaloblastic anemia:
>Diamond-Blackfan anemia
>Liver disease
>Alcoholism
29
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!)
30
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 .
31
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.
32
Another name for dimercaprol is?
British anti-Lewisite/BAL.
33
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)
34
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!!
35
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)
36
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!!!)
37
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.
38
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!
39
Direct and Indirect Coomb's test?
Direct---> Anti-Ig Antibodies are put into the patient's RBC's.
Indirect Coombs--> Normal RBCs are added.
(Indirect log normal baat kertay hein. aur direct log antiiii)
40
OCP use will bring what changes to iron studies?
INCREASE TIBC, DECREASED transferrin saturation.
| Increased fucking/BC
41
How does exogenous use of corticosteroids affect neutrophils, Eosinophils, Lymphocytes?
INCREASED NEUTROPHILS---> impaired migration of neutrophils to their site of action, and they remain in the vessels---> because of decreased activation of neutrophil adhesion molecules.
DECREASED EOSINOPHILS---> traps/sequesters eosinophils in LN.
DECREASED LYMPHOCYTES----> lymphocyte apoptosis,
42
Which disease can be treated with Hemin and Glucose?
Here's the catch in this concept that is why it is supposedly high-yield.
Hemin and Glucose are the treatement for Acute intermittent Porphyria in which porphyrinogen deaminase is defective.
But it DOWN-REGULATES ALA SYNTHASE.
43
How is iron toxic to cells?
1. Formation of free radicals
| 2. Peroxidation of membrane lipids (strange)
44
Iron poisoning causes which metabolic abnormality?
ANION-GAP metabolic acidosis.
45
A kid ingested iron pills in his childhood. As an adult, he'll present with which abnormality?
Iron causes GI scarring----> leads to GI OBSTRUCTION.
46
Desmopressin is given as a treatment in which hemophilia, and what is its mechanism of action?
Hemophillia A.
Increases circulating factor VIII & endothelial secretion of vWF to stop bleeding.
(Hence, also used to treat vWF disease)
47
PT and PTT values in Hemophilia ABC, vs Vitamin K deficiency?
PTT--> raised in Hemophilia ABC
| PTT AND PT--> Both raised in Vitamin K deficiency.
48
For which platelet disorders you can give steroids to treat?
ITP, and TTP.
49
Triad seen in TTP, HUS?
>Thrombocytopenia
> Microangiopathic hemolytic anemia--> Helmet cells/Schistocytes, increased LDH, decreased Hb)
> Acute kidney injury to creatinine will be raised.
50
TTP occurs due to a deficiency of _______________.
ADAMTS13 (a vWF metalloprotease)
51
Cause of hyperkalemia after Blood transfusion?
(RBCs may lyse in old blood units)
52
Hodgkin's lymphoma is more common in men except for _______________?
nodular sclerosing type
53
Hodgekin's lymphoma has what kind of cells?
1-5%--> Reed-Sternberg cells ( CD15+ and CD30+ B-cell origin)
The rest are---> reactive cells!
54
Treatment of Hodgekin's lymphoma?
```
ABVD!
A--> Adriamycin (Doxorubicin)
B---> Bleomycin
V--> Vinblastine
D---> Dacarbazine.
```
55
There's a subtype of Hodgekin's lymphoma, and it is very peculiar. What is it called and what is peculiar about it?
A subtype of hodgekin's lymphoma is--> Nodular Lymphocyte proliferative (LP cells/Popcorn cells)
The peculiar thing is that it doesn't show Reed-Sternberg cells on biopsy, and has cells with are CD2+ which is a B-cell marker!
56
CML translocation mnemonic?
Camel is able to go to Bhakkar at 9:22.
Translocation is 9:22 (philadelphia chromosome)
BCR-ABL is a fusion protein.
CML is the disease (Camel)
57
```
Tell mnemonic for:
Burkitt
Follicular
Mantle
Marginal
```
All are going to be CD20+ because they are neoplasms of B-cells.
Lymphomas are supposed to have a 14 translocation--> because this is the gene location for Ig-heavy chian.
>Burkitt--> B looks like 8---> so (8:14) translocation. C-myc overexpression VERY HIGH-YIELD.
>Follicular---> Imagine a razor to cut hair follicles---> BREAK AND CUT LONG HAIR (BCL2 overexpression.)
Shaving starts at the age of 18---> so, t(14;18)
>Mantle--> Fireplace with mantles (pillars on sides making a fire place and there's a cycle above it)----> Cyclin D1 overexpression---> T(11;14)---> CD5+ as well.
>Marginal---> t(11:18)--> peculiar such that it doesn't contain 14.
58
What's an interesting thing that you should know about a lymphoma that gives an EBV+ CSF analysis?
It is called Primary CNS lymphoma but in the exam they write it as Large B cell lymphoma because that is its type.
It is CD20+ ofcourse, and CD79a+!!!!
59
Describe the virus that causes Adult T-cell lymphoma?
HTLV--> Just like HIV it's a RETRO-VIRUS (Because it has a reverse transcriptase)--> single stranded RNA, positive sense, Enveloped.
60
Intracytoplasmic inclusions containing IgG are seen in?
Multiple Myeloma/Monoclonal Plasma Cell Neoplasm.
61
What is lymphoplasmacytic lymphoma?
| In new FA only---> obviously they'll test you on this!
It is another name for Waldenstrom macroglobulinemia
(Overproduction of IgM---> IgM is so bigg hence the name MACROGLOBULINEMIA)
BM analysis will show >10% small lymphocytes with IgM-containing vacuoles.
62
lymphoplasmacytic lymphoma will present as?
Hyperviscosity:
Raynaud Phenomenon, Blurred vision
Retinal Hemorrhage, headaches---> Only in new FA--> They'll test you on this!
63
Pseudo-Pelger-Huet anomaly?
neutrophil with bilobed (“duet”) nuclei. Typically seen
after chemotherapy!
(Nucleus of neutrophil looks exactly like an EYE MASK)
64
Why do we see Lytic lesions in Multiple Myeloma?
Basically, this hypercalcemia and bone resorption is due to TNF-Alpha and IL-1 (also called osteoclast activating factor-->asked in NBME13)----> the hypercalcemia causes a DECREASED PTH (asked in uworld, HIGH YIELD) and hence, decreased 1,25 OH-Vitamin D.
65
A woman with cough comes to you, and you prescribe her amoxicillin, the symptoms don't get better. Her cold agglutinin test is positive. The medicine didn't work on her because?
Because of lack of peptidoglycan/cell wall.
Cold agglutinin in the setting of cough means Mycoplasma pneumonie and Mycoplasma has no cell wall.
Can cause atypical variant of Stevens Johnson syndrome (It can be high-yield---> steven johnson and cold agglutinin test positive)
66
Whenever you see anemia, ask yourself if there's splenomegaly with it or not?
No splenomegaly, and Pancytopenia---> APLASTIC ANEMIA! (Here's the catch that they can test you on---> If pancytopenia with no splenomegaly---> it's called aplastic anemia. If ONLY anemia with no splenomegaly--> APLASTIC CRISIS (aik banda ho tou crisis hota hai naa, nobody to help)
Anemia WITH splenomegaly can mean--->
1. Myelofibrosis (massive splenomegaly and BM is fibrosed so pancytopenia)--> (uworld asked what will the spleen biopsy show-->islands of hematopoietic progenitor cells)
2. Hairy Cell leukemia--> massive splenomegaly (uworld once asked---> what will be the findings in spleen?--> engorged red pulp)--> The catch is its strange how HCL infilterates red pulp of spleen when normally it is enlarged related to RBCs eating.
3. CML---> Splenomegaly and Pancytopenia!
67
Blasts are seen on peripheral blood smear. They contain Auer rods. How do you differentiate between AML and CML?
It has been tested in a very confusing way, but the trick is:
If you see auer rods on a slide, and you need to know if it is AML or CML, LOOK FOR BLAST PERCENTAGE IN PERIPHERAL BLOOD SMEAR/LAB VALUES?
> Blast cells in CML are less than 2%
> On peripheral blood smear, blasts with auer rods was shown--> no other clue--> I was confused kay AML hai ya CML--> The catch was kay peripheral blood smear mein agar itnay ziaada nazar aa rahay hein aur Lab value of blast percentage is not given--> Then blasts ZIAADA hee hein 2% so the correct answer was AML.
68
AML vs CML.
On peripheral blood smear, lab values: AML will have more than 2% of blast cells, CML will have less.
For CML---> Remember CAMEL ABLE TO GO TO BCR at 9:22 pm basophilically.
Basophilia, eosinophilia (In one question, this was the only clue given that it is a CML because there was increase metameylocytes (blast cells but not more than 1%, ABSOLUTE basophilia and eosinophilia (Leukocyte count might be normal but increased percentage of basophils and eosinophils)
For AML:
APML--> highly tested---> Apple operator with glasses is a DICK, but he is down after 5.
Apple---> Vitamin A receptor mutation, management is with all-trans retinoic acid!
Glasses--> t(15;17)
DICK--> presents with DIC.
down after 5--> Down's syndrome kids get AML after the age of 5 (SOOO HIGH-YIELD)
69
Tdt+/DNA polymerase/PAS positve lymphoblasts are seen on peripheral blood smear. How do you diffrentiate between ALL and CLL.
Blast cells will be more than 20% in ALL.
70
T-ALL vs B-ALL?
B-ALL---> Ball and Bi-->
- 2 kinds of translocations: t(12;21) in kids with good prognosis,
9:20 in adults and this one has a poor prognosis
Ball--> Down's syndrome kids love balls, and B-ALL is associated with Down's, and kids get this BEFORE THE AGE OF 5---> they can ask you the translocation and that will be the one common in kids--> t(12;21)
Balls--> Goes to testis and brain, so we have to inject chemo into CSF and testis directly.
T-ALL---> presents as a thymic mass/SVC syndrome---> they'll say the person has SOB, respiratory difficulty, swelling of face, neck, arms.
71
CLL?
Remember an old lady cleaning and watching TV.
Old lady---> common in old people.
Cleaning---> sudge cells
CLL--> 3+1+1=5, so CLL is basically a B cell lymphoma but it has a T-cell CD so CERTAINLY ABNORMAL---> CD20+. CD23+ (B-cell markers), CD5+
TV--> HGTV---> Hypogammaglobulinemia, thrombocytopenia is seen but because of AIHA. Remember, CLL associated with AIHA? Hmm yess!
72
CD5+ is a T-cell marker, but is seen in which B-cell neoplasms?
CLL
| Mantle Cell Lymphoma
73
CD1a+ is seen in?
Langerhans cell histiocytosis ( also S-100 +)--> macrophages of skin or mucosa--was asked in uworld!!!
Langerr hai tou 100 log hongey hee!
Cells are functionally immature and
do not effectively stimulate primary T cells
via antigen presentation (HIGH-YIELD, has potential to be asked)
Racket shaped/Birbeck granules.
74
Tumor lysis syndrome
Everything hyperrr!
hyperkalemia (will cause arrythmia)
hyperphosphatemia,
hyperuricemia (acute kidney injury)
Increased LDH (this was specifically asked in uworld, becausue it tests the concept that in cell lysis LDH is always going to be increased)
ONLY hypocalcemia--> because increased Phosphate binds to it! (Asked so many times)
75
How does tumour lysis syndrome affect kidney?
Causes urate and calcium phosphate crystals nephropathy!
76
How can tumor lysis syndrome be treated?
hydration
allopurinol
rasburicase (It is a URIC-ASE, so splits uric acid into allantoin which is a more soluble form and can be easily excreted out of kidney)
Fun fact--> rasburicase is a recombinant version of urate oxidase enzyme which is not present in humans but in other mammals. (can be asked as experiment vignette)
77
Examples of drugs that can cause isolated thrombocytopenia include __________, ___________ and ________.
heparin, beta-lactam antibiotics, and vancomycin
78
Which drug should be given when the patient comes with pulmonary embolism?
For venous thromboembolism (VTE) (ie, PE or deep vein thrombosis)---> LMWH is given.
Why not tpA? We give that to dissolve the clot in MI so why not here---> Tissue plasminogen activator is indicated in the treatment of massive PE complicated by hemodynamic instability. However, it is not appropriate for VTE prophylaxis due to the relatively high risk of serious bleeding complications (eg, intracranial hemorrhage).
79
Heparin can cause which electrolyte abnormality?
Hyperkalemia---> because it Blocks aldosterone production! (uworld)
80
What is the difference between the mechanism of action of heparin and LMWH?
Heparin binds to antithrombin 3, and activates it to decrease the action of thrombin/factor 2 and factor 10a BOTH.
LMWH--> Binds to anti-thrombin 3 and activates it to only decrease the action of 10a.
81
HIT presents as?
| And how is it treated?
Thrombosis--> which leads to isolated thrombocytopenia.
The treatment of HIT is---> Argatroban, Dabigatran--> because they don't need anti-thrombin 3, they bind to factor 2/thrombin active site directly
82
Why does thrombocytopenia occur in HIT?
| Asked in uworld
The major manifestation is thrombocytopenia, which typically occurs 5-10 days after heparin initiation due to the destruction of antibody-coated platelets by splenic macrophages
83
The patient is given a recombinant biologic agent that has antigen homology with factor Xa but no catalytic effect. The agent is most likely to antagonize the effects of which of the anticoagulant drugs?
Because the drug is binding to FactorXa, only FactorXa inhibitors will be antagonized---> those are apixaban, rivaroxaban.
84
What will be the values of the following in VWF disease?
Platelets:
PT:
PTT:
Platelets: Normal.
PT: Normal
PTT: prolonged.
(Bleeding Time will be proloned, but they never asked it because it is too easy)
85
Intravenous heparin infusion is initiated. This medication is most likely to cause which of the coagulation changes?
Thrombin Time:
PTT
Factor Xa activity
Thrombin Time: increased (Heparin but not LMWH inhibit factor 2/thrombin too)
PTT: Increased
Factor Xa activity: decreased
86
What will the cardiac biopsy show in the following chemotherapeutic agents?
Doxorubicin
Trastuzumab
Doxorubicin- Cardiotoxicity is dose dependant. patchy fibrosis with vacuolization and lysis of myocytes are evident-->dilated cardiomyopathy.
Trastuzumab--> decreased cardiomyocyte contractility with NO fibrosis. It's cardiotoxicity in NOT dose-dependant.
87
Bleomycin affects which phase of the cell?
G2--> Bleo matlab BLEW into 2 pieces.
| G2---> Also called pre-mitotic phase
88
Which antimetabolite chemotherapeutic agent is non-cell cycle specific?
Cladrabine (ADA inhibitor)---> used for Hairy Cell leukemia.
89
Which of the alkylating agent chemotherapeutic agent is a weak MAO inhibitor?
Procarbazine--> disulfiram reactions, cheese like reactions. (Hypertensive crisis with ingestion of cheese, wine, fava beans)
(CAN COME IN THE EXAM. ONLY IN NEW FA)
90
Cisplastin nephrotoxicity can be prevented by which drug?
Amifostine (a free radical scavenger)
| Chloride saline diuresis.
91
How does inhibition of Type I and Type II topoisomerase cause cell death?
Type I topoisomerase inhibitor causes PREVENTION OF DNA UNWINDING AND REPLICATION.
Type 2 topoisomerase inhibitor causes INCREASED DNA degradation.
92
Which chemotherapeutic agent can you give to wean off patient of chronic disease from steroids?
Azathioprine, 6-MP
93
Mechanism of action of Hydroxyurea and its uses?
Inhibits ribonucleotide reductase
Used to treat:
CML
Polycythemia Vera
Sickle cell anemia (Increase HbF)
94
Bortezomib MOA and the 2 disease where it is used?
Bortezomib/car-fil-zomib--> Proteosome inhibitor.
used in treatment of:
Multiple Myeloma
Mantle Cell Lymphoma.
95
Rituximab is a ___________.
CD20 inhibitor.
96
Name drugs that cause EGFR tyrosine Kinase inhibition?
EGFR Tyrosine kinase receptor inhibitors--> ERLO-TINIB--> used in non-small cell lung carcinoma.
Monoclonal Ab against EGFR/erb-2/HER2 tyrosine kinase receptors--> trastuzumab.
97
Ankle ligament tears happen in which movement?
Super-inverted plants always tear first and leave us feeling low.
Over supination/Over inversion/Over plantarflexion--> LOW ankle sprain--> ATF torn. (ATF= Anterior Talo-fibular.
Opposite for Anterior Inferior Tibiofibular ligament. (AITF)
