Hematology 🩸 Flashcards
ABO incompatibility in pregnancy? big risk to fetus? signs?
only mild hemolysis ensues. mild jaundice within 24 hrs of birth, mild anemia, coombs positive, etc.
difference between thalassemia and IDA in regards to RBC no.
thalassemia: normal/high
IDA: low
Confirmatory tests for hereditary spherocytosis
Osmotic fragility test, or E5M binding test
Mx of febrile non haemolytic transfusion reaction (FNHTR)
Stop transfusion and give antipyretic (NSAID)
Prevent with leukoreduction
Mx if HIT
Stop heparin and give direct thrombin inhibitor
Gold standard to Dx HIT
Serotonin release immunoassay
Mx protocol for trauma based haemorrhage
Transfuse ASAP, (1:1:1 if massive haemorrhage RBC:FFP:PLT). If blood pressure very low, then give colloids first, then straight to bloods. 1L max NS
In acute haemorrhage, Why can O+ be given to men, but is generally avoided in women (need O-)
Women can become sensitised to the Rh, and can cause erythroblastosis fetalis. Rh mismatch for patients generally is ok though
When are massive transfusion requirements met
When there is concern for massive transfusion requirements (eg, SBP
<90/mm Hg, pulse ≥120/min, positive FAST, penetrating mechanism of
injury), blood products should be given in a 1:1:1 fresh frozen
plasma/packed red blood cells/platelets ratio
How to differentiate high PTT from lupus anticoagulant, and true high PTT
PTT will not correct when add plasma
Warfarin reversal. Consider if needs to be rapid or not
If rapid give PCC. If not give vitamin K
TPA overdose treatment
Aminocaproic acid, tranexamic acid, fresh-frozen plasma
Reversal agent for factor X inhibitors
Andexanet Alpha
Reversal for dabigatran
Idarucizumab
Management of bleeding due to warfarin
Stop warfarin. Give Ivy vitamin K and PCC
Patient on warfarin, INR is more than 10
Discontinue warfarin, give oral vitamin K and monitor INR
Patient on warfarin, INR is 4.5 to 10 and there is no bleeding. How to manage
Hold warfarin temporarily for a few doses. Consider giving oral vitamin K
Patient on warfarin INR is less than 4.5. How to manage
Hold the next dose of warfarin and readjust the maintenance dose
Appreciate the coag cascade
Haemophilia A cause
Haemophilia B cause
Haemophilia C cause
Factor 8
Factor 9
Factor 11
Resp
Four CIs for tPA
Active/risk of bleeding
IC lesion
<2mo trauma to spine or head
Stroke Hx within 3mo
When to use PCC vs vit K, for warfarin reversal (basics)
If immediate (do PCC)
tPA toxicity Tx
Aminocaproic acid, tranexamic acid, FFP
Reversal for factor Xa inhibitors
Andexanet alfa
Dabigatran reversal medication
Idarucizumab
Anticoag to use instead of heparin in HIT patient
Argatroban (hirudin)
Warfarin vs DOAC metabolism organ
Hepatic and renal resp.
Go through the Tx of supra therapeutic INR sue to warfarin for the following:
Bleeding:
INR >10, no bleeding:
INR 4.5-10, no bleeding:
INR <4.5 , no bleeding:
Most accurate test to diagnose haemophilia A
Specific factor VIII level
Name main indications for PLT transfusion
Hb < 10,000 if not bleeding. Or Hb < 20,000 if bleeding or going to have procedure. or <50,000 prior to surgery
Cryoprecipitate ingredients and indications to use
factor VIII, vWF, fibrinogen, fibronectin, factor XIII.
Use in: fibrinogen disorder, vWD, liver diaease, DIC, uraemia
FFP vs PCC
FFP: 1972 & 5, 8, 11, 12, 13
(And better in liver disease)
Which blood replacement product needs ABO compatibility
FFP, cryoprecipitate, RBCs
Given suspected haemophilia (patient has isolated prolonged aPTT), what is the best initial test
Mixing study
what to measure next if mixing test corrects a low aPTT
Measure factor 8, 9, 11 for haemophilia , and even vWF
If patient has isolated aPTT, and mixing test fails to correct it… what do we check. Next
If it’s temp or time dependent
(Could indicate an inhibitor is the cause)
If patient has isolated aPTT, and mixing test fails to correct it… but it is time or temperature dependent, what to do?
Measure FVIII and inhibitors to Dx cause
If patient has isolated aPTT, and mixing test fails to correct it… it is not time or temp dependent either. What next?
Test for lupus anticoag. If that’s negative, check FVIII and inhibitors
Algorithm for prolonged aPTT
Tx if mild (>5% of factor) or moderate (1-5% of factor) haemophilia
Desmopressin
Tx for severe haemophilia (factor level <1%)
Immediate transfusion of missing factor or cryoprecipitate
Type 1 vs 2 vs 3 vWD
Type 1 - mild quantitative def
Type 2 - qualitative def
Type 3 - complete def
Worsening bleeding (mucosal sites) is seen in which disease
vWD
Best initial diagnostic test for vWD? Additional test?
Ristocetin cofactor assay. Additional test could be: vWF Ag level
Best treatment for mild to moderate von Willebrand’s disease
Desmopressin
Best treatment for severe von Willebrand’s disease (major bleeds, surgery, non-responsive to desmopressin like type two)
Must give von Willebrand factor or factor eight concentrate
If a patient has recurrent thrombus episodes, before doing thrombophilia screening what should be done
Should rule out acquired causes such a surgery, pregnancy, immobilisation et cetera
Officially when should you do thrombophilia screening
In patients who have VTE and no risk factors or in patients with a first-degree relative with VTE less than 50 years old, or a first-degree relative with an actual diagnosis of thrombophilia
What is the next best step in thrombophilic cases where anticoagulation is contra indicated or if the patient has recurrent DVTs despite being on a therapeutic dose of anticoagulation
IVC filter
What’s the diagnosis. Hypercoagulable state with skin necrosis following warfarin administration
Factor C or S deficiency
What’s the diagnosis. Young, white patient with a person and family history of multiple thrombosis episodes
Factor five Leiden
Best/specific test for factor five Leiden
The APC resistance test (factor five Leiden functional assay)
Mainstay Tx for Factor V Leiden
DOAC or warfarin for 6 mo (if compliance issue risk or overweight)
Talk to me about HIT type one
A mild, non-immune mediated decrease in platelet. 1 to 4 days after heparin. Treat only with observation, do not need to stop heparin
Talk to me about HIT type II
The immune mediated type. Antibodies against PG for and platelet, leading to significant drop in platelet count. Occurs 5 to 10 days after heparin. May see skin necrosis at injection site. Discontinue heparin and give argobatran 
4 Ts To indicate HIT
Thrombocytopenia, timing of platelet count fall, thrombosis signs, thombocytopenia of other causes unlikely
Best initial test and most accurate test of HIT
PF4 antibody. Functional assay with serotonin release assay.
Treatment of heparin induced thrombocytopenia
Discontinue heparin. Give a direct thrombin inhibitor like argatroban 
Most common cause of paediatrics stroke (like underlying aetiology)
SCD
Thymoma can cause which haematological phenomenon
Pure red cell aplasia
How is fanconi anemia diagnosed
Seeing chromosomal breakages after a cross linking agent is added
Treatment for lead poisoning
Ca disodium EDTA
Tx of hereditary spherocytosis
Transfuse, folate, splenectomy
Dx of hereditary spherocytosis
Acified glycerol test or E5M binding test
What is the new therapeutic INR in patients on warfarin, who need emergency surgery.
Doesn’t matter. Come off warfarin, give PCC and vitamin K. FFP 2nd line.
Patient newly diagnosed with HL, should have what Invx done
CXR. check for mediastinal mass, since most patient will have one.
Best drug to give for PE tX In CA patient
High dose LMWH. Since DOACs are risky in malig for bleeding
Mx of urticaria reaction to blood transfusion
Stop transfusion, give anti histamine. If gets better resume the transfusé
Transfusion associated bacterial infection is most common in which transfusion product
Platelet
When to do splenectomy in ITP
Do when first line Tx didn’t work (CS, IVIg) and patient has symptoms.
Can we do PLT transfusion in ITP
Avoid unless life threat. Since it can fuel the fire
ITP, when to only observe. Consider if adult or child
Child, if only cutaneous symptoms. Adult, if cutaneous symptoms and PLTs above 30
Medications that avoid in G6PDH def
Dapsone, sulfas, primaquine, rasburicase, quinolone, chloroquine, TMO, quinine
Dx the issue
Patient on RIPE for Tb, gets microcytic anemia. Yet Fe high, and TIBC low.
Pyridoxine def
What haematological thing do we see in scleroderma renal crisis
MAHA!!!
When to test for factor V Leiden mutation?.
Do it if first VTE <45 yo. If recurrent VTE. Or thrombosis in unusual place
Anterior mediastinal mass causing high HCG and AFP. And then if only high HCG
Mixed germ cell tumour, and seminoma respectively
Sequestration (SCD) crisis Tx
Fluids, lil transfusion and then splenectomy
What is mentzer index, and what does it indicate if above or below 12
It’s MCV/RBC. If <13 it suggests thalassemia. If >13 it suggests IDA
Pretentious like Dave meltzer
And MCV of above 110 favours what Dx
A megaloblastic macrocytosis
What is the TSAT, MCV, Fe, TIBC of someone who is thalasemic
High, low, high, low resp
Managment of spinal cord compression from cancer. Consider first thing to do?
IV GCs first. Then MRI to confirm. Then neuroSx consultation
Other than TCP, what else in HIT can present
Necrosis, thrombosis, even anaphylacticoid reaction
Dx of CLL…. From symptoms to Dx
after FBC and signs, do smear to see smudges. Then do flow cytometry on the smear. BM and LN biopsy not needed
Peutz jegers syndrome screening
Do annual anemia check, and upper and lower scopes
Patients with ITP Dx, should be tested for which infx?
Test for hep c and hiv
Rhogam schedule
Give 28 weeks and within 72 hours after birth. Give 300 micoG. Higher dose needed after birth in higher risk (abruptio P), so use the kleihauer betke test to determine dose
Compare and contrast type one with type two chemotherapy induced cardiotoxicity
 type one is by your anthracycline. Usually causes myocardial damage and necrosis, is usually irreversible. Type one is usually by trastuzumab, and is associated with myocardial hibernation/stunning, and is reversible
What is acute versus chronic DIC
Acute is what you’re used to. Chronic is usually seen in chronic cancer patients. Mild lab changes and often a symptomatic. Usually the only complaint is thromboembolic disorder
What are some of the associations with TTP
SLE, malignancy, pregnancy, cyclosporine, quinidine, Clopidogrel, AIDS
Out of TTP and HUS which has higher creatinine
HUS
Out of TTP and HUS which has the worst neuro symptoms
TTP
Is erotic aciduria and Fanconi anaemia megaloblastic or non-megaloblastic macrocytic anaemia is
Megaloblastic
Name some of the causes of sideroblastic anaemia
Alcohol is most common, lead poisoning, B6 deficiency, copper deficiency, drugs like isoniazid and linezolid, myelodysplastic syndrome
Sid the alcoholic
Medication causes for aplastic anaemia
Benzene, insecticides, so fast, chloramphenicol, PTU, carbamazepine, alcohol, methimazole, chemo
Causes of warm autoimmune haemolytic anaemia
SLE, CLL, lymphoma, penicillin, methyldopa, even rifampin and phenytoin
Causes of cold autoimmune haemolytic anaemia
EBV, Mycoplasma pneumonia and waldestrom
Talk about neonatal pooycthemaia,
Caused by hypoxia IU, like eclampsia, IUGR, etc. Causes plethora, low glucose, resp issues, abd distension and more. Treat with exchange transfusion, glucose, fluids
Talk about neonatal pooycthemaia,
Caused by hypoxia IU, like eclampsia, IUGR, etc. Causes plethora, low glucose, resp issues, abd distension and more. Treat with exchange transfusion, glucose, fluids
SVC syndrome Dx’ic Invx
MRI
Risk factors for upper extremity DVT
Peripheral inserted CVC, cancer, young athletes, thoracic outlet syndrome
How to invx suspected macrovasc hemolysis due to valve
Echo
How does follicular non-Hodgkin’s lymphoma present
Very indolent lymphomas. Painless lymph nodes occurring in different areas. Generally full blood count abnormalities are rare, and the symptoms are rare. Fairly similar presentation to CLL, but CLL has full blood count abnormalities
What’s the main physical difference between myofascial pain syndrome and fibromyalgia
In myofascial pain syndrome, they have trigger points, when palpated cause pain in target zones. Fibromyalgia has pain at the point of palpation
How does EPO Tx predispose HTN? What is a lab clue that indicated elevated risk for HTN
Decreases NO release, vasoC directly, increases alpha sensitivity. A sudden increase in Hb from when EPO given, can indicate risk for HTN
AIHA are intra or extra vascular
Extra!!
CLL vs lymphoma.
Which one is b symptoms and normal FBC
Which one no b symptoms and high high Lymphocytes
Lymphoma and CLL respectively
What is post transplant lymphoproliferative disorder
Immunosuppressiion. Deceases CD8 immunosurpression, allowing for EBV replication and lymphocyte immortality
Some random lab findings for HL
High eosinophils, high LDH
Pain in chest when drink booze
HL. Alcohol causes pain in LNs
Bronchiestcatsis involving upper lobes mainly, is a sign of……what cause..?
CF
What is non diahrreal HUS?
Complement-mediated microangiopathy (also called nondiarrheal hemolytic-uremic syndrome) is a
hereditary disorder marked by unregulated complement activation and the formation of platelet-rich thrombi.
Chronic vs acute DIC
Acute DIC
Common etiologies
Sepsis
Severe trauma
Obstetric complications
Coagulation studies
You know!
chronic DIC
Malignancy (eg, pancreatic)
And coag studies studies are usually normal!!
Red papules on the trunk and lips represent what
represent cutaneous arteriovenous malformations. Could be osler Webber rendu
Mainstay Tx for aplastic crisis in SCD
Transfuse
How harlequin syndrome be seen in neuroblastomas
If it cp,pressed cervical chain. Although sweating is often difficult to appreciate in young children, absent facial flushing (ie, “harlequin” sign) can be observed in anhidrotic areas, as seen in this patient.
Dx of neuroblastoma
Surgical biopsy definitive
Why do pernicious anemia need periodic EGD
Risk of gastric CA
RF for upper extremity DVT. Name 5
Central venous cathete
• Repetitive arm motions (eg, baseball pitching)
• Weight lifting (increase scalene size causing thoracic outlet syndrome)
• Malignancy
thoracic outlet syndrome
Treatment of splenic sequestration crisis
Isotonic fluid resuscitation
• Red blood cell transfusion
• ‡ Splenectomy
SCD disease patient with:
Abdominal pain
• Palpable splenomegaly
• Signs of anemia (tachycardia, pallor, fatigue)
•Hypotensive shock 大
Splenic sequestration crisis
Tx of SCD induced stroke
• Exchange transfusion
• Simple transfusion if exchange transfusion is unavailable
All patients with cryoglob, need which infx disease test
Therefore, all patients require hepatitis serologies (even if aminotransferases
General Tx for raynauds
Avoid aggravating factors
CCB for persistent symptoms
If secondary
• Evaluate & treat underlying disorder
• CB for persistent symptoms, aspirin
for patients at risk for digital ulceration
Main symptoms difference between primary and secondary raynauds
Tissue injury or digital ulcers
• Abnormal nail fold capillary examination
In secondary
Recall muscles for shoulder abduction
Abduction of the shoulder is
initiated by the Supraspinatus;
O to 15°
The Deltoid muscle can then
abduct to 90°. Its the major
abductor. 15° to 90°
180° (elevation) is brought about by
rotation of the scapula upwards by
the Trapezius and Serratus anterior.
HbCO levels in smokers and non smoker
Nonsmokers have low levels (<3%) of carboxyhemoglobin (due to normal enzymatic reactions). Cigarette smokers may have carboxyhemoglobin levels as high as 10%.
Why do we get polycythemia in CO toxicity
Carboxyhemoglobin shifts the oxygen dissociation curve to the left, impairing the ability of heme to unload oxygen at the tissue level. This results in tissue hypoxia. The kidney responds to tissue hypoxia by producing more erythropoietin (EPO). EPO stimulates the bone marrow to differentiate more red blood cells. Chronic CO toxicity is a cause of secondary polycythemia.
Leukamoid reaction vs CML regarding shift left
Leukamoid reaction: More mature
(metamyelocytes > myelocytes)
CML: Less mature
(metamyelocytes < myelocytes)
Main issue with the G6PDH assay testing. How do we overcome this
It’s often normal during the attack. So in 3mo we do the confirmatory assay test
Clinical difference between Pyr Kinase def and G6PDH def
Unlike with G6PD deficiency, hemolysis is constant,
so there is no relationship to inciting events (eg, sulfa drug exposure).
Leukoreduction of RBCs, two benefits
Leukoreduction reduces the risk of human leukocyte antigen alloimmunization and transmission of cytomegalovirus (which typically resides in leukocytes). Also reduces risk of FNHTR
First line Tx for chemo induced N/V
Serotonin (5HT) receptor antagonists (eg, ondansetron)
Thrombosis link to IV fluids
Limiting use of crystalloids (eg, $1 L), which dilute existing coagulation (eg, clotting) factors and platelets, thereby increasing coagulopathy
Iv fluids worsen the lethal triad. What is the lethal triad
“lethal triad” (hypothermia, acidosis, coagulopathy)
Mx for TRALI
Resp support only
TRALI vs TACO BP
Low and high resp
Risk factors for rectal sheath hematoma
Abdominal trauma, forceful abdominal contractions (eg, coughing)
• Anticoagulation
• Older age, female sex
How does a rectal sheath hematoma present
Acute-onset abdominal pain with palpable abdominal mass
Worse pain on abdominal contraction (carnett sign)
• Blood loss anemia, leukocytosis
• ‡ Nausea, vomiting, fever
Why is a rectal sheath hematoma problematic below arcuate line?
The rectus sheath, which contains this muscle, does not extend posteriorly below
the arcuate line; therefore, bleeding below this line (eg, lower aspect of rectus abdominis muscle) is relatively uncontained and can result in significant hemorrhage with hematoma formation.
Bone lesions in MM vs HyperPTH
Hyper PTH are typically well-defined (vs moth-eaten appearance of MM), and other radiographic abnormalities are common (eg, subperiosteal bone resorb the middle, phalanx,
Why do infants have a Hb nadir
After birth, increased oxygenation (ie, breathing, ductus closure) triggers reduced erythropoietin (EPO)
production by the liver and kidney. Low levels of circulating EPO impair erythropoiesis in the bone marrow, which normally causes a mild, transient anemia that reaches a nadir of around 9-11 g/dL at age 2-3 months
Why do premats have a lower infant Hb nadir
htc is lower at birth, blood draws will also worsen it. Flora is less mature too
Pathophys of urticaria transfusion reaction
preformed recipient IgE antibodies reacting against a soluble allergen in the
donated plasma, or vice versa (ie, donor IgE against recipient allergen).
Tx of metastasis to bone for the high calcium and bad pain?
BPS for the Ca, and Radiation therapy can treat moderate to severe pain caused by bone metastases.
Name the risk factors for iron deficiency of infancy
- Prematurity
• Lead exposure
• Age <1
• Delayed introduction of solids
(ie, exclusive breastfeeding after 6 months)
• Cow’s, soy, or goat’s milk
• Age >1
• >24 oz/day cow’s milk
• <3 servings/day iron-rich foods
If the Coombs test is negative and there is still a high index of suspicion for AlHA…. What can be done to clinch Dx
a micro-Coombs test can be done
How to treat haemophilia. Consider if not severe and factor above 1%. Consider if severe or factor below 1%
Give desmopressin. But if severe or factor less than 1% transfuse the factor
How to properly diagnosed pseudo TCP
Draw blood using a non-EDTA tube. Platelet count should be normal now
Other than doing von Willebrand factor antigen test, What is another diagnostic test for von Willebrand’s disease
Ristocetin assay.
Interpret Ristocetin assay
If it improves the bleeding time this is indicative of Bernard Soulier disease. If it doesn’t improve bleeding time this indicates von Willebrand’s disease
If von Willebrand’s disease patient has refractory, severe, current plead, Type II, surgery. What is the treatment
Von Willebrand factor and factor eight concentrate. Not desmopressin like usual
Can you name 3 scenarios where you would do a thrombophilia screen
VTE and no risk factor.
First-degree relative had VTE test and 50 years old
1st° relative had thrombophilia
Diagnostic approach to HIT2. Consider beginning, initial diagnostic test, most accurate test
Obviously would do platelet count. The HIT PF4 Ab is first diagnostic test. Most accurate is the functional serotonin release assay
Why is testing for factor eight important in DIC
He is low in DIC, but is normal in liver disease
Antiphospholipid syndrome treatment.
Low molecular weight heparin bridge into warfarin. DOAC not so effective here
Recall of TTP management and HUS management
TTP - Plasma exchange, consider steroids and rituximab
HUS – mainly supportive. Plasma exchange of severe. Dialysis if aKI. Hydration
ITP management. If platelets above 30, And no bleeding. Or if platelets less than 30 or bleed
No treatment as long as platelets above 30 and no bleeding. Corticosteroids or IVIg otherwise. Keep in mind this is for adults
Main difference in ITP management between adults and children
Adults we give treatment if platelets are less than 30 all the patients bleeding. In children we only give treatment if bleeding
If corticosteroids or IV immunoglobulin fails for ITP, what are the things could we do
Splenectomy, rituximab, TPO
Most accurate diagnostic test for G6PD H deficiency
Enzyme levels a couple of months after the attack
Most accurate test for PNH
Flow cytometry (CD55 and CD59 absence
PNH treatment. Consider best initial, alternative, definitive
Prednisone initially. Eculizumab is an alternative. Bone marrow transplant is definitive
Hereditary spherocytosis. Treatment. Consider most cases, and considered severe cases
Most cases just give folate supplementation and transfuse of need. Severe cases usually require splenectomy
First line treatment for warm autoimmune haemolytic anaemia. What about a mild. Potential second line
Corticosteroid First line. If mild no treatment.
Splenectomy or IV Ig could be a second line
Is rituximab more for cold or warm autoimmune haemolytic anaemia
Cold
 What is the schilling test used for
Radioactive B 12/ And then check the urine. Detect whether you just have a low B12 in the diet or a problem absorbing B12
Polycythaemia main therapy combo? (Consider Susan). If resistant to main treatment can give what. What percentage do we aim haematocrit to be
HU, phlebotomy when need, aspirin. Ruxolitinib is a jack inhibitor, and is the if HU is resistant. Less than 45%
Porphyria cutanea tarda management
Phlebotomy to remove porphyrin, avoid sun, hydroxychloroquine (like lupus)
Acute intermittent porphyria management
Mainly supportive, but hemin and glucose are good
HLH management
Dexamethasone and etopside. Consider antibiotics. Transfuse if needed
Treatment ideas for mastocytosis
Prevent degranulation. Antihistamine, cromylyn, anti-leukotriene
Neutropenic fever investigations. And treatment.
Investigation: chest x-ray, CT, blood culture, urine culture, stool culture, BUN, LFT.
Give prophylactic Vanco and cephalosporin. No rectal exam. Antifungal cover if no improvement in 72 hours.
Neutropenia chronic management
If chronic consider G – CSF, and bone marrow transplant
If a patient has lymphopenia, and is asymptomatic, does not have HIV. How do I manage
Can just observe and monitor
Name three indications where an eosinophilic patient should have corticosteroids
Dress syndrome, eosinophils above 100. Eosinophilic myocarditis
What are pel Epstein fevers
10 days fever and 10 days off. Seen in Hodgkin lymphoma
Alcohol induced pain at noodle sites, is a sign of what disease
Hodgkin lymphoma
Dutcher bodies are found in which cells
Plasma cells
Patient with SCD, patient has microcytosis and also high HbA2…. What’s this?
This is heterozygous HbS with Beta Thal. These are two signs of this
Which medication reduces attacks and mortality in SCD
HU
I’m in a case of ITP, and the patient is on IV Ig and corticosteroid. The platelets are around 10, and they have discussed with TJ, but the rest of the exam is okay. What do you do
Do splenectomy or rituximab. These patients should not be given a platelet transfusion
Be careful. If you have a case of transfusion reaction. Sort of could be a TRALI or anaphylaxis. What’s the main thing to differentiate them if the presentation overlaps
Just look at the time. Anaphylaxis will be in minutes. Other than that they should be clinically easy to differentiate
Comprehensively list the glucose-6-phosphate dehydrogenase medication exacerbated
Dapsone, sulphur, TMP SMX, primaquine, quinine, chloroquine, raspberry case, quinolone
What kind of anaemia can I NAH cause
Sideroblastic, due to B6 deficiency
On US Emily, if a young patient has thrombosis, we can assume what
Presume it’s factor five Leiden (activated protein see resistance
Which one of the thrombophilia is is acquired most of the time
Antithrombin three deficienc
When calculating Meltzer index, (MCV divided by red blood cell) what is the cut-off
Less than 13 indicate thalassaemia, more than 13 indicates iron deficiency anaemia
When is basophilic stippling commonly seen
Lead poisoning, megaloblastic anaemia, benzene exposure
Two Viruses that are associated with ITP
Hep C and HIV
When an abruption p Case has RhoGAM. What do we need to consider
The dose needs to be higher for these patients. That’s why we do the Betke test
Cancel Mets to the spine causing spinal-cord compression. Before the MRI what do I do
Ivy glucocorticoids
Iron studies in anaemia of chronic disease
Ferritin hi, Iron low, TIBC low,
Sickle cell disease patient, with 1 mo increasing shortness of breath, history of painful crises. Haemoglobin is very low, reticulocyte count around one. And the MCV is high
Could be a follow deficiency. Not a cute enough and severe enough to be aplastic crisis
Tortuous retinal veins in the setting of anaemia and high-protein count
Consider Walden Strom
Young patient with Ruby coloured peppers on the lips, high haematocrit, history bleeding (epistaxis) , Increased pulse pressure
Osler webber rendu syndrome
When we have a patient with STEC and salmonella. Can we give antibiotics for the salmonella
No don’t give any antibiotics at all
Big demographic and symptom difference between Hodgkin and follicular non-Hodgkin’s lymphoma
Follicular non-Hodgkin’s usually does not have the symptoms
If we have a patient who has submandibular lymph node, chronic smoker. Maybe a bit of referred otalgia. What’s the next investigation why
Do a laryngeal pharyngeus scope . Because you’re suspicious of oral Sq cell carcinoma
I deficiency anaemia versus beta thalassaemia. Red blood cell count
Low, (normal or high) respectively
If you the question of patient has B12 deficiency signs, and they have a good diet and they’re in the West. What can you presume
Just presume there is a pernicious in a
Chronic SLE is a risk factor for which lymphoma
NHL
When does gestational thrombocytopenia take place in preg

Second half
Is graft versus host always immediate
No. Usually takes time. Sometimes even up to 80-100 days
If you want to do a workout for protein C deficiency, what drug cannot be taken two weeks prior
Warfarin. As it can decrease its levels naturally
What things do you give to prevent a KI in a patient that have chemotherapy for leukaemia
Normal saline and allopurinol
