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USMLE Step 2 - Top 5% > Hematology 🩸 > Flashcards

Hematology 🩸 Flashcards

1
Q

ABO incompatibility in pregnancy? big risk to fetus? signs?

A

only mild hemolysis ensues. mild jaundice within 24 hrs of birth, mild anemia, coombs positive, etc.

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2
Q

difference between thalassemia and IDA in regards to RBC no.

A

thalassemia: normal/high
IDA: low

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3
Q

Confirmatory tests for hereditary spherocytosis

A

Osmotic fragility test, or E5M binding test

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4
Q

Mx of febrile non haemolytic transfusion reaction (FNHTR)

A

Stop transfusion and give antipyretic (NSAID)

Prevent with leukoreduction

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5
Q

Mx if HIT

A

Stop heparin and give direct thrombin inhibitor

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6
Q

Gold standard to Dx HIT

A

Serotonin release immunoassay

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7
Q

Mx protocol for trauma based haemorrhage

A

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

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8
Q

In acute haemorrhage, Why can O+ be given to men, but is generally avoided in women (need O-)

A

Women can become sensitised to the Rh, and can cause erythroblastosis fetalis. Rh mismatch for patients generally is ok though

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9
Q

When are massive transfusion requirements met

A

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

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10
Q

How to differentiate high PTT from lupus anticoagulant, and true high PTT

A

PTT will not correct when add plasma

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11
Q

Warfarin reversal. Consider if needs to be rapid or not

A

If rapid give PCC. If not give vitamin K

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12
Q

TPA overdose treatment

A

Aminocaproic acid, tranexamic acid, fresh-frozen plasma

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13
Q

Reversal agent for factor X inhibitors

A

Andexanet Alpha

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14
Q

Reversal for dabigatran

A

Idarucizumab

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15
Q

Management of bleeding due to warfarin

A

Stop warfarin. Give Ivy vitamin K and PCC

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16
Q

Patient on warfarin, INR is more than 10

A

Discontinue warfarin, give oral vitamin K and monitor INR

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17
Q

Patient on warfarin, INR is 4.5 to 10 and there is no bleeding. How to manage

A

Hold warfarin temporarily for a few doses. Consider giving oral vitamin K

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18
Q

Patient on warfarin INR is less than 4.5. How to manage

A

Hold the next dose of warfarin and readjust the maintenance dose

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19
Q

Appreciate the coag cascade

A
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20
Q

Haemophilia A cause
Haemophilia B cause
Haemophilia C cause

A

Factor 8
Factor 9
Factor 11

Resp

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21
Q

Four CIs for tPA

A

Active/risk of bleeding
IC lesion
<2mo trauma to spine or head
Stroke Hx within 3mo

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22
Q

When to use PCC vs vit K, for warfarin reversal (basics)

A

If immediate (do PCC)

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23
Q

tPA toxicity Tx

A

Aminocaproic acid, tranexamic acid, FFP

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24
Q

Reversal for factor Xa inhibitors

A

Andexanet alfa

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25
Q

Dabigatran reversal medication

A

Idarucizumab

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26
Q

Anticoag to use instead of heparin in HIT patient

A

Argatroban (hirudin)

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27
Q

Warfarin vs DOAC metabolism organ

A

Hepatic and renal resp.

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28
Q

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:

A
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29
Q

Most accurate test to diagnose haemophilia A

A

Specific factor VIII level

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30
Q

Name main indications for PLT transfusion

A

Hb < 10,000 if not bleeding. Or Hb < 20,000 if bleeding or going to have procedure. or <50,000 prior to surgery

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31
Q

Cryoprecipitate ingredients and indications to use

A

factor VIII, vWF, fibrinogen, fibronectin, factor XIII.
Use in: fibrinogen disorder, vWD, liver diaease, DIC, uraemia

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32
Q

FFP vs PCC

A

FFP: 1972 & 5, 8, 11, 12, 13
(And better in liver disease)

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33
Q

Which blood replacement product needs ABO compatibility

A

FFP, cryoprecipitate, RBCs

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34
Q

Given suspected haemophilia (patient has isolated prolonged aPTT), what is the best initial test

A

Mixing study

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35
Q

what to measure next if mixing test corrects a low aPTT

A

Measure factor 8, 9, 11 for haemophilia , and even vWF

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36
Q

If patient has isolated aPTT, and mixing test fails to correct it… what do we check. Next

A

If it’s temp or time dependent
(Could indicate an inhibitor is the cause)

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37
Q

If patient has isolated aPTT, and mixing test fails to correct it… but it is time or temperature dependent, what to do?

A

Measure FVIII and inhibitors to Dx cause

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38
Q

If patient has isolated aPTT, and mixing test fails to correct it… it is not time or temp dependent either. What next?

A

Test for lupus anticoag. If that’s negative, check FVIII and inhibitors

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39
Q

Algorithm for prolonged aPTT

A
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40
Q

Tx if mild (>5% of factor) or moderate (1-5% of factor) haemophilia

A

Desmopressin

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41
Q

Tx for severe haemophilia (factor level <1%)

A

Immediate transfusion of missing factor or cryoprecipitate

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42
Q

Type 1 vs 2 vs 3 vWD

A

Type 1 - mild quantitative def
Type 2 - qualitative def
Type 3 - complete def

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43
Q

Worsening bleeding (mucosal sites) is seen in which disease

A

vWD

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44
Q

Best initial diagnostic test for vWD? Additional test?

A

Ristocetin cofactor assay. Additional test could be: vWF Ag level

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45
Q

Best treatment for mild to moderate von Willebrand’s disease

A

Desmopressin

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46
Q

Best treatment for severe von Willebrand’s disease (major bleeds, surgery, non-responsive to desmopressin like type two)

A

Must give von Willebrand factor or factor eight concentrate

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47
Q

If a patient has recurrent thrombus episodes, before doing thrombophilia screening what should be done

A

Should rule out acquired causes such a surgery, pregnancy, immobilisation et cetera

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48
Q

Officially when should you do thrombophilia screening

A

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

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49
Q

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

A

IVC filter

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50
Q

What’s the diagnosis. Hypercoagulable state with skin necrosis following warfarin administration

A

Factor C or S deficiency

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51
Q

What’s the diagnosis. Young, white patient with a person and family history of multiple thrombosis episodes

A

Factor five Leiden

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52
Q

Best/specific test for factor five Leiden

A

The APC resistance test (factor five Leiden functional assay)

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53
Q

Mainstay Tx for Factor V Leiden

A

DOAC or warfarin for 6 mo (if compliance issue risk or overweight)

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54
Q

Talk to me about HIT type one

A

A mild, non-immune mediated decrease in platelet. 1 to 4 days after heparin. Treat only with observation, do not need to stop heparin

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55
Q

Talk to me about HIT type II

A

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 

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56
Q

4 Ts To indicate HIT

A

Thrombocytopenia, timing of platelet count fall, thrombosis signs, thombocytopenia of other causes unlikely

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57
Q

Best initial test and most accurate test of HIT

A

PF4 antibody. Functional assay with serotonin release assay.

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58
Q

Treatment of heparin induced thrombocytopenia

A

Discontinue heparin. Give a direct thrombin inhibitor like argatroban 

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59
Q

Most common cause of paediatrics stroke (like underlying aetiology)

A

SCD

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60
Q

Thymoma can cause which haematological phenomenon

A

Pure red cell aplasia

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61
Q

How is fanconi anemia diagnosed

A

Seeing chromosomal breakages after a cross linking agent is added

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62
Q

Treatment for lead poisoning

A

Ca disodium EDTA

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63
Q

Tx of hereditary spherocytosis

A

Transfuse, folate, splenectomy

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64
Q

Dx of hereditary spherocytosis

A

Acified glycerol test or E5M binding test

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65
Q

What is the new therapeutic INR in patients on warfarin, who need emergency surgery.

A

Doesn’t matter. Come off warfarin, give PCC and vitamin K. FFP 2nd line.

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66
Q

Patient newly diagnosed with HL, should have what Invx done

A

CXR. check for mediastinal mass, since most patient will have one.

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67
Q

Best drug to give for PE tX In CA patient

A

High dose LMWH. Since DOACs are risky in malig for bleeding

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68
Q

Mx of urticaria reaction to blood transfusion

A

Stop transfusion, give anti histamine. If gets better resume the transfusé

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69
Q

Transfusion associated bacterial infection is most common in which transfusion product

A

Platelet

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70
Q

When to do splenectomy in ITP

A

Do when first line Tx didn’t work (CS, IVIg) and patient has symptoms.

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71
Q

Can we do PLT transfusion in ITP

A

Avoid unless life threat. Since it can fuel the fire

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72
Q

ITP, when to only observe. Consider if adult or child

A

Child, if only cutaneous symptoms. Adult, if cutaneous symptoms and PLTs above 30

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73
Q

Medications that avoid in G6PDH def

A

Dapsone, sulfas, primaquine, rasburicase, quinolone, chloroquine, TMO, quinine

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74
Q

Dx the issue

Patient on RIPE for Tb, gets microcytic anemia. Yet Fe high, and TIBC low.

A

Pyridoxine def

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75
Q

What haematological thing do we see in scleroderma renal crisis

A

MAHA!!!

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76
Q

When to test for factor V Leiden mutation?.

A

Do it if first VTE <45 yo. If recurrent VTE. Or thrombosis in unusual place

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77
Q

Anterior mediastinal mass causing high HCG and AFP. And then if only high HCG

A

Mixed germ cell tumour, and seminoma respectively

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78
Q

Sequestration (SCD) crisis Tx

A

Fluids, lil transfusion and then splenectomy

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79
Q

What is mentzer index, and what does it indicate if above or below 12

A

It’s MCV/RBC. If <13 it suggests thalassemia. If >13 it suggests IDA

Pretentious like Dave meltzer

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80
Q

And MCV of above 110 favours what Dx

A

A megaloblastic macrocytosis

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81
Q

What is the TSAT, MCV, Fe, TIBC of someone who is thalasemic

A

High, low, high, low resp

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82
Q

Managment of spinal cord compression from cancer. Consider first thing to do?

A

IV GCs first. Then MRI to confirm. Then neuroSx consultation

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83
Q

Other than TCP, what else in HIT can present

A

Necrosis, thrombosis, even anaphylacticoid reaction

84
Q

Dx of CLL…. From symptoms to Dx

A

after FBC and signs, do smear to see smudges. Then do flow cytometry on the smear. BM and LN biopsy not needed

85
Q

Peutz jegers syndrome screening

A

Do annual anemia check, and upper and lower scopes

86
Q

Patients with ITP Dx, should be tested for which infx?

A

Test for hep c and hiv

87
Q

Rhogam schedule

A

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

88
Q

Compare and contrast type one with type two chemotherapy induced cardiotoxicity

A

 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

89
Q

What is acute versus chronic DIC

A

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

90
Q

What are some of the associations with TTP

A

SLE, malignancy, pregnancy, cyclosporine, quinidine, Clopidogrel, AIDS

91
Q

Out of TTP and HUS which has higher creatinine

A

HUS

92
Q

Out of TTP and HUS which has the worst neuro symptoms

A

TTP

93
Q

Is erotic aciduria and Fanconi anaemia megaloblastic or non-megaloblastic macrocytic anaemia is

A

Megaloblastic

94
Q

Name some of the causes of sideroblastic anaemia

A

Alcohol is most common, lead poisoning, B6 deficiency, copper deficiency, drugs like isoniazid and linezolid, myelodysplastic syndrome

Sid the alcoholic

95
Q

Medication causes for aplastic anaemia

A

Benzene, insecticides, so fast, chloramphenicol, PTU, carbamazepine, alcohol, methimazole, chemo

96
Q

Causes of warm autoimmune haemolytic anaemia

A

SLE, CLL, lymphoma, penicillin, methyldopa, even rifampin and phenytoin

97
Q

Causes of cold autoimmune haemolytic anaemia

A

EBV, Mycoplasma pneumonia and waldestrom

98
Q

Talk about neonatal pooycthemaia,

A

Caused by hypoxia IU, like eclampsia, IUGR, etc. Causes plethora, low glucose, resp issues, abd distension and more. Treat with exchange transfusion, glucose, fluids

99
Q

Talk about neonatal pooycthemaia,

A

Caused by hypoxia IU, like eclampsia, IUGR, etc. Causes plethora, low glucose, resp issues, abd distension and more. Treat with exchange transfusion, glucose, fluids

100
Q

SVC syndrome Dx’ic Invx

A

MRI

101
Q

Risk factors for upper extremity DVT

A

Peripheral inserted CVC, cancer, young athletes, thoracic outlet syndrome

102
Q

How to invx suspected macrovasc hemolysis due to valve

A

Echo

103
Q

How does follicular non-Hodgkin’s lymphoma present

A

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

104
Q

What’s the main physical difference between myofascial pain syndrome and fibromyalgia

A

In myofascial pain syndrome, they have trigger points, when palpated cause pain in target zones. Fibromyalgia has pain at the point of palpation

105
Q

How does EPO Tx predispose HTN? What is a lab clue that indicated elevated risk for HTN

A

Decreases NO release, vasoC directly, increases alpha sensitivity. A sudden increase in Hb from when EPO given, can indicate risk for HTN

106
Q

AIHA are intra or extra vascular

A

Extra!!

107
Q

CLL vs lymphoma.

Which one is b symptoms and normal FBC

Which one no b symptoms and high high Lymphocytes

A

Lymphoma and CLL respectively

108
Q

What is post transplant lymphoproliferative disorder

A

Immunosuppressiion. Deceases CD8 immunosurpression, allowing for EBV replication and lymphocyte immortality

109
Q

Some random lab findings for HL

A

High eosinophils, high LDH

110
Q

Pain in chest when drink booze

A

HL. Alcohol causes pain in LNs

111
Q

Bronchiestcatsis involving upper lobes mainly, is a sign of……what cause..?

A

CF

112
Q

What is non diahrreal HUS?

A

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.

113
Q

Chronic vs acute DIC

A

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!!

114
Q

Red papules on the trunk and lips represent what

A

represent cutaneous arteriovenous malformations. Could be osler Webber rendu

115
Q

Mainstay Tx for aplastic crisis in SCD

A

Transfuse

116
Q

How harlequin syndrome be seen in neuroblastomas

A

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.

117
Q

Dx of neuroblastoma

A

Surgical biopsy definitive

118
Q

Why do pernicious anemia need periodic EGD

A

Risk of gastric CA

119
Q

RF for upper extremity DVT. Name 5

A

Central venous cathete
• Repetitive arm motions (eg, baseball pitching)
• Weight lifting (increase scalene size causing thoracic outlet syndrome)
• Malignancy

thoracic outlet syndrome

120
Q

Treatment of splenic sequestration crisis

A

Isotonic fluid resuscitation
• Red blood cell transfusion
• ‡ Splenectomy

121
Q

SCD disease patient with:

Abdominal pain
• Palpable splenomegaly
• Signs of anemia (tachycardia, pallor, fatigue)
•Hypotensive shock 大

A

Splenic sequestration crisis

122
Q

Tx of SCD induced stroke

A

• Exchange transfusion
• Simple transfusion if exchange transfusion is unavailable

123
Q

All patients with cryoglob, need which infx disease test

A

Therefore, all patients require hepatitis serologies (even if aminotransferases

124
Q

General Tx for raynauds

A

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

125
Q

Main symptoms difference between primary and secondary raynauds

A

Tissue injury or digital ulcers
• Abnormal nail fold capillary examination

In secondary

126
Q

Recall muscles for shoulder abduction

A

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.

127
Q

HbCO levels in smokers and non smoker

A

Nonsmokers have low levels (<3%) of carboxyhemoglobin (due to normal enzymatic reactions). Cigarette smokers may have carboxyhemoglobin levels as high as 10%.

128
Q

Why do we get polycythemia in CO toxicity

A

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.

129
Q

Leukamoid reaction vs CML regarding shift left

A

Leukamoid reaction: More mature
(metamyelocytes > myelocytes)
CML: Less mature
(metamyelocytes < myelocytes)

130
Q

Main issue with the G6PDH assay testing. How do we overcome this

A

It’s often normal during the attack. So in 3mo we do the confirmatory assay test

131
Q

Clinical difference between Pyr Kinase def and G6PDH def

A

Unlike with G6PD deficiency, hemolysis is constant,
so there is no relationship to inciting events (eg, sulfa drug exposure).

132
Q
A
133
Q

Leukoreduction of RBCs, two benefits

A

Leukoreduction reduces the risk of human leukocyte antigen alloimmunization and transmission of cytomegalovirus (which typically resides in leukocytes). Also reduces risk of FNHTR

134
Q

First line Tx for chemo induced N/V

A

Serotonin (5HT) receptor antagonists (eg, ondansetron)

135
Q

Thrombosis link to IV fluids

A

Limiting use of crystalloids (eg, $1 L), which dilute existing coagulation (eg, clotting) factors and platelets, thereby increasing coagulopathy

136
Q

Iv fluids worsen the lethal triad. What is the lethal triad

A

“lethal triad” (hypothermia, acidosis, coagulopathy)

137
Q

Mx for TRALI

A

Resp support only

138
Q

TRALI vs TACO BP

A

Low and high resp

139
Q

Risk factors for rectal sheath hematoma

A

Abdominal trauma, forceful abdominal contractions (eg, coughing)
• Anticoagulation
• Older age, female sex

140
Q

How does a rectal sheath hematoma present

A

Acute-onset abdominal pain with palpable abdominal mass
Worse pain on abdominal contraction (carnett sign)
• Blood loss anemia, leukocytosis
• ‡ Nausea, vomiting, fever

141
Q

Why is a rectal sheath hematoma problematic below arcuate line?

A

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.

142
Q

Bone lesions in MM vs HyperPTH

A

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,

143
Q

Why do infants have a Hb nadir

A

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

144
Q

Why do premats have a lower infant Hb nadir

A

htc is lower at birth, blood draws will also worsen it. Flora is less mature too

145
Q

Pathophys of urticaria transfusion reaction

A

preformed recipient IgE antibodies reacting against a soluble allergen in the
donated plasma, or vice versa (ie, donor IgE against recipient allergen).

146
Q

Tx of metastasis to bone for the high calcium and bad pain?

A

BPS for the Ca, and Radiation therapy can treat moderate to severe pain caused by bone metastases.

147
Q

Name the risk factors for iron deficiency of infancy

A
  • 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

148
Q

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

a micro-Coombs test can be done

149
Q

How to treat haemophilia. Consider if not severe and factor above 1%. Consider if severe or factor below 1%

A

Give desmopressin. But if severe or factor less than 1% transfuse the factor

150
Q

How to properly diagnosed pseudo TCP

A

Draw blood using a non-EDTA tube. Platelet count should be normal now

151
Q

Other than doing von Willebrand factor antigen test, What is another diagnostic test for von Willebrand’s disease

A

Ristocetin assay.

152
Q

Interpret Ristocetin assay

A

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

153
Q

If von Willebrand’s disease patient has refractory, severe, current plead, Type II, surgery. What is the treatment

A

Von Willebrand factor and factor eight concentrate. Not desmopressin like usual

154
Q

Can you name 3 scenarios where you would do a thrombophilia screen

A

VTE and no risk factor.

First-degree relative had VTE test and 50 years old

1st° relative had thrombophilia

155
Q

Diagnostic approach to HIT2. Consider beginning, initial diagnostic test, most accurate test

A

Obviously would do platelet count. The HIT PF4 Ab is first diagnostic test. Most accurate is the functional serotonin release assay

156
Q

Why is testing for factor eight important in DIC

A

He is low in DIC, but is normal in liver disease

157
Q

Antiphospholipid syndrome treatment.

A

Low molecular weight heparin bridge into warfarin. DOAC not so effective here

158
Q

Recall of TTP management and HUS management

A

TTP - Plasma exchange, consider steroids and rituximab

HUS – mainly supportive. Plasma exchange of severe. Dialysis if aKI. Hydration

159
Q

ITP management. If platelets above 30, And no bleeding. Or if platelets less than 30 or bleed

A

No treatment as long as platelets above 30 and no bleeding. Corticosteroids or IVIg otherwise. Keep in mind this is for adults

160
Q

Main difference in ITP management between adults and children

A

Adults we give treatment if platelets are less than 30 all the patients bleeding. In children we only give treatment if bleeding

161
Q

If corticosteroids or IV immunoglobulin fails for ITP, what are the things could we do

A

Splenectomy, rituximab, TPO

162
Q

Most accurate diagnostic test for G6PD H deficiency

A

Enzyme levels a couple of months after the attack

163
Q

Most accurate test for PNH

A

Flow cytometry (CD55 and CD59 absence

164
Q

PNH treatment. Consider best initial, alternative, definitive

A

Prednisone initially. Eculizumab is an alternative. Bone marrow transplant is definitive

165
Q

Hereditary spherocytosis. Treatment. Consider most cases, and considered severe cases

A

Most cases just give folate supplementation and transfuse of need. Severe cases usually require splenectomy

166
Q

First line treatment for warm autoimmune haemolytic anaemia. What about a mild. Potential second line

A

Corticosteroid First line. If mild no treatment.

Splenectomy or IV Ig could be a second line

167
Q

Is rituximab more for cold or warm autoimmune haemolytic anaemia

A

Cold

168
Q

 What is the schilling test used for

A

Radioactive B 12/ And then check the urine. Detect whether you just have a low B12 in the diet or a problem absorbing B12

169
Q

Polycythaemia main therapy combo? (Consider Susan). If resistant to main treatment can give what. What percentage do we aim haematocrit to be

A

HU, phlebotomy when need, aspirin. Ruxolitinib is a jack inhibitor, and is the if HU is resistant. Less than 45%

170
Q

Porphyria cutanea tarda management

A

Phlebotomy to remove porphyrin, avoid sun, hydroxychloroquine (like lupus)

171
Q

Acute intermittent porphyria management

A

Mainly supportive, but hemin and glucose are good

172
Q

HLH management

A

Dexamethasone and etopside. Consider antibiotics. Transfuse if needed

173
Q

Treatment ideas for mastocytosis

A

Prevent degranulation. Antihistamine, cromylyn, anti-leukotriene

174
Q

Neutropenic fever investigations. And treatment.

A

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.

175
Q

Neutropenia chronic management

A

If chronic consider G – CSF, and bone marrow transplant

176
Q

If a patient has lymphopenia, and is asymptomatic, does not have HIV. How do I manage

A

Can just observe and monitor

177
Q

Name three indications where an eosinophilic patient should have corticosteroids

A

Dress syndrome, eosinophils above 100. Eosinophilic myocarditis

178
Q

What are pel Epstein fevers

A

10 days fever and 10 days off. Seen in Hodgkin lymphoma

179
Q

Alcohol induced pain at noodle sites, is a sign of what disease

A

Hodgkin lymphoma

180
Q

Dutcher bodies are found in which cells

A

Plasma cells

181
Q

Patient with SCD, patient has microcytosis and also high HbA2…. What’s this?

A

This is heterozygous HbS with Beta Thal. These are two signs of this

182
Q

Which medication reduces attacks and mortality in SCD

A

HU

183
Q

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

A

Do splenectomy or rituximab. These patients should not be given a platelet transfusion

184
Q

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

A

Just look at the time. Anaphylaxis will be in minutes. Other than that they should be clinically easy to differentiate

185
Q

Comprehensively list the glucose-6-phosphate dehydrogenase medication exacerbated

A

Dapsone, sulphur, TMP SMX, primaquine, quinine, chloroquine, raspberry case, quinolone

186
Q

What kind of anaemia can I NAH cause

A

Sideroblastic, due to B6 deficiency

187
Q

On US Emily, if a young patient has thrombosis, we can assume what

A

Presume it’s factor five Leiden (activated protein see resistance

188
Q

Which one of the thrombophilia is is acquired most of the time

A

Antithrombin three deficienc

189
Q

When calculating Meltzer index, (MCV divided by red blood cell) what is the cut-off

A

Less than 13 indicate thalassaemia, more than 13 indicates iron deficiency anaemia

190
Q

When is basophilic stippling commonly seen

A

Lead poisoning, megaloblastic anaemia, benzene exposure

191
Q

Two Viruses that are associated with ITP

A

Hep C and HIV

192
Q

When an abruption p Case has RhoGAM. What do we need to consider

A

The dose needs to be higher for these patients. That’s why we do the Betke test

193
Q

Cancel Mets to the spine causing spinal-cord compression. Before the MRI what do I do

A

Ivy glucocorticoids

194
Q

Iron studies in anaemia of chronic disease

A

Ferritin hi, Iron low, TIBC low,

195
Q

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

A

Could be a follow deficiency. Not a cute enough and severe enough to be aplastic crisis

196
Q

Tortuous retinal veins in the setting of anaemia and high-protein count

A

Consider Walden Strom

197
Q

Young patient with Ruby coloured peppers on the lips, high haematocrit, history bleeding (epistaxis) , Increased pulse pressure

A

Osler webber rendu syndrome

198
Q

When we have a patient with STEC and salmonella. Can we give antibiotics for the salmonella

A

No don’t give any antibiotics at all

199
Q

Big demographic and symptom difference between Hodgkin and follicular non-Hodgkin’s lymphoma

A

Follicular non-Hodgkin’s usually does not have the symptoms

200
Q

If we have a patient who has submandibular lymph node, chronic smoker. Maybe a bit of referred otalgia. What’s the next investigation why

A

Do a laryngeal pharyngeus scope . Because you’re suspicious of oral Sq cell carcinoma

201
Q

I deficiency anaemia versus beta thalassaemia. Red blood cell count

A

Low, (normal or high) respectively

202
Q

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

A

Just presume there is a pernicious in a

203
Q

Chronic SLE is a risk factor for which lymphoma

A

NHL

204
Q

When does gestational thrombocytopenia take place in preg


A

Second half

205
Q

Is graft versus host always immediate

A

No. Usually takes time. Sometimes even up to 80-100 days

206
Q

If you want to do a workout for protein C deficiency, what drug cannot be taken two weeks prior

A

Warfarin. As it can decrease its levels naturally

207
Q

What things do you give to prevent a KI in a patient that have chemotherapy for leukaemia

A

Normal saline and allopurinol

USMLE Step 2 - Top 5% (34 decks)

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