Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine MBBS year 2 > Haematology > Flashcards

Haematology Flashcards

1
Q

what happens in antithrombin deficiency?

A

decreased inhibition of factor IIa and Xa

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

symptoms of DVT?

A

swelling, redness, warmth, pain

post-thrombotic syndrome (damage to valves)

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

Absence of GpIb surface glycoprotein results in?

A

Bernard Soulier syndrome
( only 1 b in Gp1b and in Bernard soulier)

It is a Platelet adhesion problem

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

clinical features of coagulation disorders?

A
  1. bleeding into deep tissues muscles and joints

2. bleeding delayed but prolonged

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

what questions would you ask a patient whose labs suggest iron deficiency aneamia?

A 
Menstrual/postmenopausal bleeding 
Diet - vegetarian/vegan 
GI symptoms - dysphagia/dyspepsia/abdominal pain/change in bowel habit/hematemesis/rectal bleeding/melaena
Aspirin/NSAIDs
Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

role of coagulation?

A

To generate thrombin (IIa), which will convert fibrinogen to fibrin

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

Why is aspirin used as anti platelet therapy?

A

Decreases thromboxane A2. Decreases platelet activation

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

what happens in factor V leiden?

A

Mutant factor 5. The coagulation factor is resistant to degradation by activated protein C

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

functions of B12?

A

DNA synthesis, homocysteine metabolism

Integrity of the nervous system

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

What is used to treat hemophilia A?

A

Desmopressin

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

below which platelet count is spontaneous bleeding common?

AND severe spontaneous bleeding?

A
  1. <40 x 10^9

2. for severe spontaneous bleeding <10 x 10^9

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

What is the effect of direct Xa inhibitors on PT and PTT?

A

Prolong both

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

What is the result of absence of factor XI?

A

bleed after trauma but not spontaneous

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

conditions associated with AIHA?

A

SLE - polyarthritis, renal impairment, facial skin rashes, hepatitis, tiredness
CLL

*positive dat test. Splenomegaly

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

what do lab tests show in DIC?

A

increase in FDPs (D-dimers) - due to activation of fibrinolysis
decrease in fibrinogen

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

what causes a prolonged PT and normal APTT

A

factor 7 deficiency

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

mechanism of ITP

A

anti-GpIIb/IIIa antibodies bind to platelets -> destruction by splenic macrophages

  • blood smear will show megakaryocytes but other cell counts will be fine
  • May be associated with viral illness
  • decrease in platelet count
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Give two possible investigations you would undertake if a disorder of primary heamostasis is suspected.

A

platelet count
vWF assay
clinical examination

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

signs of B12 deficiency?

A

paresthesia
Pale Yellow tinge to skin
Changes in the way you move or walk around
Reversible dementia

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

causes of vessel wall disorder?

A
  1. hereditary hemorrhagic telangiectasia, Ehlers-Danlos Syndrome
  2. Acquired - steroid therapy, aging (senile purpula), vasculitis, scurvy
    Usually affect collagen synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

causes of thrombocytopenia (low platelet count)?

A
  1. Bone marrow failure - leukemia, B12 deficiency
  2. Accelerated clearance - Immune (ITP) is common, Disseminated Intravascular Coagulation (DIC)
  3. Pooling and destruction in enlarged spleen (e.g cirrhosis and portal hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the result of absence of prothrombin (Factor II)?

A

lethal

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

a patients VWF is found to show reduced platelet adhesion, what type of Von
Willebrand disease does this indicate?

A

type 2

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

how does LMWH work?

A

enhances antithrombin- predominantly inactivates Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Direct Xa inhibitors decrease the formation of —

A

Thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

If a patient with iron deficiency anemia reports weight loss and intermittent abdominal pain, what investigations do you order?

A
  1. FIT for blood in stool
  2. Upper Gi endoscopy, duodenal biopsy, colonoscopy (GI investigations)
  3. Coeliac antibody testing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

causes of megaloblastic aneamia?

A

Vitamin B12 and folate deficiency
Agents or mutations that impair DNA synthesis:
azathioprine cytotoxic chemotherapy
Folate antagonists - methotrexate
Bone marrow cancers - myelodysplastic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is DIC?

A

widespread activation of clotting factors leading to deficiency
platelets also consumed -> thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are common symptoms of anemia?

A

Fatigue, pallor, dyspnea, tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

absence of GpIIb/IIIa surface glycoprotein results in?

A

Glanzmann’s thrombasthenia

2 A’s, 3’s in Glanzmann’s = GpIIb/IIIa

It is a platelet aggregation problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are some causes of DIC?

A
  1. sepsis
  2. major tissue damage
  3. inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Patient with Rheumatoid Arthritis, low hb, slightly low MCV, reticulocytes on low end
Low serum iron. Low transferrin. High ferritin. Normal transferrin saturation. High ESR. blood film shows microcytic hypochromic rbcs. Elevated platelet count. What is the diagnosis?

A

aneamia of chronic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

warfarin is a substrate for cytochrome p450

name some p450 inhibitors that would cause increased plasma levels of warfarin -> bleeding on warfarin

name some p450 inducers

A

inhibitors:
- fluconazole
- erithromycin/clarithromycin
- ciprofloxacin
- omeprazole
- some anti-HIV drugs, especially protease inhibitors
- grapefruit juice

inducers

  • st. johns wort
  • Rifampicin (anitbiotic used to treat TB)
  • Antiepileptics - carbamazepine, phenytoin, phenobarbitone, primidone
  • griseofulvin (antifungal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

treatment for hereditary spherocytosis?

A

Folic acid to help make new red blood cells

Splenectomy if severe to increase rbc life span

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

other causes of normocytic aneamia?

A

Recent blood loss:
- Gastrointestinal haemorrhage, trauma

Failure of production of RBCs:

  • Early stages of iron deficiency
  • Bone marrow failure or suppression (e.g. chemotherapy)
  • Bone marrow infiltration (e.g. leukaemia)

Pooling of RBCs in spleen:
Hypersplenism, e.g. liver cirrhosis
Splenic sequestration in sickle cell anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

state causes of Folic acid deficiency

A
  1. diet - alcoholics, poverty
  2. malabsorption - coeliac disease, jejunal resection
  3. increased demand - hemolytic aneamia, pregnancy

treat with oral supplements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

increase of which coagulant proteins can result in thrombosis?

A
  1. prothrombin mutation/ Factor II
  2. Factor 5 leiden
  3. Factor 8 mutation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

4 side effects of Warfarin?

A
  1. bleeding
  2. skin necrosis
  3. purple toe syndrome
  4. teratogenic - chondrodysplasia punctata
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

A patient with a disorder of primary haemostasis shows no evidence of petetchiae. What cause of the symptoms might this allow you to rule out?

A

thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

causes of macrocytic aneamia?

A

Lack of vitamin B12 or folic acid: megaloblastic anaemia
Use of drugs interfering with DNA synthesis
Liver disease and ethanol toxicity
Haemolytic anaemia (reticulocytes increased)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is virchows triad?

A

SHE

  1. stasis of blood flow - surgery, long haul flights, pregnancy
  2. hypercoagulability - dominant in venous thrombosis
  3. endothlial damage - dominant in arterial thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

differentiate between purpura and petechiae

A

purpura dont blanch when pressure is applied

pupura are larger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what deficiencies can result in thrombosis?

A

of anticoagulant proteins

  1. antithrombin deficiency
  2. protein C or S deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

State Important deactivators of coagulation. Deficiency Of them lead to what

A
  1. Antithrombin lll
  2. Protein C and protein S(cofactor)
  3. Tissue factor pathway inhibitor
    Hypercoagulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what neurological disorders can present with B12 and folate deficiencies?

A 
Folate = neural tube defect 
B12 = Dementia and SACD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

state 3 situations that require use of anticoagulants as prophylaxis

A
  1. following surgery
  2. during hospital admission
  3. during pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

findings in hereditary spherocytosis?

A

signs of hemolytic anemia
Spherocytes on blood film - small, spherical, no central pallor
Splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which type of heparin medication requires monitoring?

A

UFH - results in prolongation of APTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the main function of Plasmin?

A
  • Degrade clots to FdPs and D-dimers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

signs and symptoms of iron deficiency aneamia?

A

Symptoms - fatigue, conjunctival pallor, pica, spoon nails
Labs show Low ferritin and serum iron. High transferrin/TIBC. Low transferrin saturation
Hb electrophoresis shows no increase in HbA2 (ruling out b- thalassemia)
Blood film shows small hypochromic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what happens in protein C or S deficiency?

A

decreased ability to inactivate Va and VIIIa

52
Q

why does warfarin cause skin necrosis?

A

initial risk of hyper-coagulation when using the drug - protein C depletes initially before the other clotting factors get depleted. So blood clots form which block blood flow to skin

53
Q

findings in G6PD deficiency

A
  1. Labs consistent with hemolytic anemia
  2. Blood film shows heinz bodies (precipitated oxidised haemoglobin) and bite cells
  3. Ghost cells and hemighost cells from intravascular hemolysis
54
Q

Effect of factor XII deficiency?

A

no bleeding.
doesn’t cause bleeding problems
But it causes prolonged PTT
This because Thrombin instead can activate other parts of the clotting cascade

55
Q

spontaneous joint bleeding in hemophilia is called?

A

haemarthrosis

56
Q

causes of iron deficiency aneamia?

A 
Blood loss (most common cause in adults) due to :
Hookworm (most common worldwide)
 menorrhagia
GI loss
 Insufficient GI iron intake:
Dietary - vegetarians, vegan	
Malabsorption -  Coeliac disease,  H. pylori gastritis	
Increased iron requirements:
 Pregnancy, infancy
57
Q

findings in AIHA?

A 
signs of hemolytic anemia 
DAT test (adding anti-human globulin to patient RBC and antibody complex) = positive
58
Q

name some triggers in a patient with G6PD deficiency

A

fava beans, oxidant drugs, napthalene, infection

59
Q

What diagnostic tests can be used to determine B12 deficiency

A

Methylmalonic acid test - will be high

Test for intrinsic factor antibodies - used to diagnose pernicious aneamia

60
Q

functions of folate?

A

DNA synthesis, homocysteine metabolism

61
Q

state 4 causes of resistance to warfarin

A

Diet - increased vitamin k intake
Lack of medication compliance
Increased metabolism from drug interactions
Reduced binding

62
Q

what do you monitor when administering LMWH?

A

anti-xa activity

63
Q

what are the clinical features in disorders of primary haemostasis?

A
  1. superficial prolonged bleeding from cuts/ after trauma/surgery - immediate
  2. mucosal bleeding (epistaxis, menorrhagia, gum bleeding)
  3. ecchymosis
  4. Petechiae - from thrombocytopenia
  5. purpura - from platelet or vascular disorders

*severe VWD can result in haemophilia-like bleeding due to low FVIII

64
Q

what anticoagulant do you use for atrial fibrillation?

A

DOACs or Warfarin

65
Q

what anticoagulant do you use for a prosthetic heart valve?

A

Warfarin

66
Q

which drug works by increasing anticoagulant activity?

A

heparin

67
Q

functions of haemostasis?

A
  1. prevent blood loss from injured vessels
  2. arrest bleeding from injured vessels
  3. enable tissue repair
68
Q

When a patient presents with a normocytic nonhemolytic anemia, what is the next investigation you order?

A

iron studies - as condition may be caused by iron deficiency or aneamia of chronic disease or things that are not iron related

69
Q

causes of increase in fibrinolytic factors

A
  1. tPA

2. Heparin - potentiates antithrombin

70
Q

functions of VWF?

A
  1. Binding to collagen and capturing platelets

2. Stabilising factor VIII - may be low if VWF is low

71
Q

how does aspirin work

A

irreversibly blocks COX enzyme

inhibits the production of thromboxane A2 from arachidonic acid

72
Q

Why is an elevated d-dimer used for DVT/PE diagnosis

A

Indicates clot breakdown

73
Q

state some direct Xa inhibitors

A

rivaroXaban

apiXaban

74
Q

state 4 causes of prolonged APTT and PT

A
  1. Liver disease
  2. anticoagulant drugs
  3. DIC
  4. blood transfusion
  5. vitamin K deficiency?
75
Q

state some direct thrombin inhibitors

A

Digabatran

76
Q

which drug/s work by lowering procoagulant factors

A

warfarin, DOACS

77
Q

state 4 causes of prolonged APTT and normal PT

A
  1. haemophilia A
  2. haemophilia B
  3. factor XII deficiency
  4. factor XI deficiency

*PTT Is intrinsic pathway - play Table Tennis Inside

78
Q

Low MCH, MCHC and MCV are found in what type of anemia?

A

Microcytic hypochromic anemia

79
Q

_ FDPs and d-dimers and _ fibrinogen are hallmarks of DIC

A

High

Low

80
Q

what is the normal range for platelet count

A

150 x10^9 - 400 x10^9

81
Q

describe some novel treatments for haemophilia

A
  1. gene therapy
  2. bispecific antibodies in Haemphilia A
  3. RNA silencing - targets antithrombin
82
Q

symptoms of pulmonary embolism

A

Tachycardia (palpitations), hypoxia, shortness of breath
Chest pain, hemoptysis,
Sudden death

83
Q

causes of bleeding?

A
  1. reduction in coagulation factors and platelets (failure of production or increased consumption vs defective function)
  2. increase in fibrinolytic factors and anticoagulant proteins
84
Q

how do DOACs work?

A

Factor Xa (direct Xa inhibitors) or IIa (direct thrombin inhibitors).

85
Q

what is warfarins mechanism of action?

A

Warfarin inhibits vitamin K epoxide reductase

thus preventing the vitamin K-dependent carboxylation of factor II, VII, I, Protein C, Protein S

86
Q

storage pool disease results in?

A

reduction in granular content of dense granules of platelets - ADP, calcium, serotonin

87
Q

how do you monitor warfarin administration?

A

using INR = PT/PTc. normal = 1

target with warfarin = 2-3

88
Q

what is chondrodysplasia punctata?

A

early fusion of epiphyses

89
Q

which clotting factor does warfarin reduce most quickly

A

VII

90
Q

A 35 year old woman presents suffering regular prolonged nosebleeds and has noticed she bruises
easily when playing sport. She also notes that her menstrual bleeding has been heavier than usual in
recent months.

What phase of haemostasis is likely to be disrupted in this patient?

A

primary

91
Q

causes of extrinsic hemolytic aneamia?

A
  1. Immune mediated - AIHA, Allo immune/post blood transfusion
  2. None immune- Microangiopathic (HUS leads to this), macroangiopathic, infections. snake venom, drugs.
92
Q

describe the pathophysiology of aneamia of chronic disease

A
  1. IL-6 released during inflammation. This Increases hepcidin levels which blocks iron absorption and release by binding to ferroportin on intestinal mucosal cells and macrophages
  2. Decrease EPO production
93
Q

what are the classic findings in hemolytic aneamia?

A
  1. normocytic aneamia
  2. ↑reticulocyte count
  3. ↑ LDH
  4. ↑ unconjugated bilirubin
  5. ↓ haptoglobin (lower in intravascular)
  6. Urine Hb and hemosiderin (intravascular)
94
Q

how does UFH work?

A

Enhances antithrombin - helps bind and inactivate Factor Xa and thrombin
IV drug

95
Q

what are the 3 main causes of coagulation disorders

A
  1. Deficiency of coagulation factor production
  2. Dilution - blood transfusions (red cell transfusions do not contain plasma. Must replace plasma in major hemorrhage as well as red cells and platelets)
  3. Increased consumption - DIC, autoimmune (production of coagulation factor inhibitors)
96
Q

consequence of DIC?

A

fibrin deposition in vessels can cause organ failure

97
Q

Direct thrombin inhibitors decrease formation of___

A

Fibrin

98
Q

state causes of B12 deficiency and how to treat it

A
  1. diet
    treat with supplements
  2. gastric/intrinsic factor - pernicious aneamia and gastrectomy
    treat with hydroxocobalamin injections
  3. terminal ileum - chron’s disease, ileal resection
    treat with the injections
99
Q

name 3 conditions that require a therapeutic use of anticoagulants?

A
  1. venous thrombosis
  2. atrial fibrillation
  3. mechanic prosthetic heart valve
100
Q

causes of impaired function of platelet?

A
  1. Glanzmann’s thrombasthenia
  2. Bernard Soulier Syndrome
  3. Storage pool disease
  4. Aspirin, NSAIDs, Clopidogrel
101
Q

A patient is on warfarin. Why might malnutrition result in an increase in their INR?

A

Metabolism of some drugs affected by malnutrition

Malnutrition decreases plasma protein levels (warfarin is heavily plasma protein bound):

  • Decreases oxidative metabolism
  • Decreased GFR
102
Q

What is INR? What does a fall in INR signify?

A

International normalised ratio - Standardised measure of blood clotting time
PT patient/PTnormal
Fall in INR = Increased clotting, decreased bleeding
If INR falls below 2.0 thrombosis risk increases for a patient predisposed to clotting

103
Q

how does clopidogrel work?

A

inhibits ADP from binding to its P2Y12 receptor on platelet)

104
Q

state some common causes of anaemia of chronic disease

A

chronic infections(TB, HIV), autoimmune disorders like RA, malignancy

105
Q

causes of von willebrand disease?

How does it manifest?

A
  1. Hereditary decrease of quantity (Type 1 or 3) or function of the factor (Type 2)
  2. May be acquired due to antibody
  • NORMAL Platelet count and PT. PTT may or may not be elevated due to factor 8 deficiency
106
Q

what tests are carried out for coagulation disorders

A
  1. clotting screen - APTT, PT, platelets
  2. assays for factor 8
  3. test for inhibitors
107
Q

5 causes of deficiency of coagulation factor production?

A
  1. factor 8 deficiency - hemophilia A
  2. factor 9 deficiency - hemophilia B
  3. liver disease
  4. anticoagulant drugs - warfarin, DOACs
  5. vitamin k deficiency
108
Q

what is purple toe syndrome?

A

disrupted atheromatous plaques bleed

cholesterol emboli lodge in extremeties

109
Q

which anticoagulant has some renal dependence?

A

DOACs

110
Q

A Patient with hemolytic anaemia later presents with upper right abdominal pain, more marked jaundice and higher bilirubin which is mainly conjugated. What is the cause?

A

pigment Gallstones from increased breakdown of hb to bilirubin
Has obstructed common bile duct - buildup of conjugated bilirubin that cant pass to duodenum

111
Q

how do you slowly and rapidly reverse warfarin action?

A

Slowly - vitamin k administration

Rapidly - infusion of coagulation factors- PCC or FFP

112
Q

when do you use FFP?

A

to replace all coagulation factors

113
Q

what lab tests are carried out for disorders of primary haemostasis.

A
  1. platelet count - normal or low depending on condition
  2. bleeding time - prolonged
  3. assays of von Willebrand factor
  4. coagulation screen - NORMAL except in mixed disorders. PT and APTT prolonged in DIC. PTT may be prolonged in severe cases of VWD

*primary, think PLATELET problem

114
Q

what anticoagulant do you use in pregnancy?

A

LMWH (DOACs not safe)

115
Q

how do you treat abnormal primary haemostasis?

A
  1. failure of production - replace missing factors or platelets. stop aspirin/NSAIDs
  2. immune destruction - steroids(prednisolone) or splenectomy for refractory ITP
  3. increased consumption - replacement and treatment of cause
  4. VWD - desmopressin to release vWF
  5. tranexamic acid (anti-fibrinolytic), fibrin glue, OCP for menorrhagia
116
Q

when do you use cyroprecipitate?

A

coagulation factor deficiencies of fibrinogen and factor 8

117
Q

how do you treat coagulation disorders?

A
  1. factor replacement:
    - factor concentrates
    - FFP
    - cyroprecipitate
  2. desmopressin, tranexamic acid, fibrin glue, OCP
118
Q

findings in megaloblastic aneamia?

A

Hypersegmented neutrophils, RBC macrocytosis elevated MCV

119
Q

What protein transports iron in the blood?

A

Transferrin

120
Q

What protein stores iron? Where?

A

Ferritin

In macrophages of liver and bone

121
Q

What happens to transferrin when iron stores are low?

A

Transferrin levels rise

122
Q

What key molecule causes anaemia of chronic disease?

A

Hepcidin

It binds ferroportin in enterocytes and macrophages

123
Q

What are the iron studies in anaemia of chronic disease?

A

Increased ferritin - iron trapped in storage form
Decreased serum iron
Decreased transferrin

124
Q

How would you treat anaemia of chronic disease?

A

Ibuprofen

125
Q

In a patient with SLE, state one way of differentiating between AIHA and Anemia of chronic disease being the cause of anaemia

A

AIHA will have a high reticulocyte count (hemolytic)

And will also be normocytic

126
Q

Spherocytes have _ MCHC

A

Elevated

Medicine MBBS year 2 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions