blood

Question 1

Which of the following correctly describes the changes in hemoglobin composition during human development?

A) HbA2 levels increase significantly after birth, becoming the dominant form in adults.
B) HbF (fetal hemoglobin) predominates in fetal life but decreases after birth, replaced mostly by HbA (adult hemoglobin).
C) HbF levels remain constant throughout life, while HbA only appears in late childhood.
D) HbA is the dominant form in fetal life, while HbF becomes the primary form in adulthood.

Answer 1

B) HbF (fetal hemoglobin) predominates in fetal life but decreases after birth, replaced mostly by HbA (adult hemoglobin).

Alpha Always, (α)
Gamma Goes, (γ)
Becomes Beta (β)
=> HbF (α2γ2) predominant form during fetal form and decline after birth,
and HbA (α2β2) becomes the dominant form instead

Question 2

definition of anemia

Answer 2

decrease in Hb
and/or decrease in RBC

Question 3

how does anemia lead to fatigue

Answer 3

low Hb and/or RBC
[definition of anemia]
-> low oxygen-carrying capacity
-> hypoxia
-> lower rate of aerobic resp
-> less ATP released
=> fatigue

Question 4

3 types of anemia
(based on MCV)

Answer 4

• microcytic = decreased MCV
• normocytic = normal MCV
• macrocytic = increased MCV

Question 5

cause of microcytic anemia

Answer 5

insufficient/abnormal Hb synthesis,
usually due to iron deficiency
OR thalassemia

Question 6

2

causes of normocytic anemia

Answer 6

1. increased RBC destruction
   a. blood loss
   b. haemolysis
2. decreased RBC production
   a. kidney damage -> decreased EPO production
   b. anemia of chronic disease -> suppress EPO production

erythropoietin (EPO) signals bone marrow to produce more RBCs,
is produced by kidney
and is increased in response to drop in pO2

Question 7

cause of macrocytic anemia

Answer 7

impaired DNA synthesis and cell div,
usually due to vitamin B12 or folate deficiency

Question 8

when is erythropoietin (EPO) produced

Answer 8

when there is low O2 levels (hypoxia)
-> stimulates bone marrow to increase RBC production
=> increase O2 delivery to tissues

produced by kidneys

Question 9

what will ferritin levels be like in iron-deficiency anemia

Answer 9

low
<- depleted iron stores

ferritin stores iron

Question 10

what will
transferrin levels, transferrin saturation and total iron binding capacity (TIBC)
be like in iron deficiency anemia

Answer 10

liver increases transferrin production
to maximise iron transport
=> high levels of transferrin

thus more available binding sites for iron
=> high TIBC

however less iron available to bind transferrin
=> low transferrin saturation

Question 11

in which scenario will there be LOW reticulocyte count?

A) Folate or B12 deficiency
B) Hemolytic anemia
C) Acute blood loss

Answer 11

A) Folate or B12 deficiency

-> impairs DNA synthesis
-> premature destruction of RBC precursors in the bone marrow before they can mature into reticulocytes and be released
(intramedullary hemolysis from ineffective erythropoiesis)
=> fewer reticulocytes released

Reticulocytes are immature RBCs released by bone marrow into bloodstream

high reticulocyte count = increased production of RBCs by bone marrow as COMPENSATION
for (B), compensating for RBCs which are destroyed in circulation
for (C), compensating for RBCs lost through blood loss

Question 12

early/late, any cons

comment on ferritin levels as indicator of iron deficiency

Answer 12

• good as earliest indicator of iron deficiency
• bad as inflammation or infection can also increase ferritin levels
  <- ferritin is acute-phase reactant

increased production of ferritin during inflammation/infection
to sequester iron away from pathogens which need it to grow

Question 13

difference in site of bleeding
in platelet disorders vs coagulation factor disorders

Answer 13

• platelet disorders: skin, mucous membranes (e.g. gum, epistaxis)
• coagulation factor disorders: deep soft tissues (joints, muscles)

Question 14

which is the intrinsic pathway?
aPartial Thromboplastin Time (aPTT)
or Prothrombin Time (PT)

Answer 14

aPTT
Table Tennis is played indoors,
while extrinsic pathway is PT as Tennis is played outdoors

Question 15

clotting pathway

What are the coagulation factors involved in common pathway

Answer 15

Factor I, II, V and X
bcos 1 x 2 x 5 = 10

Question 16

clotting pathway

What are the coagulation factors involved in intrinsic pathway

Answer 16

Factors VIII, IX, XI and XII
bcos count down from 12 to 8
but exclude 10 as it is alr in common pathway

Question 17

clotting pathway

What are the coagulation factors involved in extrinsic pathway

Answer 17

Factor VII

Question 18

Hemophilia A and Hemophilia B are caused by deficiencies in which clotting factors?

A) Factor VII & Factor IX
B) Factor VIII & Factor IX
C) Factor V & Factor X
D) Factor VIII & Factor X

Answer 18

B) Factor VIII & Factor IX

Haemophilia A = Haemophilia Ate (8)
Haemophilia B = B is 1 letter after A = 9 (1+8)

Question 19

Which does Haemophilia A and B affect,
aPTT or PT?

Answer 19

aPTT
as factors VIII (Haem A) and IX (Haem B) are both part of intrinsic pathway

recall!
factors in intrinsic pathway is 12 -> 8 (except 10)
intrinsic pathway is aPTT as Table Tennis is played indoors

Question 20

Why does a deficiency of Factor VIII or IX lead to impaired clotting?

A) They directly convert fibrinogen to fibrin
B) They are necessary for the activation of Factor X in the coagulation cascade
C) They prevent platelet aggregation
D) They break down fibrin clots

Answer 20

B) They are necessary for the activation of Factor X in the coagulation cascade

Factor VIII (Haem A) and Factor IX (Haem B) are part of the intrinsic pathway
-> Factor X cannot be activated without them
-> no Factor X to activate thrombin
=> impaired clot formation

Factor VIII stabilises fibrin clot by cross-linking fibrin strands

recall!
factors in intrinsic pathway are 12 -> 8 (except 10)
factors in common pathway are 1 x 2 x 5 = 10

implication!
since Factors VIII and IX are part of intrinsic pathway,
aPTT is affected in Haem A and B!
(aPTT = Table Tennis is played indoors)

Question 21

What factors will be deficiency if there is a Vitamin K deficiency?

Answer 21

• Factor II (prothrombin)
• Factor X
• Factor VII
• Factor IX

as Vit K act as a cofactor for the carboxylation and thus activation of these factors

Question 22

Which does Vit K deficiency affect,
aPTT or PT?

Answer 22

Both!
Factor IX is from intrinsic pathway,
(countdown from 12 to 8, exclude 10)
Factor VII is from extrinsic pathway

the remaining Factors II and X are from common pathway
(1 x 2 x 5 = 10)

Question 23

What factors will be deficiency if there is liver disease?

Answer 23

All factors except Factors III and IV
as liver produces most clotting factors

Factor VI does not exist!

Factor III = tissue factor
-> produced by tissues when damaged and initiates extrinsic coagulation pathway

Factor IV = Ca2+
-> coemes from diet and bones
and essential for several steps in clotting pathway

Question 24

Which does liver disease affect,
aPTT or PT?

Answer 24

Both!
Since all factors involved will be deficient

Question 25

Why does Hemophilia (A and B) NOT cause excessive bleeding from small cuts but leads to joint and deep tissue bleeding? A) The vascular response is unaffected B) Platelets function normally C) The coagulation cascade defect mainly affects fibrin clot formation D) All of the above

Answer 25

D) All of the above Hemophilia does not affect platelets -> normal primary hemostasis (initial plug formation) but results in deficiency of Factor VIII or IX -> defective clot stabilization (secondary hemostasis) => deep bleeding (joints, muscles, GI tract, brain, etc.)

Question 26

# platelet count (PC), bleeding time (BT), PT or aPTT what does vWF disease affect

Answer 26

* increases BT as defect in **platelet adhesion to exposed collagen** * increases (or no change in) aPTT <- decreased levels of Factor VIII <- vWF **stabilises Factor VIII** "**v**olks**W**agen **F**actories make gr**8** cars" ## Footnote usually, vWF binds to exposed subendothelial collagen at sites of vascular injury -> platelets adhere to vWF via their GPIb receptor => platelet plug formation recall! intrinsic pathway = aPTT as table tennis is played indoors and it involves factors 12 -> 8 (exclude 10)

Question 27

Which of the following best describes the underlying mechanism of Disseminated Intravascular Coagulation (DIC)? A) Isolated platelet destruction leading to thrombocytopenia B) Widespread activation of the coagulation cascade, leading to thrombosis and depletion of clotting factors C) Overproduction of clotting factors without platelet involvement D) Deficiency of von Willebrand Factor leading to abnormal platelet adhesion

Answer 27

B) Widespread activation of the coagulation cascade, leading to thrombosis and depletion of clotting factors **Trigger** (e.g. sepsis, trauma) -> excessive release of **TF** -> activation of **extrinsic pathway** -> widespread **clotting** -> **depletion** of platelets and clotting factors => increased **bleeding risk**

Question 28

are D-dimer levels increased or decreased in DIC

Answer 28

increased D-dimer are **fibrin degradation products** -> **excessive clots** broken down => increase in D-dimer

Question 29

how does DIC affect PC, BT, PT and aPTT

Answer 29

* decreases PC <- depletion of platelets for excessive clot formation * increases BT <- less platelets to form clots and stop bleeding * increases PT and aPTT <- depletion of platelets for excessive clot formation

Question 30

mechanism of Factor V Leiden

Answer 30

**mutated** form of Factor V -> **resistant to degradation** by **APC/S complex** -> more prothrombin is converted to thrombin -> excessive clot formation (hypercoagulability) => increased risk of DVT/PE

Question 31

what does Tissue Factor Pathway Inhibitor (TFPI) do

Answer 31

regulates **extrinsic pathway** of coagulation by **inhibiting Tissue Factor-Factor VIIa** (TF-FVIIa) complex

Question 32

# aPTT and PT do heparin and warfarin affect diff timings

Answer 32

Heparin prolongs aPTT * as it primarily affects factors in common and intrinsic pathways (XII, XI and IX) while Warfarin prolongs PT * as it FIRST affects extrinsic pathway <- **Factor VII** has the **shortest half-life**

Question 33

What is the primary purpose of a mixing test in coagulation studies? A) To differentiate between clotting factor deficiency and the presence of an inhibitor B) To measure the overall platelet count C) To diagnose thrombocytopenia D) To assess fibrinogen levels

Answer 33

A) To differentiate between clotting factor deficiency and the presence of an inhibitor if clotting time corrects => clotting factor deficiency if clotting time remains prolonged => factor inhibitor present ## Footnote Process: 1. patient's plasma + **normal** plasma mixed together in **1:1 ratio** 2. clotting test is repeated

Question 34

# the types and how many gene copies each have types of thalassemia

Answer 34

* Alpha thalassemia: **4** gene copies (bcos each person has 4 α-globin gene copies) 4 mutations = fatal * Beta thalassemia: **2** gene copies (bcos each person has 2 β-globin gene copies)

Question 35

symptoms of thalassemia

Answer 35

1. jaundice, anemia and splenomegaly bcos excess β or α chains -> **HbH (β4) or toxic aggregates** -> premature destruction (**haemolysis**) => excessive RBC breakdown 2. target cells bcos decreases α or B globin chain production -> low Hb content (hypochromia) -> **more membrane relative to Hb** => cell membrane folds on itself ## Footnote In fetuses, 4 α-globin gene mutations -> excess γ chains -> **Hb Barts (γ4)** -> higher oxygen affinity than HbH -> cannot release O2 to fetal tissues => severe hypoxia and **hydrops fetalis**

Question 36

# name of enzyme, requires/inhibited by, clinical implication 1st enzyme in heme synthesis

Answer 36

ALA synthase 2 * needs B6 * inhibited by heme and iron

Question 37

# name of enzyme, requires/inhibited by, clinical implication 2nd enzyme in heme synthesis

Answer 37

ALA dehydratase * inhibited by lead * lead poisoning -> **bluish** line on gums

Question 38

# name of enzyme, requires/inhibited by, clinical implication 3rd enzyme in heme synthesis

Answer 38

Uroporphyrinogen decarboxylase * affected in porphyria cutanea tarda -> red urine, photosensitivity

Question 39

# name of enzyme, requires/inhibited by, clinical implication 4th enzyme in heme synthesis

Answer 39

Ferrochelatase * inhibited by lead * lead poisoning -> **bluish** line on gums

Question 40

how does heme → bilirubin (unconjugated)

Answer 40

heme → biliverdin → bilirubin in **macrophages**

Question 41

how is bilirubin transported in bloodstream? A) Bound to transferrin B) Bound to albumin C) In free form as unconjugated bilirubin D) Bound to hemoglobin

Answer 41

B) Bound to albumin unconjugated bilirubin is **insoluble** → binds to **albumin** for **transport to liver**

Question 42

# during heme breakdown what happens in the liver

Answer 42

bilirubin **conjugation** occurs -> making it **soluble**

Question 43

what are the 2 pathways of conjugated bilirubin in liver

Answer 43

upon secretion into bile and conversion nto **urobilinogen** in *gut*, 1. some are **oxidised** to **stercobilin** -> excreted in **feces** => give feces its **brown colour** 2. others are **reabsorbed by liver** -> transported to *kidneys* -> converted to **urobilin** -> excreted in **urine** => giving urine its **yellow colour**

Question 44

signs of haemolysis

Answer 44

* rise in **LDH** bcos it's an **enzyme** found in RBC * rise in unconjugated bilirubin due to RBC breakdown * decrease in haptoglobin bcos **haptoglobin binds to free Hb** -> RBC breakdown -> more Hb -> more haptoglobin binding to Hb

Question 45

what causes prehepatic jaundice

Answer 45

too much **Hb breakdown** -> too much heme

Question 46

# bilirubin, urine, lab levels findings in prehepatic jaundice

Answer 46

1. increase in **unconjugated bilirubin** 2. normal urine OR (if severe) dark urine <- too much Hb to be broken down, thuss excreted instead 3. decrease in **haptoglobin** levels <- haemolysis

Question 47

what causes post hepatic jaundice

Answer 47

something which obstructs bile FLOW, usually **bile duct OBSTRUCTION**

Question 48

# bilirubin, urine, lab levels findings in post hepatic jaundice

Answer 48

1. increase in **conjugated bilirubin** 2. **tea coloured** urine cos bile flow is obstructed -> conjugated bilirubin backs up into bloodstream -> eventually excreted by kidneys 3. increase in **ALP and GGT** levels cos bile flow is obstructed -> bile buildup and subsequent **damage to bile duct cells** => release of enymes into bloodstream

Question 49

types of hepatic jaundice

Answer 49

* defect in conjugation: (similar to prehepatic jaundice) increase in unconjugated bilirubin * defect in excretion (similar to post hepatic jaundice) increase in conjugated bilirubin * mixed defect

Question 50

# think abt word HEPATIC findings in hepatic jaundice

Answer 50

* increase in **AST and ALT** levels cos liver damage -> leakage of liver enzymes into bloodstream * decreased liver fuction -> decreased **albumin** (impaired protein synthesis) -> increased **clotting times, aPTT and PT** (impaired clotting factor synthesis)

Question 51

# 1st child, 2nd child haemolytic disease of newborn (Rh incompatibility)

Answer 51

1. Sensitisation **1st** child has **RhD** antigen (inherited from father, mother doesn't have) -> causes **mother** to produce **antibodies against RhD** 2. Next fetus Mother's anti-RhD antibodies **cross placenta** -> **bind to RhD antigen** on *RBC* of 2nd Rh+ child

Question 52

treatment for haemolytic disease of newborn (Rh incompatibility)

Answer 52

**anti D injection** where body will treat ANY fetal RBCs that cross over as foreign and **eliminate** it -> mother **does not sensitise** against RBCs w/ RhD antigen

Question 53

what is added to blood plasma samples when measuring aPTT

Answer 53

* **Kaolin** -> activates clotting factors (in intrinsic pathway) * Ca2+ -> activates clotting factors (in coagulation cascade in general) * phospholipids -> mimic cell membrane envt

Question 54

what is added to blood plasma samples when measuring PT

Answer 54

thromboplastin -> **TF** and thus activates **extrinsic pathway**

Question 55

Virchow triad consists of ...

Answer 55

**H**ypercoagulability **E**ndothelial damage **S**tasis "**HE**'**S** Virchow" ## Footnote one risk factor of endothelial damage is **smoking**, but NOT alcohol!

Question 56

What is the main protein responsible for iron storage in cells? A) Transferrin B) Ferritin C) Haptoglobin D) Hemosiderin

Answer 56

B) Ferritin primary and most abundant storage of iron in contrast, **hemosiderin** stores iron during **iron overload**

Question 57

What is the primary protein responsible for transporting iron in the bloodstream? A) Ferritin B) Transferrin C) Hemoglobin D) Myoglobin

Answer 57

B) Transferrin binds to iron in **Fe3+ state** thus iron is **oxidised** from Fe2+ to Fe3+ by **hephaestin** beforehand

Question 58

Which form of iron is absorbed most efficiently by the body? A) Ferric iron (Fe³⁺) B) Ferrous iron (Fe²⁺) C) Iron bound to heme D) Iron bound to transferrin

Answer 58

B) Ferrous iron (Fe²⁺) thus iron is **absorbed as Fe2+** into intestinal cells by DMT, then **reduced to Fe3+** by ferric reductase in cell

Question 59

What enhances the absorption of non-heme iron from the diet?

Answer 59

Vitamin C **non-heme iron** is usually in **Fe3+ form** → Vit C helps to **reduce Fe3+** to the more absorbable Fe2+

Question 60

What is the role of hepcidin in iron regulation? A) It promotes the absorption of iron from the intestines B) It prevents the release of iron from enterocytes into the bloodstream C) It increases the synthesis of ferritin D) It binds to transferrin to transport iron

Answer 60

B) It prevents the release of iron from enterocytes into the bloodstream hepcidin binds to **ferroportin**, causing its internalisation and degradation → **inhibit release of iron** from enterocytes into bloodstream ## Footnote hepcidin is a hormone produced by liver to control iron levels ⇒ high iron levels = more hepcidin

Question 60

What is the body's response to a low iron state

Answer 60

1. increase **DMT-1** -> **absorb more** iron 2. increase **ferroportin** -> **excrete more** iron out of intestinal cells 3. increase **transferrin receptor** -> bind to more iron to **transport more** iron

Question 61

definition of lymphoma

Answer 61

malignancies of lymphoid system that manifests **outside** the bone marrow ## Footnote malignancies of **lymphoid system** = abnormal growth and proliferation of **lymphocytes**

Question 62

# and their differences in terms of characteristics types of lymphomas

Answer 62

* aggressive lymphomas fast BUT localised and **responsive and curable** w/ aggressive therapy * indolent lymphomas slow BUT widespread and mostly **incurable**

Question 63

characteristics of Hodgkin lymphoma

Answer 63

Reed-Sternberg cells - large - "owl's eyes"

Question 64

Which of the following is the most common type of B-cell lymphoma? A) Burkitt Lymphoma B) Mantle Cell Lymphoma C) Diffuse Large B-Cell Lymphoma (DLBCL) D) Follicular Lymphoma

Answer 64

C) Diffuse Large B-Cell Lymphoma (DLBCL)

Question 65

Which B-cell lymphoma is associated with the **"starry sky" appearance** on histology and is **linked to Epstein-Barr Virus (EBV)**? A) Diffuse Large B-Cell Lymphoma B) Burkitt Lymphoma C) Follicular Lymphoma D) Mantle Cell Lymphoma

Answer 65

B) Burkitt Lymphoma t(8;14) transolcation -> **C-MYC** now under control of lgH promotor -> **upregulated expression** of C-MYC (transcription factor regulating cell proliferation and growth) => **uncontrolled cell proliferation** "can rmb as number **8** in front which looks like **infinity sign ∞** = translocation result in cell **multiplying constantly** => uncontrolled cell **proliferation**" | t(8;14) bcos burkitt has 7 letters so 7+1=8, 14 always at the back ## Footnote all 3 (burkitt, mantle cell and follicular) lymphoma are due to translocation of gene segment -> gene under control of lgH promotor => overexpression

Question 66

Which lymphoma is associated with overexpression of BCL-2, preventing apoptosis? A) Diffuse Large B-Cell Lymphoma B) Burkitt Lymphoma C) Mantle Cell Lymphoma D) Follicular Lymphoma

Answer 66

D) Follicular Lymphoma t(14;18) translocation -> **BCL-2** now under control of lgH promotor -> **upregulated expression** of BCL-2 (transcription factor regulating apoptosis) => **blockade of apoptosis** and cell survival "can rmb as number **4** in front = translocation result in cell 不能**死** => prevents **apoptosis**" | only one where cannot count letters + 14 at the front instead of back

Question 67

Which B-cell lymphoma is considered **indolent** and slow-growing compared to the others? A) Burkitt Lymphoma B) Diffuse Large B-Cell Lymphoma C) Mantle Cell Lymphoma D) Follicular Lymphoma

Answer 67

D) Follicular Lymphoma Why? A-HA its bcos mutation in * follicular lymphoma allow cells to **resist apoptosis** (recall! translocation is t(1**4**;18) and the number **4** in front = cell 不能**死**) * BUT NOT undergo rapid proliferation (like in Burkitt or Mantle Cell)

Question 68

what are the ferritin levels like in haemolytic anaemia? | haemolytic anaemia is a form of normocytic anaemia

Answer 68

High * increased **iron release** from hemolyzed RBCs * also present as **acute phase reactant** <- haemolysis can trigger inflammation

Question 69

# type of anaemia what is jaundice commonly associated with

Answer 69

haemolytic anaemia results in **increased release of Hb** from destroyed RBCs → increased conversion of Hb to **unconjugated bilirubin** → elevated levels of unconjugated bilirubin, exceeds **liver processing capacity** (i.e. rate at which liver conjugates bilirubin) ⇒ **yellow** unconjugated bilirubin **deposit in skin and other tissues**, causing the characteristic yellowing seen in jaundice ## Footnote also seen in other conditions where there is elevated levels of unconjugated bilirubin (e.g. megaloblastic anaemia where there is premature desturction of RBCs)

Question 70

blood smear finding for megaloblastic anaemia

Answer 70

**hypersegmented** neutrophil due to impaired DNA synthesis → nucleus does not **divide and segment** properly ⇒ nucleus ends up with **many lobes** (> 6) | usually 3-5 lobes

Question 71

how can G6PD or PK deficiency lead to pre-hepatic jaundice

Answer 71

* G6PD is crucial for production of **NADPH** → helps **protect RBCs from oxidative stress** * PK is essential for **glycolysis** → by which RBCs **generate energy** * Lack of either → RBCs are **more easily destroyed** (i.e. haemolysis) ⇒ lead to pre-hepatic jaundice

Question 72

mechanism of neonatal jaundice

Answer 72

due to **liver immaturity** → lower levels of **UDP-glucuronosyltransferase** (enzyme responsible for conjuation) → **production > conjugation** for bilirubin → **buildup** of unconjugated bilirubin ⇒ jaundice

Question 73

what does positive Direct Coombs Test indicate

Answer 73

jaundice (or any other disease) has an **immune cause**

Question 74

what should be given for immediate restorance of hemostatic competence? | e.g. during excessive anticoagulation due to warfarin overdose

Answer 74

fresh frozen plasma bcos it contains **ready-to-use clotting factors**

Question 75

treatment for mild to moderate vWD

Answer 75

desmopressin 1st-line treatment as it * stimulates **vWF release** from Weibel-Palade bodies * **increases Factor VIII levels** | can also be used **prophylactically**

Question 76

treatment for haemophilia if patient develops **inhibitors** against clotting factor replacement | i.e. recombinant factors ## Footnote how it works: body produce **antibodies** against the clotting factor replacement -> preventing replacement factor from working

Answer 76

Activated Prothrombin Complex Concentrates (APCC) which contain a **mix of several clotting factors** which are already **partially activated** → bypass need for factor that is deficient ## Footnote compared to fresh frozen plasma which also has many clotting factors, but are all **inactivated** and thus may **require activation by the inhibited factors** ⇒ will not work

Question 77

An 8-year-old boy was found to have a swollen right knee. Investigations revealed blood in the right knee. While the bleeding time and aPTT was prolonged, PT was normal. The levels of factors VIII and IX were also normal. Which is MOST LIKELY to be true? A. Both coagulation pathways are expected to be normal B. Factor V is deficient C. Factor VIII function is impaired D. Serum calcium is expected to be low E. Prothrombin is low

Answer 77

C. Factor VIII function is impaired * * bleeding time and aPTT was prolonged → indicative of haemophilia * The levels of factors VIII and IX were also normal → seems to not be haemophilia ⇒ haemophilia where there are **normal levels** BUT **abnormal function**

Question 78

Which is the MOST LIKELY potential side effect of a massive blood transfusion? A. Hyperthermia B. Raised conjugated bilirubin level in blood C. Reduced total body iron stores D. Low ionised calcium level in blood E. Increased thrombosis

Answer 78

D. Low ionised calcium level in blood as blood that is transfused likely has **citrate** (acts as calcium chelator to prevent blood from coagulating before transfusion) -> **liver** may be unable to **metabolise citrate** in transfused blood quickly -> excess chelate **binds to calcium ions** => lower levels of calcium ions in blood

Question 79

most common thymic pathology in children and adult respectively? A) thymoma B) non-hodgkin lymphoma C) germ cell tumours D) hodgkin lymphoma | thymic pathology = conditions affecting thymus

Answer 79

* children: non-hodgkin lymphoma * adults: thymoma

Question 80

# petechiae, purpura, ecchymosis difference in size of haemorrhages

Answer 80

petechiae: less than 1/2 cm purpura: up to 1 cm ecchymosis: 2-3 cm

Question 81

what type of haemorrhage usually present in coagulation factor deficiency

Answer 81

ecchymosis

Question 82

definition of oedema

Answer 82

excessive **extravascular** accumulation of **fluid** in interstitial tissues and body cavities

Question 83

presence of (...) is used to diagnose amniotic fluid embolism ## Footnote when **amniotic fluid** enters **maternal circulation** via tears in placenta during childbirth/parturition or abortions => **occlusion of pulmonary arteries**

Answer 83

presence of foetal **squames** (i.e. foetal squamous cells) in mother's blood

Question 84

# general, not for specific antigens like Rh what test is done to check for compatibility bet donor and recipient blood before blood trasfusion

Answer 84

**crossmatching** where we we mix **donor RBCs** with **recipient PLASMA** and check for **agglutination** ## Footnote must rmb that it is always **PLASMA** from **donor** which may then react with (antigens on) *RBCs* from *recipient*

Question 85

How to differentiate iron deficiency anemia and thalassemia?

Answer 85

by RBC **distribution width** (i.e. variation in cell size) * iron deficiency: **high** as **iron availability** is more *random* (more random distribution) -> **AMT of Hb synthesis** *varies* => **size** of RBC *varies* * thalassemia: **low** as **Hb production** is *consistently poor* => RBCs are **unformly small**