Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Linganguliguliguli > Blood > Flashcards

Blood Flashcards

1
Q

Process of erythropoiesis

A

Myeloid stem cells differentiate and proliferate into proerythroblasts (w EPO)
Further division of cells (w folate and B12)
Mature into reticulocytes
Filling of Hb (w Fe) and reabsorb nucleus
Migration into capillaries and mature into RBCs

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

Growth factor for erythropoiesis

A

EPO

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

Required for DNA synthesis for erythropoiesis

A

B12 and folate

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

Required for filling RBCs with Hb

A

Fe

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

Regulation of erythropoiesis

A

Decrease in arterial PaO2 produces HIF-1a transcription factor
Increases EPO production and released from kidney
Increases RBC count and o2 carrying capacity
Increase PaO2 (negative feedback loop)

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

What determines anaemia

A

Hb count

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

What does RBC index indicate

A

Type/cause of anaemia

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

What are the components of RBC index

A

Hematocrit = V of RBCs
MCV = RBC size
MCH = Hb per RBC
MCHC = Hb per V per RBC (colour)

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

What does microcytic anaemia suggests

A

Impaired Hb synthesis (Fe deficiency/ Hbpathies)

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

What does normocytic anaemia suggests

A

RBC loss (blood loss)
Decreased RBC production (renal disease)

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

What does hypochromic anaemia suggests

A

Impaired Hb synthesis (Fe deficiency/ Hbpathies)

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

What does macrocytic anaemia suggests

A

Impaired DNA synthesis & cell division (Folate/B12 deficiency)

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

What does presence of inclusion bodies suggests

A

Hbpathy

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

What does normochromic anaemia suggests

A

Less likely due to Hb production issues

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

What are the characteristics of hyperchromic anaemia

A

Spherocytes due to overfilling of Hb
Loss of biconcave shape
Loss of elasticity => bursts easily
Less SA:V => Less O2 delivery

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

Explain symptoms of anaemia

A

Fatigue - Tissue hypoxia from decreased O2 carrying capacity
SOB - Acidosis from increased glycolysis causes increased respi drive
Palpitations - Decreased PaO2 heart compensate by increasing HR to increase blood flow

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

Describe heavy metal poisoning

A

Pb inhibits ALA dehydratase (XPBG) & Ferro-chelatase (XHeme) => anaemia and neuropathy
Pb deposition causes bluish colouration @gum line

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

What does presence of RBC fragments suggests

A

Haemolytic anaemia

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

Describe the characteristics of hepatic jaundice excretion defect

A

Increased conjugated bilirubin
Indicated by increased AST/ALT; PTT and aPTT

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

Describe the characteristics of Hepatic jaundice conjugation defect

A

Increased unconjugated bilirubin
indicated by increased AST/ALT; PTT and aPTT

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

Describe the characteristics of prehepatic jaundice

A

Caused by hemolysis
Increased unconjugated bilirubin
Increased urine urobillinogen -> Dark urine
Indicated by decreased haptoglobin

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

Describe the characteristics of hepatic jaundice mixed defect

A

Indicated by increased AST/ALT; PTT and aPTT
a/w viral hepatitis & alcoholic liver disease

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

Describe the characteristics of obstructive jaundice

A

Obstruction of bile duct
Increased conjugated bilirubin
Decreased urobilinogen
Tea coloured urine and pale stools
Indicated by increased ALP/GGT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the pathology of A-thalassemia

A

Decreased A-globin -> Decreased HbA and increased B-globin -> B4 precipitates -> hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
What does presence of HbF suggests
Sickle cell anaemia
6
What are the different Hb types and what are their components
Hb Gower (E1Z1) -> HbF (A2G2) -> HbA (A2B2) & HbA2 (A2D2)
6
Which Hb is highest in adulthood
HbA
7
Describe the different severities of A-thalassemia
1 mutated gene = carrier 2 mutated genes = mild anaemia 3 mutated genes = severe HbH disease 4 mutated genes = fatal
7
Which Hb is absent in adulthood
Hb Gower
7
Which Hb is highest in embryos
Hb Gower
7
What is the nature of thalassemia
Autosomal recessive
8
What does presence of HbH suggests
Thalassemia
8
What happens to excess Fe2
Excess Fe2 -> Ferretin -> Excess ferritin -> Hemosiderin
8
Describe the general pathology of thalassemia
Synthesis defect of A&B globin =>abnormal Hb -> Hemolysis - > Splenomegaly & anaemia -> Increased liver & bone marrow hematopoiesis (Hepatomegaly) => Increased heme (jaundice) and Fe (organ dmg)
8
Describe the pathology of B-thalassemia
Decreased B-globin -> Decreased HbA and increased A-globin -> A4 precipitates -> hemolysis
8
Describe the different severities of B-thalassemia
0 mutated genes = asymptomatic 1 mutated gene = thalassemia minor 2 mutated genes = thalassemia major
9
What is the response to low iron
Upregulation of DMT-1, ferroportin (decreased hepcidin) and transferrin receptors
9
Describe how iron is transported and stored
Fe2 => Fe3 via hephastin => stored as ferritin Fe2 transported out via ferroportin => Fe3 via hephastin => bind to transferrin => ferritin (short term) / hemosiderin (long term)
9
Describe how iron is absorbed
- Direct transport of heme - Fe3 reduced to Fe2 via ferric reductase and transported via DMT-1
9
What is the response to high iron
Increase hepcidin => downregulate ferroportin and DMT1 Downregulate transferring receptors
9
What must be given to prevent iron overload during blood transfusions
Iron chelators
9
What is plasma iron
Fe3-transferrin
9
What is unsaturated iron binding capacity
Total unbound transferrin
9
What is total iron binding capacity
Total transferrin
9
What is transferrin saturation %
Plasma iron/TIBC -> bound transferrin/total transferrin
9
What are the findings of iron deficiency
Decrease plasma iron, ferritin/hemosiderin Increase plasma transferrin
9
What are the findings of excess iron
Increase plasma iron, ferritin/hemosiderin Decrease plasma transferrin
9
Describe platelet plug formation
Platelet adhesion to exposed collagen & activation by vWF Platelets aggregate via released granules containing platelet agonists (platelet agonist) Forms plug and releases more platelet attracting substances (positive feedback loop)
9
How is unintentional platelet activation inhibited
Intact endothelial cells release NO and prostacyclins
9
What is the function of vWF
Binds platelets to exposed collagen & activates them
9
What is the function of ADP
Attracts and activates more platelets
9
What is the function of TBXA2
Aggregation and vasoconstriction
9
What is the function of fibrinogen
Link platelets through glycoprotein receptors
9
Describe the extrinsic coagulation pathway
Damaged tissue releases thromboplastin allowing VII -> VIIa X -> Xa (VIIa & Ca2) Prothrombin -> Thrombin (Xa, Va & Ca2) Fibrinogen -> fibrin (Thrombin) & XIII -> XIIIa (Thrombin) Fibrin crosslinks into fibrin meshwork (XIIIa)
9
Describe the intrinsic coagulation pathway
Exposure to foreign surface / collagen fibres releases platelet phospholipids allowing XII -> XIIa XI -> XIa (XIIa) IX -> XIa (XIa & Ca2) X -> Xa (VIIIa, IXa & Ca2) Prothrombin -> Thrombin (Xa, Va & Ca2) Fibrinogen -> fibrin (Thrombin) & XIII -> XIIIa (Thrombin) Fibrin crosslinks into fibrin meshwork (XIIIa)
9
Where are most of the coagulation factors produced
Liver except for thromboplastin
10
What is the consequence of liver damage on the coagulation pathway
Increased bleeding due to impaired factor production
10
Which factors require vitamin k for their production
II, VII, IX, X
10
What is the nature of haemophilia
X-linked recessive
10
Which are the coagulation factors missing for haemophilia A & B respectively
A = VIII deficient B = IX deficient
11
Which pathway does haemophilia affect
Intrinsic pathway
11
What is the treatment for haemophilia
Desmopressin for mild Recombinant coagulation factors for severe
11
What is the MOA of dabigatron
Inhibits thrombin
12
What is the MOA of rivaroxaban
Inhibits Xa
12
What are the 3 main anti-coagulation factors
TFPI APC-PS Anti-thrombin
13
What is the function of TFPI
Binds and inhibits thromboplastin
13
What is the function of protein C & S
PC binds to thrombin -thrombomodulin complex Activate PC which binds to circulating PS APC-PS complex formation Cleaves and inactivates Va & VIIIa
14
What does a prolonged PT indicate
Impaired extrinsic pathway
15
What does a prolonged PTT indicate
Impaired intrinsic pathway
16
What is the function of Anti-thrombin
Serine protein inhibitors that sequester thrombin leaked from clots Inhibits IXa & Xa
17
How are clots removed
Injured tissue release TPA => plasminogen -> plasmin => fibrinolysis of fibrin -> fibrin degradation products
18
What does the presence of D-dimers indicate
Thrombotic event
18
What are the causes of haemorrhage
Trauma Abnormal vessels Platelet (Thrombocytopenia) Coagulation factor deficiency
19
What are the different types of bruises
Petechiae Purpura Ecchymoses
20
What might cause petechiae or purpura
Thrombocytopenia or Abnormal vessels
21
What might cause ecchymoses
Trauma Vasculitis Factor deficiency
22
What is Virchow's triad
Endothelial damage Venous stasis Hypercoagulability
22
How does endothelial damage potentiate thrombosis
Endothelial damage -> disrupts inhibition of plug formation (hypertension, smoking, atherosclerosis)
22
How does venous stasis potentiate thrombosis
Venous stasis -> slow blood flow decreases anti-coagulant-coagulation factor interaction (Prost trauma/surgery)
23
How does hyper coagulability potentiate thrombosis
Hypercoagulability -> increase clotting tendency (Cancer, oral contraceptives)
24
What are the 4 types of embolism
Pulmonary, Fat, Air, Amniotic fluid
24
Describe pulmonary embolism
Embolism from DVT => IVC => R heart => Pul. artery occlusion Death/ Pul. Hypertension/Infarction/Necrosis
24
Describe fat embolism
Caused by soft tissue injury, liposuction, orthopaedic trauma Vascular occlusions in brain and lungs
24
Describe air embolism
Air emboli travels to brain and lungs Breathlessness, pain, loss of balance
24
Describe amniotic fluid embolism
Amniotic fluid enters uterine veins Fetal squamous cells and PGs in mothers blood => triggers coagulation cascade => DIVC, pul occlusion and HF
24
Name 4 classes of anti platelet drugs
Aspirin (NSAID) GPIIB/IIIA blockers Clopidogrel Dipyridamole
24
What is the MOA of aspirin
Inhibits COX -> Inhibits PGI2, TXA2 , PGE2 => inhibits platelet aggregation
24
What are the uses of aspirin
Prophylactic transient cerebral ischemia Reduce recurrent MI Reduce mortality post MI
24
What are the adverse effects of aspirin
Increased bleeding (TXA2) GI bleeding and ulcers (PGE2)
24
What is GPIIB/IIIA
Platelet membrane surface protein -> complex acts as a receptor for fibrinogen & vWF -> platelet aggregation
25
Name 3 GPIIB/IIIA blockers
Abciximab Eptifibatide Tirofiban
25
What is the MOA of Abciximab
Reversibly inhibits fibrinogen binding
25
What is the MOA of eptifibatide
Analog of extreme carboxyl terminal of fibrinogen D chain
26
What is the MOA of tirofiban
GPIIB/IIIA receptor blocker
26
What is the MOA of clopidogrel
inhibits P2RY12 => inhibits ADP activation
26
What is the MOA of Dipyridamole
PDE blocker inhibiting cAMP -> amp
27
What is the use of GPIIB/IIIA blockers
Prevent restenosis after coronary angioplasty
28
Name 2 anticoagulants
Heparin Warfarin
28
What is the MOA of heparin
Binds to ATIII and causes conformational change -> expose active site -> increase interaction w and inactivates clotting factor proteases
28
What is the MOA of warfarin
Inhibits vitamin K reductase -> decrease production of II, VII, IX & X
29
What are the uses of anticoagulants
DVT, AMI, pul.embolism use with GP11B/11A blockers for coronary angioplasty use with thrombolytics for revascularisation
29
Which anticoagulant can be used for pregnancy
Heparin
30
What are the adverse effects of Heparin
Thrombocytopenia Haemorrhage (treat w protamine sulphate and stop heparin dose)
31
What are the contraindications of warfarin
CYP450 inhibitor Bleeding Pregnancy
31
What is the MOA of thrombolytic agents
Increase plasminogen -> increase plasmin
31
What are the uses of thrombolytics
Coronary artery thrombosis Peripheral arterial thrombosis and emboli Ischemic stroke (<4.5h)
31
What are the adverse effects of thrombolytics
Bleeding and impaired wound healing
31
Can thrombolytics be used in pregnancy?
No
31
What are the clinical presentations of lymphomas
enlarged masses, fever, night sweats, weight loss
31
Which lymphomas are indolent
Follicular cell lymphoma MALT
32
What are the characteristics of Hodgkins lymphoma
Reed-sternberg cells (owl eye inclusions) Surface antigens CD15, 30 Spreads contiguously via lymphatics a/w EBV
32
Which lymphomas involve T/NK cells
Peripheral T cell Anaplastic large cell lymphoma
32
What are the characteristics of Follicular cell lymphoma
Surface antigens CD10, BCL6 t(14;18) -> increase BCL2 anti-apoptotic factor in B cells
33
Which organism can cause MALT if found in thyroid or stomach
H. pylori
34
What are the characteristics of Burkitts lymphoma
Starry sky appearance due to high macrophages CD10, BCL6 t(8;14) -> increase C-MYC => auto transcription of growth factors a/w HIV, EBV Presents as jaw lesion
34
What are the characteristics of Mantle cell lymphoma
t(11;14) -> increase cyclin D1 under IgH promoter
35
Describe how the clinical presentations of acute leukaemia come about
Suppression of normal marrow function - Decrease RBC = anaemia + fatigue - Immature leukocytes = infection + fever - Thrombocytopenia = easy bleeding
35
What are the non-specific symptoms of chronic leukaemia
Fatigue, weight loss, anaemia Splenomegaly -> abnormal abdominal sensation
36
What differentiates acute and chronic leukaemia
Acute = immature blast cells Chronic = more differentiated and mature cells
37
Which chromosome is involved in leukaemia
philadelphia chromosome t(9;22)

Linganguliguliguli (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions