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Semester 1 > Tired all the time > Flashcards

Tired all the time Flashcards

1
Q

What does the structure of the RBC provide

A

biconcave shape and no nucleus - pliable, high surface area/volume

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2
Q

What is reticulin?

A

remnants of mRNA left once the nucleus of a maturing RBC has been extruded (removed by spleen in 1-2 days)

a useful measure of marrow response to anaemia or treatment

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3
Q

What is hepcidin?

A

regulates iron absorption and release from macrophages - increased in inflammatory disease hence less iron available

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4
Q

How is iron transported and stored?

A

transferrin: transport/regulation –> transferin receptors increased in iron deficiency
ferritin: insoluble form of storage –> better measure of iron stores

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5
Q

Folic Acid:
Where is it absorbed?
How can deficiency come about?

A

Absorbed in the upper small bowel

Deficiency due to poor intake/absorption/increased need

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6
Q

B12/Cobalamin:
Where is it absorbed?
How is it transported?
How does deficiency come about?

A

Absorbed in the terminal ileum
transported on transcobalamin II via portal circulation to liver
dietary deficiency in vegans or pernicious anaemia

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7
Q

How is erythropoiesis switched on?

A

tissue hypoxia or anaemia
high altitude
epo producing tumors e.g. renal

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8
Q

Structure of Hb and abnormalities

A

2 alpha chains (chromosome 16)
2 beta like chains (chromosome 11)
Hb (adult) is 2 alpha, 2 beta
Hb (foetal) is 2 alpha, 2 gamma

Thalassaemia: inherited defect in globin chain production
sickle cell disease: one amino acid change in beta chain

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9
Q

neutrophils morphology and function

A

Morphology – large, copious cytoplasm lobed nucleus.

  • chemokines released by activated tissues and immune cells attract neutrophils to sites of infection
  • phagocytose microbes and digest in cytoplasmic vesicles
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10
Q

lymphocytes features and functions

A
  • Circulate in the blood and reside in lymph nodes
  • Unique antgen specific surface receptor
  • B cell receptors recognise soluble antigen
  • T cells can only recognize antigen presented in MHC class I or class II molecules.
  • MHC are host identifiers, class I on all cells at risk of infection or damage.
  • Class II only on professional antigen presenting cells – macrophages, B lymphocytes and Dendritic cells
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11
Q

Natural Killer cells features

A

• Large lymphocyte cells with granular cytoplasm.

  • do not have antigen specific receptors
  • recognise virus ingected cells
  • part of the innate lymphoid cell group
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12
Q

monocytes: function and features

A

• Morphology – large cells with a kidney shaped nucleus and copious cycoplasm

  • blood monocytes can phagocytose, degrade and present antigen
  • monocytes continually migrate to tissues and differentiate to become machrophages
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13
Q

macrophage functions

A
  • phagocytosis
  • disposal of infected/damaged cells
  • induce inflammation: secrete cytokines and chemokines and inflammatory mediators
  • actively recruit other cells to site of infection
  • present antigen from degraded pathogen to MHC class II t-helper cells
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14
Q

dentritic cells features

A
  • immature dendtritic cells migrate from the bone marrow through the blood stream to mature in the tissues
  • degrade pathogens that they take up
  • main role = present antigens to T-cell and send signals to immune mediators
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15
Q

what inhibtits thrombin production?

A

Heparin and thrombomodulin produced in the endothelial cells

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16
Q

What reduces platelet adhesion?

A

prostaglandin and Nitric Oxide produced in the endothelial cells

17
Q

coagulation cascade

A

Diagram

18
Q

Coagulation tests

A
  • bleeding time
  • prothrombin time (PT)
  • Activated partial thromboplastin test (APTT)
  • Fibrinogen (final substrate for making fibrin)
  • Correction tests and factor assays
19
Q

Inherited blood disorders

A
  • Haemophillia A+B: X linked defect in VIII or IX gene
  • Von-Willebrand disease: autosomal dominant defect in platelet adhesion and binding of VIII
  • Acquired coagulation disease - liver disease: bleeding due to abnormal clotting (all clotting factors made in liver)
  • Acquired coagulation diseae - DIC: activation of coagulation cascade due to multiple reasons e.g. trauma, malignancy, sepsis etc.
  • thrombocytopaenia: abnormal marrow function
  • thrombophilia: Inherited defects in coag inhibitors
20
Q

Symptoms of anaemia

A

shortness of breath
muscle pain on exersion
dizziness
angina

21
Q

clinical signs of anaemia

A
  • palor in skin and conjuctiva
  • tachycardia
  • rapid breathing
  • peripheral oedema if severe
  • Peripheral oedema if severe anaemia
22
Q

name classification of anaemia according to MCV

A

microcytic, normocytic and macrocytic

23
Q

describe the classification of anaemia according to MCV

A
  • normocytic: blood loss, anaemia of chronic disease, renal impairment
  • macrocytic: megaloblastic anaemia - B12/folate deficiency, myelodysplasia
  • microcytic: iron deficiency, thalassaemia
24
Q

describe the Buffer system in the red cell

A

diagram

25
Q

Composition of circulating white blood cells

A
  • Neutrophils 60-70%
  • Lymphocytes 20-30%
  • Eosinophils 2-4%
  • Basophils <1%
  • Monocytes 3 – 8%
  • Mast cell precursors
  • Not macrophages
26
Q

What are the main constituents of coagulation?

A
  • Vessel wall lined by endothelium
  • Platelets- derived from megakaryocytes in marrow
  • Coagulation factors in un-activated state
  • Inhibitors of coagulation
  • Fibrinolytic system and inhibitors
27
Q

What are endothelial cells?

A

• Line blood vessels and form a barrier

• Produce:
- thrombomodulin and heparin
sulphate to inhibit thrombin production
- Enzymes to degrade platelet granule- derived molecules
- Prostacyclin and nitric oxide (NO) to reduce platelet adhesion

28
Q

What are the coagulation inhibitors?

A
  • Protein C activated by thrombomodulin-thrombin complex
  • With co-factor- Factor S- Va and VIIIa are degraded
  • Antithrombin inhibit Xa and IIa • Heparin cofactor II inhibits Ila
  • Heparin stimulates antithrombin and heparin cofactor II
29
Q

What is B12 anaemia?

A

• macrocytic anaemia
- Often bilirubin and LDH raised
• Can also cause peripheral neuropathy- demyelination and posterior column damage
• B12 result can be falsely low in pregnancy/oral contraceptive/on metformin
• Pernicious anaemia- gastric atrophy and auto antibodies to parietal cells and intrinsic factor preventing absorption
• Strict vegan or terminal ileal disease also possible

30
Q

B12 deficiency treatment

A
  • Hydroxocobalamin 1mg IM

* Cyanocobalamin available orally

31
Q

Describe anaemia of chronic disease

A
  • normocytic anaemia associated with chronic inflammatory disease
  • Plentiful iron stores but poor transfer to RBC due to hepcidin and cytokines
32
Q

Describe thalassaemia

A
  • Inbalance of globin chain production
  • Beta thalassaemia- as Hb F (2 alpha, 2 gamma chains) declines after birth
  • Progressive iron overload
33
Q

what is the difference between race and ethnicity?

A

Race: Biological division of the species into groups based on the frequency of hereditary traits

Ethnicity: Social division of people into groups based on their identification with shared origin

34
Q

Explain cultural competency and cultural humility

A

Cultural competency:

  • Mastery of a finite body of knowledge and information
  • Endpoints defined by exams
  • Commitment to competency

Cultural humility:
Humility
- To assess anew the cultural dimensions of each patient
- To engage in self-reflection
- To check the power imbalances in clinical relationship
No endpoint
Commitment to social justice

35
Q

What are the anaemia drugs?

A 
Ferrous Sulfate 
Iron Dextran
Hydroxocobalamin
Folic Acid
Darbepoeitin Alfa
Hydroxycarbamide
36
Q

Indications, MOA, dose and side effects of Ferrous Sulfate

A

Iron deficiency anaemia

replaces iron stores. Ferrous ion absorbed in small intestine, bound to transferrin in the
plasma and used for haemoglobin synthesis

200mg orally once (prophylaxis) or 2-3 times (treatment)

Abdominal
cramping,
diarrhoea or constipation,
nausea.

37
Q

Indications for Iron Dextran

A

Parenteral iron is reserved for use when oral therapy is unsuccessful due to intolerance or noncompliance, continuing blood loss or malabsorption.

38
Q

Indications for folic acid

A

Folic acid must not be used alone in undiagnosed megaloblastic anaemia due to the risk of vitamin
B12 deficiency leading to peripheral neuropathy.

Given with hydroxocobalamin

39
Q

Indications of Hydroxycarbamide

A

used for reduction of elevated platelet counts in ‘at risk’

patients with essential thrombocythaemia.

Semester 1 (13 decks)

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