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ESA1-4 revision sessions > MEH > Flashcards

MEH Flashcards

1
Q

energy metabolism is all about producing

A

acetyl-COA - which will be used to produce ATP to be used as energy by cells

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2
Q

acetyl- CoA produced by

A

breakdown of fats, alcohol, carbohydrates, protein

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3
Q

fats –> acetyl co A

A

fats –> fatty acids + gylcerol

fatty acids used to produce acetyl CoA and ATP via B-oxidation

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4
Q

carbhoydrates

A

carbhoydrates –> glucose- 6 P –> glycolysis –> pyruvate –> acetyl CoA –> TCA cycle –> ATP

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5
Q

proteins –> acetyl co a

A

protein –> amino acids –> pyruvate –> acetyl CoA–> TCA cycle

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6
Q

which metabolites can be used in glucoseneogensis to produce glucose 6-P

A

amino acids

glycerol

lactate

this glucose 6-P will then be used to produce acetyly coA

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7
Q

pyyruvate is converted to ….. when low oxygen

A

lactate

lactate can then be used in glucoseneogensis –> glucose -6-P to be used to produced acetyl- CoA and be used in TCA cycle

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8
Q

glycolysis

A

glucose –> pyruvate

investment (2ATP) and payback phase (4ATP)

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9
Q

key regulator of glycolysis

A

phosphofructokinase

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10
Q

citric acid cyle (TCA)

A

acetyl coA (2 carbons) feeds into CAC and combines with oxaloacetate (C4) to produce citrate (C6)

  • citrate (loses 2C as CO2 during the cycle) metabolised to produce NADH, GTP and FADH2
  • NADH and FADH2 used as reducing power to drive the electron transport chain
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11
Q
A
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12
Q

electron transport chain and ATP synthesis

A

NADH and FADH2 supply high energy electrons (reducing power)

  • electrons pass through series of compelexes pumping H+ ions into the intermembrane space and finally reducing oxygen to form water

- ATP synthases used proton gradient to convert ADP to ATP

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13
Q

fatty acid oxidation

A
  1. fatty acid activation by fatty acyl CoA synthaise
  2. fatty acid transported into mitochdondria there used carinitine shuffle
    • transport inhibited by malonyl CO 9prevents newly synthesised FA from being immediatley transported into mitochondria and oxidsed
  3. oxidation by B-oxidation pathway
    • repeated removal of C2 unit (acetyl CoA–> TCA cycle) and NADh and FADH2 –> ETC
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14
Q

ketone bodies

A
  • made in the liver mitochdornia from acetykl-CoA
  • improtant source in starvation - spare glucose
  • brains adapts to use ektone odies if glucose is critically low
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15
Q

give an example of when ketones are produced byt he body

A

untreated diabetes , severe dieting and fasting convert acetyl-CoA from fatty acis to ketone bodies

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16
Q

high levels of ketons can

A

cause ketoacidosis

  • acetone (pear drop smell) on breath
  • synthesis controlled by insulin/glucagon
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17
Q

lipoproteins

A
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18
Q

types of lipoproetiens

A
  • Chylomicrons (lipids from our diets) drain into the lymphatic system and enter the the blood stream at the thoracic duct which enters the left subclavian vein
  • VLDL- way liver exports fat - circulates fat around then body and gives to tissue that needs it e.g. adipose tissue and as an energy source for muscle
  • LDL -depleted VLDL - caused atherosclerotic plaques - very long lived and therefore suscpetive to lipid peroxidation (regonsied by macrophages and these become foam cells which form fatty streak and enbed in smooth muscle)
  • HDL- produced by the liver (empty) and travela roudn the body collecting excess fat and take it back to the liver top be processed
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19
Q

lipoprotein size

A
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20
Q

summary of lipoprotein fucntion

A
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21
Q

alcohol oxidation

A

overall can cause

  • lactic acidosis
  • gout
  • hypoglycamia
  • fatty liver
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22
Q

alcohol metabolism produces

A

NADH which can be used as energy production (ETC)

this process uses up NAD+ which causes lactate to accumulate in blood :

  1. kidneys abiltiy to excrete uric acid decreased = urate crystals in tissue causing gout
  2. deficit in glucoseneogensis = hypoglycameia
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23
Q

disulifiram

A

alcohol depndent

  • inhibits aldheyde dehydrogenase which causes acetaldehyde to huild up = hangover symptoms
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24
Q

reactive oxyegn species

A

free radicals:

reactive oxyegn species

  • superoxide
  • ydrogen peroxide
  • hydroxyl radical

reactive nitrogen species

  • nitric oxide
  • peroxynitirre
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25
Q

cellular defences to free radical

A

glutathione

  • needs to be recycles
  • requires NADPH (sourced by the pentose ohosphate pahtway)
  • people with glucose glucose 6- phosphate dehydrogenase deficiency cant produce suffieicnet amoutn sof NADPH and therefore become suscpetible to oxidative damage to RBC

–> causing haemolysis and cataracts

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26
Q

iron

A

required for oxygen carriers and co-factors in many enzymes

  • free iron= toxic to cells
  • body has no emchanisms for excreting iron
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27
Q

ferric vs ferrous iron

A

we absorbed both haem iron (Fe2+) and non-haemi (mixture of Fe2+ and Fe3+) in our diet

Ferric (Fe3+) must be reduced to ferrous (Fe2+) before it can be absorbed from diet

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28
Q

haem vs non-haemi iron

A

absorption occurs in dueodenuma nd upper jejunum (haem iron best source)

spme foods foritfied with iron e.g. cereal

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29
Q

dietry absorption of iron

A

haem iron absorbed dierctly

non-haem needs to be reduced from fe3+ to Fe2+ and then absorbed by the cell

stored as ferritin or exproted intot he blood via ferroportin

Fe2+ is then oxidised to Fe3+ via hephaestin

transported around the body via Transferrin

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30
Q

hepicidin

A

produced by the liver

inhibits ferroportin

  • anaemia of chronic disease shows increased hepcidin –> microcytic anaemia due to low iron
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31
Q

the adrenal gland

A
  • cushings disease
  • addisons disease
  • hypothryoidism se..g hashimotos

hyperthyroidsm- graves

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32
Q

cushins syndrome

A

external and endogenous causes

external - prescribed glucocorticosterois

endogenous causes

  • benign pituitary adneoma secreting ACTH - cushins disease
  • excess cortisol produce dby adrenal tumour- adrenal cushins
  • non-pituitary adrenal tuimours producing ACTs e.g. small cell lung cancer
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33
Q
A
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34
Q

physiological life cycle of RBC

A

120 days

RES- spleen and liver

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35
Q
A
  • Symptoms: shortness of breath, tiredness, palpitations, headache, cardiac failure
  • Signs: pallor, tachycardia, tachypnoea, hypotension
  • Other signs and symptoms specifically associated with the cause of anaemia
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36
Q

possible causes of anaemia think

A

bone marrow

peripheral red bloo cells

removal

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37
Q

what can you use to differentiate cause of anemia

A

reticulocyte count

low= bone marrow issue

high= peripheral problem

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38
Q

reticulocytes

A
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39
Q

evalutation of anaemia

A
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40
Q

high reticulocytes usually causes

A

macrocytic cells

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41
Q

cause of macrocytic anaemia

A
  • Vitamin B12 deficiency
  • Folate deficiency
  • Myelodysplasia
  • Liver disease
  • Hypothyroidism

• Alcohol

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42
Q

normocytic anameia causes

A
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43
Q

microcytic anaemia causes

A
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44
Q
A

is there an appropriate reticulocyte response? YES

is there haemolyis? cause

is there evidence of bleeding?

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45
Q

in patients where there is an appropriate reticulocyte response what is expected

A

LDH released when RBC breakdown

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46
Q

evidence of bleeding?

A
  • anti-inflammaotries causing gastric bleed etc
  • heavy epriods
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47
Q

haemolytic anaemia

A

– within blood vessels (intravascular haemolysis)
– or in the spleen or wider RES (extravascular haemolysis)

Red cells normal lifespan ~120 days

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48
Q

haemolytic anaemia results in

A
  • Symptoms of anaemia – severity worse if Hb v low or if an acute fall in
    • Accumulation of bilirubin leading to jaundice and associated risk of complications such as pigment gallstones.Hb rather than in chronic disease
  • Overworking of the red pulp leading to splenomegaly
  • Massive sudden haemolysis (as can happen in an incompatible blood transfusion) can cause cardiac arrest due to:
    • Lack of oxygen delivery to tissues
    • Hyperkalaemia as a result of release of intracellular contents
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49
Q

inherited defects in red cell membrane structures

A
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50
Q

acuired cauaed of defects in red cell membrane structure

A

will see schistocytes (red blood cell fragements)

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51
Q

defects in red cell metabolism

A
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52
Q

defects in Hb synthesis

A
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53
Q

thalassaemia

A

reduced rate of synthesis of normal α- OR ß- globin chains (the α- and ß- thalassaemias)

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54
Q

Sickle cell disease:

A

synthesis of an abnormal haemoglobin

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55
Q

removal of excess cells by RES

A
  • The spleen and other tissues of RES removes damaged or defective red cells
  • It will do this in many of the causes of anaemia already covered eg membrane disorders, enzyme disorders, haemoglobin disorders
  • In Haemolytic anaemias, (Session 5) red cells are destroyed more quickly as they are abnormal or damaged
    • This can occur within the blood vessels intravascular or outside (within the RES macrophages in spleen. Liver, bone marrow) extravascular
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56
Q

eg Autoimmune Haemolytic anaemia

A
  • In this condition autoantibodies (ie Immunoglobulin -Ig – protein produced by own B lymphocytes) bind to the red cell membrane proteins
  • Cells in the RES recognise part of the antibody, attach to it and remove it and the red cell from the circulation
  • Broadly classified as
  • – warm autoimmune haemolytic anaemia (IgG, maximally active at 370C) – cold autoimmune haemolytic anaemia (IgM, maximally active at 40C)
  • Causes can be infections (eg chest infections in children causing the cold form) or cancers of the lymphoid system (eg B cell lymphoma)
  • The spleen recognises the red cell as ‘abnormal’ and removes it .. So reducing the life span
57
Q

Haemolytic anaemia

A

• More on the subtypes, investigation and treatment of Haemolytic anaemia will be covered in more detail later in the course

• Some key laboratory features:
– increased reticulocytes (as the marrow tries to compensate)

– raised bilirubin (breakdown of Haem)
– raised LDH (red cells rich in this enzyme)

58
Q
A

Haematocrit/Packed Cell volume (PCV)

  • Proportion of blood that is made up of RBC – Centrifuged blood allows visualisation
  • Used to assess anaemia but more often polycythaemia

– Diagnosis and treatment

59
Q

Haemoglobin

A

Reference ranges vary between labs but generally

 <135g/L adult men

 < 115g/L adult women

 <110g/L children (3/12 – puberty)

 <150g/L newborns

  • Haemoglobin concentration in the blood i.e. amount of Hb mass/plasma volume
  •  Acute bleed  Dehydration
  • In vitro haemolysis will reduce Hb
60
Q

Red Cell Count (RCC) (x1012/L)

A

Number of RBC in given volume of blood (single cell column of blood passing through a detector)

Used for assessment of anaemia

  • Microcytic anaemia, RCC is
    • reduced in iron deficiency anaemia
    • increased in thalassemia trait
61
Q

Mean Cell Volume (MCV) (fL)

A
  • Mean size of RBC, measured using the amount of light scattered as they pass in a single file past a laser.
  • The most important parameter used to screen the cause of anaemia
62
Q

Red Cell Distribution Width (RDW)

A

Variation in size of the RBC

  • If increased = anisocytosis
  • Used to help assess cause of anaemia
    • Increased in iron deficiency (the first parameter to rise as iron stores fall)
    • Usually normal in thalassaemiatrait.
    • Increased following transfusion
63
Q

Mean Cell Haemoglobin (MCH) (pg)

A
  • Average measure of the amount of Hb in each RBC (e.g. Hb/RCC)
  • Used in assessment of anaemia

• Usually
– reduced in iron deficiency but
– normal or increased in macrocytic anaemias

64
Q

Mean Cell Haemoglobin Concentration (MCHC) (g/L)

A

• Mean concentration of Hb in RBC (Hb/MCV x RCC)

• One of least useful parameters:
– usually reduced if hypochromia present – increased if spherocytosis.

• Most useful in laboratory in the identification of cold agglutinins (e.g. viral/ mycoplasma infections etc.)

65
Q

Reticulocyte Count (x109/L)

A

• Measurement of the number of young erythrocytes

• Identified using size and RNA content.

66
Q

reticulocytes identified using

A

size and RNA content

67
Q

Vitamin B12 and/or folate deficiency causes

A

causes a deficiency in building blocks for DNA synthesis

Red cells become enlarged ie this is a form of a macrocytic anaemia

68
Q

vitamin B12 absorption

A

B12 from food (meat, fish, eggs and cheese)

  • binds to Haptocorrin (produced by salivary glands)
  • in the stomach HCL is secreted and cause B12 to bind to intrinsic factor (both produced by parietal cells)

- absorbed in the terminal ileum

69
Q

Causes of low Vit B12

70
Q

Folate

A

Folate present in most foods, yeast, liver and leafy greens especially rich source

5mg stores for about 3-4 months
• Absorptionoccursintheduodenumandjejunum

71
Q

Deficiency of Folate could result from:

72
Q

The Vit B12/folate link

A
  • Both B12 and folate play a role in converting homocysteine to methionine and the 2 vitamins are dependent on one another to do this.
  • Vitamin B12 is responsible for reactivating folic acid, back into tetrahydrofolate, the form of folic acid which the body can use.
    • so low B12 causes a functional folate deficiency
  • THF is essential for: serine-glycine conversion, histidine catabolism, purine synthesis, and most importantly, thymidylate synthesis which is needed throughout the body for DNA synthesis
  • Vitamin B12 needs folic acid to convert homocysteine to methionine. MTHF gives off its methyl group to vitamin B12 (cobalamin), which becomes methylcobalamin. At the same time, the MTHF folic acid is converted back into its bioactive form, tetrahydrofolate
  • Methylcobalamin then gives off its methyl group to homocysteine, to create methionine
  • Methionine is converted to S-adenosyl methionine (SAM) – very important in the production of various neurotransmitters and for DNA methylation.
73
Q

Why does Vit B12 and folate deficiency cause a megaloblastic anaemia?

A

So….both folate and Vit B12 deficiency ultimately lead to thymidylate deficiency

  • In the absence of thymine, uracil is incorporated into DNA instead
  • DNA repair enzymes detect the error and DNA strands are destroyed
  • This causes asynchronous maturation between the nucleus and the cytoplasm.
    • The nucleus (lacking DNA) does not fully mature,
    • The cytoplasm ,in which RNA production and haemoglobin synthesis continues, matures at the normal rate
74
Q

Deficiency in building blocks for DNA synthesis lead to anaemia – Vitamin B12 and/or folate deficiency

A

The peripheral blood film shows megaloblastic features:

  • macrocytic red cells
  • anisopoikilocytosis with tear drops
  • hypersegmented neutrophils
  • Can see white cell precursors also
75
Q

Deficiency in building blocks for DNA synthesis due to Vit B12 or folate deficiency lead to

A

neurological disease

• Vitamin B12 (not folate) deficiency is also associated with neurological disease – focal demyelination affecting the spinal cord, peripheral nerves and optic nerves.

• Folate deficiency in pregnancy can cause neural tube defects

76
Q

Investigation of megaloblastic anaemia

77
Q

treatment for folate deficiency

A

oral folic acid

78
Q

treatment for B12 deficiency

A
  • Pernicious anaemia: Hydroxycobalamine (intramuscular) for life
    • Beware hypokalaemia (low potassium) !
  • Other cause: oral cyanocobalamine

Transfusion in patients with Vit B12 deficiency can cause high output cardiac failure

79
Q

White cells

A
  • Neutrophils
  • Lymphocytes (B/T/ NK)
  • Monocytes
  • Eosnophils
  • Basophils

Raised mainly in reactive conditions but can be associated with underlying haematological disorders-but very rare

80
Q
A

macrophages

81
Q
A

interleukin 6

82
Q
A
  • Janus kinase
    • Tyrosine kinases which increase proliferation and survival of haemotopoetic precurosrs
83
Q

Polycythemia vera

A

(pol-e-sy-THEE-me-uh VEER-uh) is a type of blood cancer. It causes your bone marrow to make too many red blood cells. These excess cells thicken your blood, slowing its flow, which may cause serious problems, such as blood clots.

84
Q
A

microangiopathic haemolytic anaemia

85
Q
A

anisocytosis

86
Q
87
Q
A
  • Iron is not made available for the bone marrow
  • Hepcidin cause the ferroprotein to be internalised and degraded
  • In chronic diseases, high hepcidin production inhibits iron release from macrophages and intestinal absorption of iron. This consequently induces an anaemic condition. The interaction between hepcidin and ferroprotein determines the plasma iron transport.
88
Q

DIC

A

Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body.

  • Secondary to other disorders- uncontrolled coagulopathy
89
Q
A
  • Sequestration and phagocytosis of old and abnormal rbc
90
Q
91
Q
A

teardrop cells

92
Q
A

Howell-Jolly bodies are remnants of RBC nuclei that are normally removed by the spleen. Thus, they are seen in patients who have undergone splenectomy (as in this case) or who have functional asplenia (eg, from sickle cell disease). Target cells (arrows) are another consequence of splenectomy.

93
Q
A
  • Aspirin only if she was over 18
    • Causes reyes syndrome in children
      • Liver and brain damage
  • Wouldn’t use warfarin because its hard to get the dosage right (anticoagulant not an antiplatelet)
94
Q

immature RBC

A

reticulocyte

95
Q
A

kidney

  • Produced when blood oxygen is deficient (hypoxia)
  • Promotes RBC progenitor survival in the bone marrow
96
Q
A

phlebotomy

97
Q

Disulphide bond in a proteinc can ebe formed btween two residues of which amino acid?

98
Q
99
Q
A

decreased activity

100
Q
A
  • Pentose phosphate cycle
101
Q
A
  • They involve the synthesis of larger molecules from intermediary metabolites
102
Q
104
Q
A
  • Accumulation of acetaldehyde
105
Q

alcohol dependence

106
Q
A

Stimulates fatty acid synthesis via dephosphorylation of acetyl-CoA carboxylase

107
Q
108
Q
A

enter glycolysis

109
Q
110
Q
111
Q
A
  • Lipoprotein lipase
112
Q
A
  • Glycolysis
113
Q
  • Alanine aminotransferase
114
Q
A
  • C (18:3- 3 means 3 double bonds)
115
Q
A
  • Calcitonin

Parathyroid hormone is secreted by the parathyroid gland

116
Q
  • T3 and T4 are produced by the
A
  • thyroid gland follicular cells
    • Arranged in follicles full of colloid
117
Q

Parafollicular cells (C cells)

A

located in the space between thyroid follicles

  • calcitonin
118
Q

thyroid hormone synthesis

119
Q
A
  • hypopituitarism resulting in ACTH deficiency
121
Q
A
  • large hands and feet
122
Q
A
  • bromocriptine
    • prolactinomas are well controlled by medication and does not require surgery
123
Q
A
  • galactorrhea
124
Q
A

insulin secretion would increase

125
Q
A

supraoptic nucleus

126
Q

arcuate nucleus repsonsible for

127
Q
A
  • osteoclasts
129
Q
A
  • peptide hormone
130
Q
A

steroid hormone

131
Q
A

alpha cells- glucagon

132
Q
A
  • increased sunlight exposure
134
Q
A

ketoacidosis

135
Q
137
Q
A
  • Decreased maternal utlisisation of glucose
138
Q

ESA1-4 revision sessions (17 decks)

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