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Primary FRCA > Physiology 3 > Flashcards

Physiology 3 Flashcards

1
Q

Describe the structure of a chylomicron

A

Roughly spherical complexes ~100 um in diameter.
87% triglycerides
9% phospholipids + cholesterol
3% cholesterol esters
1% fat soluble vitamins enveloped in apolipoproteins

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2
Q

Which apolipoproteins are found on chylomicrons?

A

APO B-48
APO C-II
APO C-III

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3
Q

How and where are chylomicrons formed?

A

In the golgi apparatus of epithelial cells

Formed from long chain fatty acids which have been re-esterified into triglycerides in the SER of the epithelial cells

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4
Q

What happens to chylomicrons in the systemic circulation?

A

Attach to binding sites in capillaries of adipose and muscular tissues.
APO C-II activates lipoprotein lipase on capillary endothelium -> cleavage of chylomicron.
Triglycerides delivered to peripheral tissues. Cholesterol is taken up by the liver.

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5
Q

Contrast absorption of long and short-to-medium chain fatty acids

A

Long-chain absorbed via micelles and transported in chylomicrons
Short and medium-chain absorbed directly and bind to albumin

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6
Q

Where is APO B100 found?

A

VLDL and IDL

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7
Q

What is the normal daily volume of capillary ultrafiltrate produced by an adult?

A

20L

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8
Q

What is the approximate daily volume of lymph drained by an adult?

A

2-4L

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9
Q

What is the rate of lymph flow returning to the circulation?

A

100-125ml/h

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10
Q

What is Meige’s/Milroy’s Disease?

A

Autosomal dominant condition causing multiple defects including:

  • Primary lymphoedema
  • Sensorineural hearing loss
  • Extradural cysts
  • Vertebral abnormalities
  • Yellow nails
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11
Q

What percentage of protein found in erythrocytes is haemoglobin?

A

95%

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12
Q

How do erythrocytes produce ATP?

A

Anaerobic metabolism

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13
Q

What is the average functional life span of an erythrocyte?

A

120 days

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14
Q

How does the biconcave structure of the erythrocyte contribute to its function, and thus benefit respiratory gas transport?

A
  1. Increased surface area to volume ratio

2. Increased flexibility, allowing cell to bend when passing through capillaries

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15
Q

Approximately how many erythrocytes are produced by an adult per day?

A

10^12

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16
Q

Which nutrients are essential for red cell production?

A 
Vitamin B12
Folate
Iron
Pyridoxine
Riboflavin (Vit B2)
Vitamin E
Copper
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17
Q

What type of molecule is erythropoietin?

A

Glycoprotein

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18
Q

Where is EPO produced?

A

90% in inner cortex and outer medulla of kidney

10% by liver

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19
Q

What is the molecular weigh of a Hb molecule?

A

Approx 64450 D

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20
Q

How many Hb molecules per RBC?

A

Approx 640 million

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21
Q

Where does Hb synthesis take place?

A

Haem: In the mitochondria of the immature erythrocyte in several steps ending in the combining of Fe2+ (from transferrin) with protoporphyrin to form haem.
Globin: Produced by ribosomes

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22
Q

When does the switch from foetal to adult haemoglobin take place?

A

3-6m

23
Q

Discuss the links between polypeptides in the structure of Hb

A

Non-covalent bonds
alpha1-beta1 and alpha2-beta2 bonds stabilise the molecule.
alpha1-beta2 and alpha2-beta1 bonds undergo conformational change with oxygenation of the nearby haem groups. Following oxygenation of the first haem group, subsequent oxygen binding becomes easier as more bonds are broken.
When oxygen dissociates, the beta chains offer more affinity for 2,3-DPG which lowers affinity for O2

24
Q

A shift of the Hb-O2 dissociation curve to the LEFT indicates what?

A

Increased affinity

25
Q

A shift of the Hb-O2 dissociation curve to the RIGHT indicates what?

A

Decreased affinity

26
Q

What factors shift the Hb-O2 dissociation curve to the LEFT?

A

Lower [H+]
Lower pCO2
Lower temp
HbF

27
Q

What factors shift the Hb-O2 dissociation curve to the RIGHT?

A

Higher [H+]
Higher pCO2
Higher temp
2,3-DPG

28
Q

Where is 2,3-DPG found

A

In the cytoplasm of the erythrocyte

29
Q

How does CO affect the Hb-O2 dissociation curve?

A

Moves to the LEFT (increases affinity thus reducing O2 delivery to tissues)

30
Q

How does HbS affect the Hb-O2 dissociation curve?

A

Moves to the RIGHT (decreases affinity compared to HbA thus increasing O2 delivery to tissues)

31
Q

On which chromosome are ζ and α globin chains found?

A

Chromosome 16

32
Q

On which chromosome are ε, γ, δ and β globin chains found?

A

Chromosome 11

33
Q

What are the stages of Hb development?

What types of Hb correspond with each stage?

A

Embryonic -> Foetal -> Adult

Embryo: Gower 1 (ζ2, ε2), Portland (ζ2, γ2). Gower 2 (α2, ε2)
Foetus: HbF (α2, γ2)
Adult: HbF (α2, γ2), HbA2 (α2, δ2), HbA (α2, β2)

34
Q

What are the prevalences of the three types of Hb in normal adult erythrocytes?

A

HbA: 96-98%
HbA2: 1.5-3.2%
HbF: 0.5-0.8%

35
Q

What are the effects of an abnormal HbS gene?

A

Homozygotes: haemolytic anaemia
Heterozygotes: no anaemia, normal blood film

36
Q

What are the effects of an abnormal HbC or D gene?

A

Homozygotes: mild haemolytic anaemia + splenomegaly
Heterozygotes: asymptomatic

37
Q

What are the effects of an abnormal HbE gene?

A

Homozygotes: mild anaemia with thalassaemic indices
Heterozygotes: Thalassaemic indices only

38
Q

What are the effects of a (rare) abnormal Hb Zurich?

A

Autosomal dominant traits of Heinz body haemolytic anaemia

39
Q

What is the effect of methaemoglobinaemia (HbMs)?

A

Failure of reduction of Fe within Hb -> cyanosis

40
Q

What is the gene defect in sickle cell disease?

A

Adenine -> Thymidine mutation leading to glutamic acid -> valine substitution at position 6 of β globin chain.

41
Q

What is the effect of sickle cell trait on perioperative morbidity/mortality?

A

No increase in perioperative morbidity/mortality with HbAS

42
Q

Where, globally, is the sickle cell gene most common?

A

Africa, parts of Asia, Arabian peninsula, Mediterranean Europe

43
Q

What are the main problems associated with sickle cell disease?

A 
Haemolytic anaemia
Vasoocclusive crises (VOC)
Visceral sequestration crises
Aplastic crises
Haemolytic crises
44
Q

What factors increase risk of VOC in sickle cell disease?

A
  • Infection
  • Acidosis
  • Dehydration
  • Hypoxia
45
Q

What are the possible VOCs associated with sickle cell disease?

A
  • Bony pain
  • Acute chest syndrome
  • Stroke
  • Acute abdomen
  • Splenic infarct
46
Q

Outline the traditional pathophysiological theory of vascular dysfunction in sickle cell disease

A

Altered physiology -> Increased sickling -> venous sludging -> occlusion

47
Q

Outline some newer ideas about the pathophysiological theory of vascular dysfunction in sickle cell disease

A

Innate instability of HbS -> Breakdown of Hb -> cell membrane disruption -> increased vascular endothelium adhesion and damage -> chronic vascular inflammation -> potentiated by HbS binding extracellularly to free NO, reducing its effect on vascular homeostasis

48
Q

Outline an updated theory of the pathophysiology of VOCs in sickle cell disease

A

Insult -> Increased circulating stress molecules -> vascular endolthelial activation -> compouding of sickle vascular dysfunction -> VOC due to vasoconstriction, thrombosis and possibly secondary sickling

49
Q

What is a visceral sequestration crisis in the context of sickle cell disease?

A

Massive pooling of RBCs in spleen -> splenomegaly, AP, anaemia, hypotension.
Mainly occurs in infants

50
Q

What are the main causes of aplastic crisis in sickle cell disease?

A

Parvovirus infection

Folate deficiency

51
Q

Blood film findings in sickle cell disease?

A

Sickle cells
Target cells
Howell-Jolly bodies (in splenic atrophy)

52
Q

How is sickle cell disease diagnosed?

A

Haemoglobin electropheresis

53
Q

What happens to the spleen in sickle cell disease?

A

Enlarged in childhood

Atrophic in adulthood due to cumulative effects of infection/infarct etc.

54
Q

Management of sickle cell disease?

A

-Mainly supportive.
-Vaccinations for asplenia
Folate supplementation
-Severe disease may be treated with Hydroxyurea which stimulates HbF production (thus decreasing the relative amount of HbS)
-Allogenic BMT in children <16 can be curative

Primary FRCA (34 decks)

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