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Principles 2018 > Clinical Biochemistry > Flashcards

Clinical Biochemistry Flashcards

1
Q

What does insulin stimulate?

A
  • Glucose uptake in muscle and adipose tissue
  • Glycolysis
  • Glycogen synthesis
  • protein synthesis
  • uptake of ions (especially K+ and PO43-)
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2
Q

What does insulin inhibit?

A
  • Glucogenesis
  • Glyconeogenesis
  • Lipolysis
  • Ketogenesis
  • Proteolysis
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3
Q

What does reduced cellular uptake of glucose result in?

A

Hyperglycaemia

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4
Q

What does hyperglycaemia cause?

A

Excess glucose spills into urine

  • glycosuria
  • osmotic diureses
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5
Q

What results from dehydration?

A

Hypotension and shock

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6
Q

What happens if the body is resistant to insulin or deficient?

A

Body tries to source insulin from other fuels

-triglycerides

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7
Q

What are ketones?

A

Intermediates of fat breakdown- strongly acidic, dissociate and release protons

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8
Q

What do ketones cause?

A

Vomitting

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9
Q

What does hypotension and shock cause?

A 
Stimulate release of hormones which exacerbate the process (anti-insulin)
>AVP
>Growth hormone
>Cortisol
>Catecholamine
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10
Q

What is lipolysis?

A

Breakdown of lipids

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11
Q

What is the role of hormone sensitive lipase?

A

> Releases free fatty acids and glycerol

>occurs when energy is needed

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12
Q

Where are ketone bodies formed?

A

Liver mitochondria

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13
Q

Where do ketone bodies diffuse to?

A

Blood stream and peripheral tissues

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14
Q

What is ketone body acid load?

A

Highly acidic ketone bodies release hydrogen ions into the blood

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15
Q

What happens to bicarbonate buffering in blood during keto-acidosis?

A

excess hydrogen ions mop up most of the available bicarbonate ions

Because carbon dioxide is blown off the reaction never reaches equilibrium

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16
Q

What is kussmaul breathing?

A

Deep sighing respiration

acidotic breathing

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17
Q

How can DKA be identifies?

A

Ketones= dipstick
DKA can be smelt from across the room
Air hunger

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18
Q

Why can some people mobilise glycogen stores?

A

Lack of enzyme

  • Phosphorylase
  • Transferase
  • a-1,6-glucosidase
19
Q

What is the problem with lactate?

A

Yields much less energy than oxidative metabolism

20
Q

What is the long term consequence of not being able to bread down glycogen?

A

Accumulates;

  • hepatomegaly, portal hypertension
  • fibrosis of the liver
21
Q

What are the clinical features of not being able to break-down glycogen?

A

Hypoglycaemia in early llife
Hepatomegaly
Heart can be affected- heart failure, lung failure, death

22
Q

What are the main components of the plasma membrane?

A

Phospholipid
Sphingomyelin
Cholesterol

23
Q

What does cholesterol do in the membrane?

A

Maintain structure and fluidity of cell membrane

24
Q

What is cholesterols role in cell singnalling?

A

Form lipid ‘rafts’ that form bridges between receptor proteins and second messengers
-lipid rafts are parts of membrane that serve as centres for assembly of signalling molecules

25
Q

What is cholesterol a precursor of?

A

Bile/bile acids (important in digestion and absorption of fat soluble vitamins), vitamin D and steroid hormones

26
Q

What is the function of triglycerides in health?

A

Similar to cholesterol in membranes- polar and non polar

Highly concentrated energy stores

27
Q

How are lipids carries around the body?

A

Lipoproteins in the blood

28
Q

How do lipoproteins vary?

A

Physical properties vary according to the specific composition of their lipids

29
Q

Describe lipoproteins from the liver?

A

Comparatively triglyceride rich, progressively lose TG content as they travel through the blood

30
Q

How is triglyceride removed from lipoproteins?

A

Lipoprotein lipase snips off as they travel through the blood (lines blood vessels)

31
Q

What is the densest lipoprotein and its function?

A

HDL

Carries cholesterol from the tissues to the liver

32
Q

What is the formation of lesions mediate by?

A

Oxidised LDL

33
Q

What is cholesterol transport from liver to tissues controlled by?

A

Bouyant lipoproteins like VLDL which after progressive dilapidation become denser IDL, LDL)

34
Q

What is cholesterol transport from tissues to liver mediated by?

A

Principally by HDL

35
Q

What happens when LDL is not effectively cleared?

A

Accumulates, gets chemically modified (oxidised) and aggregates. This acts as a trigger for macrophages- mediate inflammation and swallow stuff

36
Q

What does inflammation do to cholesterol transport?

A

Inhibits reverse cholesterol transport, exacerbating the imbalance and a feedforward or vicious circle of increasing LDL and increasing inflammation

37
Q

What is a case-control study?

A

two existing groups differing in outcome are identified and compared on the basis of some supposed causal attribute

38
Q

What is a cohort study?

A

follows a group of people over time, e.g. with reference to risk factors for a disease

39
Q

What is a systematic review?

A

literature review focused on a research question; tries to synthesize all relevant high-quality evidence

40
Q

What is meta-analysis?

A

Statistical technique for combining findings from independent studies

41
Q

What is a randomised clinical trial?

A

experiment in which trial participants are randomly allocated to treatment under study.

42
Q

What do statins do?

A

Lower cholesterol.
Interfere with cholesterol synthesis in the liver cell, which then expresses more LDL receptors in an attempt to get more cholesterol into the cell

43
Q

What do statins inhibit?

A

Smooth muscle migration

Foam cell formation

T-cell activation

Adherence and aggregation of platelets

Adherence and entry of leukotrienes

Principles 2018 (34 decks)

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