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ESA 2 > Esa1 > Flashcards

Esa1 Flashcards

0
Q

What is the difference between a meta analysis and a systematic review?

A

Systematic review: an overview of primary studies that are explicit and reproducible
Meta analysis: a quantity synthesis of two or more studies that address the same hypothesis in the same way.

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1
Q

What is the difference between bias and confounding?

A

Bias is unrepresentative sample or systematic mistake - a flawed study.

Confounding is a characteristic of the population.

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2
Q

Random effects modelling can account for heterogeneity but how can we explain it?

A

Sub group analysis

Grouped by Study characteristics or participant profile (which is better but harder to get data)

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3
Q

How is variable quality assessed and accounted for?

A

Define criteria the study must meet.
Give each study a score and encorporate it into weighting, do sub group analysis of high quality vs low quality, use meta-regression analysis.

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4
Q

Secondary structure

A

Local spartial arrangement of polypeptide backbone

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5
Q

Nucleoside?

A

Base and sugar

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7
Q

MRNA modifications to stabilise it

A

5’ 5’ capping
Polyadenylation- endonucleases cleaves and polyA polymerase extends 200
Splicing - exo and endo nucleases.

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8
Q

Peptide bond formation enzyme in translation?

A

Peptidyl transferase

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9
Q

Non stop secretion?

A

Constitutive vs regulated.

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10
Q

Function of diolichol?

A

N linked glycosylation

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11
Q

O linked glycosylation?

A

Glycosyltransferase.

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12
Q

Roles of propyl and lysyl oxidises?

A

P for h bonds

L for cross links

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13
Q

Types of base repair

A

Base excision - 1-5 oxidative
Nucleotide- 30 uV and carcinogens
Mismatch- 1, DNA synthesis.

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14
Q

How are slides prepared histiologically?

A 
Fixed using glutaldehyde or formaldehyde Dehydrated alcohol
Cleared xylene or toluene
Embedded in paraffin
Rehydrated
Stained
Dehydrated
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15
Q

Types of microscopy

A

Confocal - focus to remove glare 3D
Phase contract- live cells and refeaction
Dark field - shadows?
Fluerescent

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26
Q

Describe endochondral ossification

A

Perineal bone appears
Primary ossification centre the central cartilage appears supplied by the nutrient artery.
Medulla becomes cancellous bone and secondary ossification sites appear.
Ossification in epi thesis.
Plates continue to grow, cartilage grows and ossifies.

27
Q

Osteogenesis imperfecta

A

Type I collagen deficient. Autosomal dominant.

28
Q

Effects of botulism toxins

A

Inhibits ACH release

29
Q

What inhibits acetylcholine?

A

Organophosphates

30
Q

Describe duchenne muscular dystrophy

A

Recessive x-linked condition
Lack of dystrophin so muscles rip apart
Calcium causes necrosis

31
Q

Erythrocyte production?

A

Erythropoietin production at the kidneys in response to hypoxia. Reticulocyte is precursor, organelles extracted

32
Q

Astrocytes and micro glial cells

A

Astrocytes - mediate metabolic exchange at neurone

Micro glial cells- form blood brain barrier.

33
Q

Types of mesoderm and what they become

A

Paraxial- repeating structures of muscles, bones and dermis.
Somatic- connective tissues of limb
Splanchnic- smooth muscle, gut wall connective tissue and vasculature.
Intermediate-kidneys, ureter, gonads

34
Q

Describe galactose metabolism

A

To galactose 1 P via galactokinase.
To glucose 1 P via epimerase (UDP) and galactose 1 P ur idyl transferase.
To 6 P

35
Q

Probs in galactose metabolism

A

Transferase - hepatomegaly and jaundice

Galactokinase - cataracts (aldose reductase), galactose in urine.

36
Q

Synthesis of fatty acids

A

Acetyl CoA+ Co2 -> malonyl CoA (acetyl CoA carboxylase)
Malonyl CoA -> 2faC and co2 (fatty acid synthase complex)
Carboxylase limits rate - regulated by citrate and amp.
Insulin increases and glucagon/inhibit.

37
Q

Enzymes in glycogen breakdown?

A

Glycogen phosphorylase.
Phosphoglucomutase
Glucose 6 phosphatases.

38
Q

How is step 10 avoided in gluconeogenesis

A

PEPCK - increased by glucagon, cortisol and decreased by insulin
Pyruvate carboxylase

39
Q

Describe the reactions involved in transamination

A

Aa + a-ketoglutarate -> glutamate + keto acid
Aa+ oxaloacetate -> aspartate + keto acid
ALT - alanine -> glutamate
ASP- aspartate <- glutamate

40
Q

Ammonia detoxification including the role of glutamine

A 
NH3 + glutamate-> glutamine
Kidneys- excreted directly
Liver- used to synthesise urea
Broken down to ammonia by glutaminase
Also by urea cycle - aspartate can enter.
41
Q

Results of high ammonia/ defect in urea cycle?

A

Reacts with aketo so disrupts TCA and energy. So lethargy.
Low pH so vomiting
Affects CNS neurotransmitter synth.
Coma, irritability, mental retardation

42
Q

Describe phenylketonuria (PKU)

A

Phenylalanine cannot go to tyrosine because of no phenylalanine hydroxylase so produces phenyl pyruvate instead. Intellectual disability and seizures. Autosomal recessive.

43
Q

Describe homocystinuria

A

Homocysteine can’t go to Cystathionine or cysteine as no CbS (v6) so goes to methionine (b12) or oxidised to homocystine.
Affects fibrillin-1 so affects muscle and cvs and CNS

44
Q

What do vldls do?

A

Tags from liver to adipose tissue

45
Q

Describe type I and IIb hyperliproteinaemias

A

I- defective lipoprotein lipase
IIb- defective LDL receptor
Treated with statins and bike salt sequestrants preventing bile salt reabsorption so less cholesterol/tag digestion.

46
Q

Enzyme which neutrophils use to generate ROS?

A

NADPH oxidas

47
Q

What is an addisonian crisis

A

Hypotension, dehydration, dizziness, nausea, confusion, coma.
Treat with saline and IV cortisol

48
Q

What is the synacthen test

A

Analogue of ACTH, should increase cortisol

ESA 2 (9 decks)

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