Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1 REVISION Bismillah > 2. Biochemistry - Nate > Flashcards

2. Biochemistry - Nate Flashcards

1
Q

PKU

  1. Full name?
  2. Type of metabolism error?
  3. Cause?
  4. Role of this enzyme?
  5. What kind of nutrient is phenylalanine?
  6. What can phenylalanine build up lead to?
  7. Best proven treatment?
  8. Type of genetic disease?
  9. Why is the baby alright whilst in the mothers belly?
  10. What is phenylalanine normally broken down into? Why is this important?
  11. What can excessive phenylalanine be metabolised into?
  12. Give examples of 3 foods high in phenylalanine
A
  1. Phenylketonuria
  2. Inborn error of metabolism
  3. Absent / virtually absent phenylalanine hydroxylase (PAH)
  4. Break down excess phenylalanine from food
  5. Protein
  6. Build up in blood and brain to toxic levels, affecting brain development + function
    This can lead to intellectual disability, seizures, hypopigmentation, hyperactivity and other serious medical problems
  7. Phenylalanine restricted diet
  8. Inherited recessive problem
  9. The mothers body can break down phenylalanine
  10. Other essential compounds especially tyrosine, which is an essential amino acid so needs to be in diet. Tyrosine is used for producing neurotransmitters like dopamine + epinephrine
  11. Phenylketones
  12. Chicken breast / egg whites / tuna
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

State 2 overall reasons why signs and symptoms are caused in inborn errors of metabolism

A
  1. Toxic accumulation of substrate behind block

2. Deficiency of product after block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the diagram which highlights the theoretical consequences of an enzyme deficiency

A

Defective enzyme in the middle

On left:
Substrate (increased)
Metabolites (increased)
Leads to box saying effect on other metabolic activity

On right:
Products (decreased)
Metabolites (decreased)
Leads to box saying effect on other metabolic activity

In the middle (under defective enzyme):
Circle = co factor A - action - co factor B - other enzymes
Both cofactors leads to box saying effect on other metabolic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

State the 2 theoretical consequences of an enzyme deficiency

A
  1. Increased substrate = toxic effect

2. Decreased product = insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

State 4 ways to test for a metabolic disease

A
  1. Test blood/bodily fluid for presence of substrate
  2. Genetic testing / genomic testing for specific base pair changes
  3. Test for decreased product
  4. Check level of enzyme / measure enzyme activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. What is is called when someone has low oxygen?
  2. Which fuel metabolism pathway will they use and why is this a problem?
  3. How long can cells go without running oxidative phosphorylation? What cells is this particularly important in?
A
  1. Hypoxia
  2. Glycolysis - less efficient at making ATP
  3. 1.5 mins
    High energy demand cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Low oxygen = do glycolysis

  1. What do you end up with?
  2. What 2 things can you not go further into?
  3. What accumulates as a result of this?
  4. What is it used for? If you convert it into lactate, what can you regenerate? What is the enzyme that is involved called?
  5. What process can now continue as there is no accumulation?
A
  1. Pyruvate
  2. Acetyl co-A / TCA cycle
  3. Pyruvate
  4. Anaerobic respiration
    NAD+
    Lactate dehydrogenase
  5. Glycolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name the uses of lactate in the liver and in muscle(including cardiac muscle)

A 
Liver = generate glucose via gluconeogenesis
Muscle = provide Pyruvate for TCA cycle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

High levels of lactate

  1. What does it reduce?
  2. What does this then lower?
  3. Give 2 examples of this
A
  1. Blood pH
  2. Oxygen carrying capacity of blood cells
  3. Severe anaemia / alcohol intoxication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Decreased blood flow results in decreased oxygen

  1. What does this reduce?
  2. So the synthesis of what is decreased?
  3. Which pump is disrupted?
  4. What is increased leading to myocytes swelling?
  5. There is an influx of which ion? This activates what? This disrupts what? What is the final outcome?
  6. There is also an increased production of what kind of atom?
A
  1. ATP
  2. ATP synthesis
  3. Na/K ATPase pump
  4. Cell membrane permeability
  5. Calcium influx = activates proteases = disrupt cell function = cell death
  6. Free radicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What 2 things do free radicals cause

A

Lipid peroxidation = membrane disruption

Protein damage = cellular dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ischaemia

  1. If there is reduced oxygen and reduced nutrients, what else is there a reduction of?
  2. This leads to which kind of fuel metabolism? What occurs as a result of this?
  3. What does this ultimately lead to? Give 4 examples of things that cause this
  4. Finally, all these things can lead to what? By which 2 methods?
A
  1. Reduced ATP
  2. Anaerobic metabolism = acidosis in cells
  3. Loss of cellular homeostasis
    Leaky membrane / Sodium potassium pump failure / cellular swelling / calcium influx
  4. Cell death via apoptosis or necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What 2 features of a myocardial protein will determine the time course of the bio marker appearance in general circulation?

A

Size

Sub cellular distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

After an infarction:

  1. What is released within the first few hours?
  2. What is released within 2-6 hours?
  3. What is released within 12-24 hours?
A
  1. Ions
  2. Metabolites
  3. Macromolecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name the 4 aspects of an ideal cardiac marker, giving it a brief description

A
  1. High sensitivity
    High concentration released after myocardial injury
  2. High specificity
    Absent in non-myocardial tissue
  3. Good analytical characteristics
    Measurable by cost-effective method
  4. Good clinical characteristics
    Influence therapy and improve patient outcome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ideal cardiac marker = high sensitivity

  1. Define
  2. For early diagnosis?
  3. For late diagnosis?
A
  1. High concentration in myocardium released after myocardial injury
  2. Rapid release
  3. Long half-life in blood
17
Q

Ideal cardiac marker = high specificity

  1. Define
  2. Non-diseased subjects?
A
  1. Absent in non-myocardial tissue

2. Not detectable in blood

18
Q

Ideal cardiac marker = analytical characteristics

  1. Define
  2. Complexity?
  3. Turnaround time?
  4. Precision and accuracy?
A
  1. Measurable by cost-effective method
  2. Simple
  3. Rapid
  4. Sufficient precision and accuracy
19
Q

Ideal cardiac marker = clinical characteristics

Define

A

Able to influence therapy and improve patient outcome

20
Q

Name the 3 cardiac markers used in order of appearance

A

Myoglobin
CK-MB
Cardiac troponin (I or T)

21
Q
  1. When does myoglobin disappear?
  2. When does CK-MB disappear?
  3. When does Troponin (T or I) disappear?
A
  1. Within 24 hours
  2. Within 2-3 days
  3. Within 5-15 days
22
Q

There is no ideal cardiac marker

  1. Which one is used for sensitivity because of its early onset (however it is not cardio-specific)?
  2. Which one if used for specificity because it is cardio-specific?
A
  1. Myoglobin

2. Cardiac troponins

23
Q

Too much LDL in circulation

  1. What does it interact with?
  2. What does this lead to?
  3. Core?
  4. Plaque?
  5. Explain a complicated plaque
A
  1. Foam cells
  2. Fatty streak
  3. Lipid core
  4. Atherosclerotic plaque
  5. Complicated atherosclerotic plaque: plaque rupture / thrombosis / haemorrhage
24
Q

Name 6 risk factors of atherosclerosis

A
  1. Hyperlipidaemia
  2. Coagulation
  3. Diabetes
  4. Genetics
  5. Age
  6. Lifestyle
25
Q

Lipoprotein metabolism and increased clotting

  1. What 2 cells are circulating?
  2. What kind of deposits on blood vessels?
  3. What kind of plaques do they turn into?
  4. What can happen to these plaques which triggers clotting?
  5. What can the two outcomes be?
A
  1. Foam cells + LDL
  2. Fat deposits
  3. Lipid rich plaques
  4. They can disrupt - they have rough surfaces - can trigger clotting
  5. Completely occlusive thrombus or partially occluded thrombus
26
Q
  1. What happens in a completely occlusive thrombus?

2. What happens in a partially occluded thrombus?

A
  1. Blood supply shut off

2. Resolve some of clot = fibrous fatty end result

27
Q

Define embolus

A

Object from another part of the body that obstructs blood flow

28
Q

Define thrombus

A

Blood clot that becomes an embolus

29
Q
  1. What do vascular endothelial cells normally secrete? Give 2 examples and explain the relation to clot formation
  2. If there is damage to smooth muscle cells in the vessel wall, what can happen? Explain the relation to clotting
A
  1. Vasodilators / PG + NO / inhibits clot formation

2. Vasoconstriction / promotes clotting

30
Q
  1. When damage results in exposure of the basement membrane, what 2 things is blood exposed to?
  2. When damage results in exposure of vessel wall, what is blood exposed to?
  3. When damage results in exposure of loses epithelial cells, what is blood exposed to?
A
  1. Collagen + subendothelial tissue factor
  2. Platelet activating factor
  3. ADP
31
Q

Activated platelets

  1. What are the 2 reasons they change shape for?
  2. What 3 reasons do they activate other molecules for?
  3. What do they adhere to?
  4. What is the initial plug?
A
  1. Facilitate movement + aggregation
  2. Activate other molecules / allow adhesion / cause vasoconstriction
  3. Vessel wall at damage site
  4. Platelet aggregation
32
Q

Name 5 things that can activate platelets

A 
ADP
Collagen
Thrombin
Immune complexes
High physical shear force
33
Q

How clotting factors work

  1. Stage the names of the 3 pathways
  2. What is the intrinsic pathway activated by?
  3. What is the extrinsic pathway activated by?
  4. What kind of state do all clotting factors start out in?
A
  1. Intrinsic pathway, extrinsic pathway and common pathway
  2. Collagen
  3. Tissue factor (from tissue injury)
  4. Inactive state
34
Q

Clotting cascade

  1. Describe the main aspect of the clotting cascade
  2. What 2 things bind to and inactives thrombin immediately? What does this stop?
A
  1. Prothrombin to thrombin
    Thrombin transforms fibrinogen to fibrin to cross linked fibrin
  2. Anti-thrombin and protein C = both stop clotting
35
Q
  1. What system breaks down fibrin clots?
  2. Via which serine protease? What is the name of the inactivate state it circulates the plasma in?
  3. What 2 things allow the activation of this serine protease?
  4. What inhibits this activation?
  5. What is the end result?
A
  1. Fibrinolytic system
  2. Plasmin
    Inactive form = plasminogen
  3. tPA = tissue type plasminogen activator
    uPA = urinary type plasminogen activator
  4. Plasminogen activator inhibitor
  5. Fibrin degraded = clot broken up

1 REVISION Bismillah (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions