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Metabolism-Alaa > Alchohol > Flashcards

Alchohol Flashcards

1
Q

which enzyme is deficient in classic galactosemia?

A

“GUT” uridyl Transferase

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2
Q

what is the front line of defence against ROS? and why

A

glutathione, bc it is the most abundant in cells

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3
Q

List 3 agents in which cell protects itself against ROS.

A
  • the enzyme superoxide dismutase/catalase
  • Glutathione
  • free radical scavengers (vit E & C)
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4
Q

how does ROS damage cells? give some examples

A

DNA>> ROS react with DNA, the base could be modified leading to mispairing and mutation

Proteins >> side chains of amino acids or the protein backbone can react with ROS modifying protein structure & leading to a loss of function

Lipids>> lipid peroxidation ex: in athersosclerosis

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5
Q

how is oxidative stress related to inflammation?

A

involved in the intracellular killing of the bacteria.

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6
Q

Describe the signs and symptoms of specific vitamin deficiencies are often seen in alcoholics

A

Neurological symptoms, due to deficiencies of thaimine (B1) or pyridoxine (B6)

Hematological problem asscoaited with folic acid defieciency common in alcholohics

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7
Q

What is galactosemia?

A

Galactosemia (British galactosaemia) is a rare genetic metabolic disorder that affects ability to metabolize the sugar galactose properly.

Galactosemia follows an autosomal recessive mode of inheritance w/ a deficiency in an enzyme responsible for adequate galactose degradation.

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8
Q

What are free radicals? ROS?

A

is any atom, molecule or ion that contains one or more unpaired electrons.

Electron esca[es the ETC and reacts with O2 to form superoxide

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9
Q

How can alchohol oxidation lead to lactic acidosis. How can gout be related in this context? What crystals accumalate in gout?

A

Increased levels of NADH due to alcholol oxidation means there is less NAD+ available for the conversion of Lactate into pyruvate >> causing a build up of lactic acid>>

lactic acidiosis can decrease the kidneys ability to excrete URIC ACID ~monosodium urate acid (MSU)

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10
Q

What is gluconeogenesis? how can alchohol have an effect on it?

A

Synthesis of new glucose from noncarb (Mostly pyruvate) it cannot be activated bc there r no substrates for it to occur. (remember alchohol decreases the ability for Pyruvate to form)

as a result we get HYPOGLYCEMIA

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11
Q

when alcohol is consumed, where does it go?

A

90 % metabolised in liver

10% excreted in urine and breath

small amounts can be oxidised by CYP2E1 in liver or catalysed by the brain

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12
Q

What r they 2 ways in which ammonia is safely removed from the body?

A

Qqq

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13
Q

what is a clinical sign in the microscope level in diagnosing someone with G6PDH deficiency?

A

the presence of heinz bodies!

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14
Q

What r the components needed to make new glucose ‘gluconeogenesis” ?

A

Lactate

Pyrvic acid

Alanine

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15
Q

name 2 antioxidant vitamins? how do they function

A

E > lipid soluble, protects against lipid peroxidation.

C > watersoluble, takes VE back to its reduced form

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16
Q

Describe the metabolism of alcohol with enzymes involved and explain how the metabolism of alcohol can cause damage to the liver.

A

alchohol—->acetalaldehyde——>Acetate—–>acetyl Coa -alchohol dehydrogenase -aldehyde dehydrogenase

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17
Q

is it marasmus or qwashqior that causes muscles wasting?

A

Marasmus> Muscle wasting (M)

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18
Q

what is oxidative stress? give examples of disorders caused by it

A

imbalance btw ROS and antioxidants

atheresclerosis, alzeheminers, parkinsons, MS, chron’s disease, COPD, CVS

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19
Q

describe a variety of effects in the body that alcohol metabolism components may cause.

A
  • effect of decrease in NAD+/NADH ratio
  • effects of increased Aceytl CoA
  • effect of the toxic aceytlaldehyde -effect on GI cell linings>> (impaired absorption) -effects in pancreas (inflammation of pancreas)
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20
Q

as we know, alcohol damages the liver, what consequences can this have?

A
  • proteins not made (ex: albumin) —->cant take up bilirubin>>jaundice
  • clotting factors not made
  • lipoproteins* not made> fatty liver
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21
Q

why do u get jaundiced during galactosmeia?

A

a

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22
Q

Explain nitrogen balance amd protein turnover

A

W

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23
Q

what r heinz bodies?

A

are inclusions within red blood cells composed of *aggregates of denatured Hb*.

***clinical sign go G6PDH deficiency.

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24
Q

how do free radical scavengers work?

A

they donate a hydrogen atom and it’s electron to free radicals.

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25
Q

what is galactitol? how is it formed?

A

galactose is reduced to galactitiol via aldose reductase & the reaction uses up NADPH. (nadiyah & pharida)

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26
Q

explain relationship btw Glutathionine and NADPH

A

needs NADPH to take it back to its reduced form.

so it can continie its job of donaiting it electron and forming another disulfide bond with another glutathione;

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27
Q

what may initiate oxidative stress?

A

infection, drugs (ex antimalarial), broad beans!

28
Q

What syndrome can thiamine defieciency lead to in alcoholic?

A

Wernicke-Korsakoff symdrome

29
Q

why is it that alchololics show signs and symptoms of specific vitamen deficiencies?

A

damages lining of GI tract > impaired absorption of certain nutrients

30
Q

what r the outcomes of a patient with Kwashiorkor?

A

results from protein deficient “MEAL”

Malnutrition

Edema

Anemia

Liver

31
Q

what is the respiratory burst?

A

neutrohills use it to kill bacteria.

  • they engulf the bacteria and have this NADPH oxidase which produces “SUPEROXIDE:”
  • either binds with NITROC OXIDE
  • or becomes H2O2 il mohim, this all leads to destroying of bacteria
32
Q

what r the effects of increased toxic acetlyaldehyde during alchohol consumption can make on the body?

A

damaged liver cells have leaky membranes loss of enzymes not blood

**these enzymes r used as an indicator of liver damage (ALT) (AST)

33
Q

what is going wrong in galactosemia?

A

deficiency in any of the 3 enzymes involved in galactose break down, favours the conversion of galactose to galactitiol resulting in galactosemia

34
Q

what is glucose-6-phosphate deficiency? what happens in RBC?

A

NADPH is necessary to keep Glutathione in its reduced form (GSH). remember GSH is an antioxidant (itha nasty chaikay shnu salfita)

Low NADPH in rbc’s leads to haemolytic anemia due to poor Rbc defence against oxidising agents (fava beans, infection).

causes heinz bodies due to clusters of denatures Hb,

Stress lets u bite into some heinz ketchup

35
Q

Explain symptoms of access alchohol intake and explain why they arise?

A

Lactic acidosis

Gout

Hypoglycemia

fatty liver

ketoacidosis

hyperbilirubineamia

hyperammonia

edema

pancreatitis (if too much alcohol is consumed)

36
Q

what r the effects that the increased Acetly Coa during alchohol consumption can make on the body?

A

it increases the synthesis of fatty acids and ketone bodies.

fatty acids r packaged into TAG>this can’t be transported out of the liver (bc can’t make Lipoprotien> trapped in liver> fatty liver.

ketone bodies can cause ketoacidosis

37
Q

what r free radical scavengers? give examples

A

reduce ROS damage by donating a hydrogen atom to free radicals in a non enzymatic reaction.

-Vitmins E &; C -Melatonin, flavenoids, carotenoids

38
Q

how do u treat a patient with galactosemia?

A

exclude galactose and lactose.

39
Q

Describe how aa r catabolised?

A

Ss

40
Q

how can u treat overdose of paracetamol? why should u act FAST?

A

give antidote ACETYLCYSTINE w/ in 8HRS! -works by restoring glutathione levels SOOO.. Acetylcysteine serves as a prodrug to ‘L-cysteine.’ it’ll act as a PRECURSOR for more glutsthione to be made. (remember glutathione is a tripeptide! Glycine-Cys-Glutamate)

41
Q

what r ROS? how r they formed? name them

A

group of oxygen related compunds that r damaging. In the ETC, Oxygen at the end of the chain is waiting for its electrons to come ,BUT in some cases, those electrons do not reach the end, 7aram, oxygen gains only 1 electron (it is reduced into SUPEROXIDE O2-) (for the rest, go to lecture pic) SUPEROXIDE HYdrogen Peroxide HYDROXYL RADICAL

42
Q

Consequences if u high acetlyaldehyde? How is it formed? How can it cause liver damage

A

Its formed from alcholhol via “alcohol dehydrogenease” by converting NAD+>>NADH.

Acetlyaldehyde is very toxic to the cell.

In prolonged alchohol consumption, acetylaldehyde can accumalate to cause LIVER DAMAGE.

43
Q

Which term is used to describe the cycle by which the lactate produced in skeletal muscle is converted back to glucose in the liver?

A

Cori cycle

44
Q

what r heinz bodies?

A

Heinz bodies >>Denatured HEmaglobin that precipitates in rbc due to oxidative stress

45
Q

What is the most damaging free radical? why?

A

Hydroxyl radical, cuz it can react with anyhithng!

46
Q

**free radical scavengers donate their hydrogen atoms to free radical in a NONENZYMATIC reaction

A

ok

47
Q

what r free radicals? what is the most reactive and most damaging and why?

A

any atom or molecule that has an unpaired electron,

this will make it very reactive with other molecules to steal their electrons.

HYDROXYL RADICAL OH* >>bc it wants to react with ay shay!

48
Q

how is the pentose phosphate pathway essential for protection against free radicals?

A

it produces NADPH which is needed by Gluathionine to go back to its original form GSH.

49
Q

Lack in kinase vs tranferase in galactomseia

A

The absence of the kinase is relatively rare and is characterised by accumulation of galactose in tissues.

The absence of the transferase is more common and more serious as both galactose and galactose 1- phosphate accumulate in tissues.

50
Q

what is the pentose phosphate pathway? how does it start? which enzyme is important in the process?

A

important source of making NADPH. and producing C5 sugar ribose.

starts from glucose-6-phosphate

glucose-6-phosphate dehydrogenase

51
Q

To make new glucose we need pyruvate, how can we get it?

A

We get it from lactate, Lactate shakes hand with NAD and loses H+, causing puruvate to form! NAD—–> NADH+H

52
Q

Describe the production of superoxide radicals by mitochondria and discuss other reactive oxygen (ROS) and reactive nitrogen (RNS) species.

A

ROS can also react with NOS. ex: superoxide can combine with nitric oxide >> PEROXYNIRATE, which itself is not a free radical but itself is a powerful oxidant bc it is can easily diffuse into cells

53
Q

What is PKU? phenylketonuria?

A

.

54
Q

Symptoms of galactosemia

A

if they drink milk…>>> yellow Cats have seizures and Vomit large livers

Renal failure

hepatomegaly

cirrhosis

vomiting

seizure

cataracts

hypoglycemia

Jaundice

55
Q

Why is aldehyde toxicity noramlly kept to aminimum instead of being so high?

A

Acetaldehyde toxicity is normally kept to a minimum by aldehyde dehydrogenase because this enzyme has a low Km for acetaldehyde

56
Q

how does ROS cause damage to DNA?

A
  • it reacts with the base (leads to mispairing and mismatching
  • it reacts with the sugar (ribose + deoxyribose)
57
Q

What deficiency is related with the defect in the nadph oxidase

A

Chronic granulamotus disease

58
Q

what r bite cells?

A

result from the phagocytic removal of Heinz bodies by splenic macrophages

“Bite into some Heinz ketchup”

59
Q

what causes the “hangover” during alchohol drinking?

A

accumulated levels of Acetylaldheyde

60
Q

is there an alternate source of tissue galactose for patients on a galactose free diet?

A

q

61
Q

A 72 year old man reports deterioration in his vision. It is difficult for him to recognise faces or to read the newspaper. He is diagnosed with age-related macular degeneration and reads that oxidative stress contributes to the development of this disease. He asks his ophthalmologist if any vitamin or mineral supplements would be helpful.

Glutathione peroxidase requires which trace element to function?

A

SELENIUM

62
Q

what is glutathione? what is its significance?

A

is a tripeptide, (Gly-cys-Glu)

it is made by the body to act as an ANTIOXIDANT.

it basically lends their electrons to free radicals then goes and reacts with another Glutathione making a disulphide bond to form (GSSH).

GSSH il7een lazy breaks up and goes back to GSH and this needs NADPH to happen!

THATS WHY PENTOSE PHOSPHTE PATHWAY IS IMPORTANT IN PROTECTING AGAINST FREE RADICALS!

63
Q

Which nutrients are impaired absorbed in the gi in alcholholics?

A

Vit K,

folic acid,

pyridoxine, b6

thiamine b1

64
Q

role of vitamins E

A
  • lipid soluble vitamin
  • important for protecting against lipid peroxidation (oxidative degradation of lipids)
65
Q

what diseases is oxidative stress related to?

A
66
Q
A

lol

67
Q

how can u treat alchoholism?

A

w/ Disulfiram

Metabolism-Alaa (23 decks)

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