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Biochemistry > High Yield > Flashcards

High Yield Flashcards

1
Q

When are you at risk for Respiratory acidosis?

A

When respiration is impaired in anyway! (inadequate CO2 elimination)
=pneumonia, emphysema, severe asthma, acute pulmonary edema, congestive heart failure, drugs that inhibit respiratory centers

-because CO2 accumulates and dissolves in the blood to form carbonic acid

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2
Q

What is the result of respiratory acidosis?

A

increased PCO2 forms:
increased carbonic acid, which breaks down to form:

Increased H+ and Increased HCO3- (so chronically elevated bicarbonate)

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3
Q

When are you at risk for Metabolic acidosis?

A

Anytime H+ is elevated or HCO3- decreases

-ketosis (from poorly controlled diabetes or starvation)
Kidney damage
Chronic diarrhea (loss of bicarb)
excessive lactate production

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4
Q

What is the result of metabolic acidosis?

A

Increased H+, which requires bicarb to bind it up, so bicarb decreases! Then CO2 combines with water to form carbonic acid, which breaks down to H+ and bicarb (to replace the bicarb)

-so we use a lot of CO2 and CO2 becomes chronically low

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5
Q

What causes respiratory alkalosis?

A

Any factor that decreases PCO2

  • hyperventilation
  • high altitude
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6
Q

So what is the result of excessive CO2 elimination (resp. alkalosis)?

A

So the Low PCO2, results in less carbonic acid formation, which results in less breakdown, and therefore less H+ and chronically low bicarb

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7
Q

Metabolic alkalosis?

A

Anything that increases bicarb or decreases H+

  • excessive ingestion of antacids
  • really prolonged vomiting
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8
Q

What is the result of metabolic alkalosis?

A

the decreased H+ causes more CO2 retention (PCO2 is chronically increased) so that we can used it to form carbonic acid, which breaks down to replace the H+, but also increases bicarb

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9
Q

A 19-year-old male with type I diabetes fails to administer his insulin, thus causing the onset of diabetic ketoacidosis. This results in deep and rapid breathing (Kussmaul breathing). Which of the following best describes how the increased breathing acts to compensate for (i.e. correct) the acidosis?

A

It reduces the concentration of CO2 and carbonic acid in the blood, thereby increasing the association of protons with bicarbonate

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10
Q

A medical student becomes extremely anxious during a Biochemistry examination and begins to hyperventilate uncontrollably. What initial effects does the hyperventilation have on the student’s PCO2 and blood pH?

A

PCO2 decreases and pH increases

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11
Q

he glycosidic linkage forms when an anomeric carbon reacts with an OH or NH group from another compound.

explain sugar, milk, potato/flour (starch - storage form of carbohydrates in plants)

glycogen = storage form of carbohydrates in humans

A 
sugar = sucrose = glucose + fructose (alpha; 1,2)
milk = lactose = glucose + galactose (Beta; 1,4)

Potato or Flour = starch = glucose + glucose (alpha 1,4 amylose / alpha 1,6 amylopectin)

maltose = glucose + glucose (alpha; 1,4)
cellulose = glucose + glucose (BETA; 1,4)
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12
Q

A 6-week-old male is admitted to the ICU with jaundice, lethargy and feeding difficulties. History is significant for intermittent vomiting since birth. Physical examination reveals hepatomegaly and the initial stages of cataract formation. A diagnosis of galactosemia is made. Which of the following is the most likely mechanism of cataract formation in this patient?

A

*Osmotic uptake of water into the lens, causing aggregation of crystallin proteins

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13
Q

simple lipid

glycerophospholipid

sphingophospholipid

glycolipid

A

= 3 FA + Glycerol (alcohol)

=2 FA + Glycerol (alcohol) + phosphate + head group

= 1 FA + Sphingosine + phosphate + head group

= 1 FA + Sphingosine + carbohydrate

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14
Q

Eicosanoids - 3 types

A

(made from nutritionally essential FAs)

  1. Prostanoids
  2. Leukotrienes - chemotaxis, inflammation, allergic rxns
  3. Lipoxins - anti-inflammatory, oppose action of Leukotrienes
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15
Q

Prostanoids

A

(one type of eicosanoid)

3 examples:

  1. Prostaglandins - inflammatory response, hormone production, ion transport
  2. Prostacyclins - inhibits platelet aggregation, promotes vasodilation
  3. Thromboxanes - promotes platelet aggregation and vasoconstriction
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16
Q

Test question asked what type of lipid is a thromboxane

A

(answer is eicosanoid)

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17
Q

oleic acid naming:

18: 1 (9)

A

18 carbons, 1 double bond, at the 9th carbon

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18
Q

The fat soluble vitamins are all

A

lipids

Vitamin D can be synthesized from cholesterol (a steroid) with adequate sunlight

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19
Q

steroids

A

characteristic picture - recognize it

cholesterol (synthesize steroid hormones, bile acid, vit D)
sterols (steroid + OH),

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20
Q

Essential fatty acids (body cant make)

A

plant sources:linoleic (omega 6) / linolenic (omega 3)
animal sources: EPA, DHA
flax seeds, almonds, fish

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21
Q

Kwashiorkor

A

protein malnutrition

  • negative Nitrogen balance
  • lack of essential AA (can’t make proteins)
  • edema caused by decreased serum proteins (albumin)
  • patient appears plump from the edema
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22
Q

Marasmus

A

caloric malnutrition

-patient is skin and bones

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23
Q

Vitamin B3 (Niacin)

A

= dairy, poultry, fish, lean meat, nuts, eggs

=deficiency can cause *pellagra (rash)

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24
Q

Vitamin K

A

= cabbage, cauliflower, spinach, other green leafy vegetables, cereal

=deficiency can cause problems with blood clotting

25
Q

Vitamin A

A

= eggs, meat, dairy, green leafy vegetables, intensely colored fruits and vegetables

=deficiency causes eye problems

26
Q

***Actual test question asked what would happened if glucose transporter were saturated

A

= this would prevent the movement of glucose from lumen into the blood

27
Q

How are proteins cleaved into AAs
Fats?
Carbs?

A

protease enzymes
lipases
amylase in mouth and primarily in small intestine

28
Q

**tough test question: after a month of starving (surviving on scraps) what would your body be getting energy from

A

ketone bodies*
remember prolonged fast is the starving state!
your body uses FA (oxidizes to KB for brain!)

29
Q

Sources of carbon for gluconeogenesis?

A

carbon skeleton of:

  • AA (from muscle protein)
  • Lactate (from muscles and RBCs)
  • Glycerol (from lipolysis)
30
Q

*test question: three hours after a meal, what is high insulin or glucagon?

A

*Fasting State
Glucagon levels increase

insulin (peaks one hour after a meal, back to normal at 2 hours post meal)

31
Q

What is a prolonged fast?

What is the role of fat?

signs of prolonged fast?

A

3 days or more.

lipolysis supplies muscle and other tissues with FAs
liver can use glycerol

liver makes less glucose - so less urea is seen in urine
increased KB (due to increased FAs in the blood)
32
Q

Short fast

signs

A

overnight to 3 days

1-2 days a lot of urea seen in urine

33
Q

what does increased Ketone bodies (+increased glucose) indicate?

A

Insulin deficiency?

Type 1 diabetes?

34
Q

How could serum albumin

and creatine be useful?

A

reatinine - used as a constant to measure urine filtration

If serum albumin is low, protein deficiency

35
Q

What determines 3D structure and biological properties of proteins?

A

The sequence of the AA that are linked together

i.e. - Information for folding is contained in the sequence of the amino acid - key fact

36
Q

Non-polar AAs

A

Glycine, Leucine, Alanine, Phenylalanine

37
Q

neutral AAs

A

Serine, Cysteine, Threonine, Tyrosine

38
Q

Asn

Asp

Gln

Glu

A

Asparagine

Aspartate

Glutamine

Glutamate

39
Q

Tell me about the formation of cystine

A

2 cysteines can spontaneously oxidize to form cystine (the sulfurs bond to each other)

*cystinuria - the transport protein that reabsorbs Arg/Lys/CYSTINE is busted. so cystine cant be reabsorbed and shows up in the urine! (Arg/Lys are soluble)

can have kidney stones (made of cystine)

40
Q

keratin

hard vs. soft keratins

A

major component of external protective layers in mammal

  • hard have a high sulfur content (nails, horns, beak)
  • soft (wool, fur, skin)
41
Q

collagen

A

major protein component of connective

forms insoluble fibers of great strength

42
Q

collagen structure

A

without vitamin C (a cofactor) there can be no hydroxylation of proline/lysine and the necessary bonds between chains cannot form (post-translational modification) that produces collagen

no vitamin C = lack of collagen = scurvy

43
Q

Prion diseases

A

degeneration of brain tissue caused by conversion of normal protein to misfolded protein

introduction of this misfolded protein by infection, ingestion, or mutation is bad news

  • genetic: CDJ (humans), BSE (cows), Scrapie (sheep)
  • infection transmitted via pig human growth hormone injection (not relevant today because we use bacteria to synthesize hormones)
44
Q

Quaternary structure

A

example = hemoglobin (interaction of 4 myoglobin subunits, each with one site for Oxygen binding)

cooperative binding of oxygen (Hb)

45
Q

Bohr effect

A

Hydrogen ions (and CO2) promote the release of oxygen

source of H+: lactic acid from active muscle tissue

  • BPG stabilizes deoxyhemoglobin
  • binding of BPG promotes release of oxygen (to tissues that need oxygen most)

Fetal Hb cant bind BPG and therefore has an enhanced affinity for oxygen

46
Q

What is a conjugated protein?

A

a protein with a non-protein component attached

lipoproteins (HDL)
glycoproteins (collagen, FSH, TSH)
nucleoproteins (histomes)

47
Q

Water Soluble Vitamins:

  • *Nicotinic Acid
  • *Riboflavin (B2)
  • Thiamin (B1)
  • Folic Acid/cobalamin (B12)
  • Pyridoxine, pyridoxal, pyridoxamine (B6)
A

= NAD+/NADP+ - hydrogen and electron carriers in oxidation and reduction

=FAD/FMN - hydrogen and electron carriers in oxidation and reduction

=TTP - decarboxylation and acyl transfer

=TH4 - one carbon transfer, rearrangements, methyl-transfers

=CoASH - Transamination, decarboxylation, acyl transfer, carboxylation

48
Q

Transferases

A

transfer functional groups

-creatine kinase

49
Q

Lyases

A

group elimination to form double bonds

50
Q

Ligases

A

bond formation coupled with ATP hydrolysis

-DNA ligase

51
Q

Km

A

substrate concentration at half the Vmax

  • small Km reflects a HIGH affinity of enzyme for substrate (it doesn’t take a lot of substrate to reach half the max vel)
  • large Km reflects a LOW affinity of enzyme for substrate
52
Q

What is the treatment for gout and what enzyme does the treatment inhibit?

A

*Allopurinol

Xanthine oxidase

53
Q

Disease associated with elevation in this enzyme(s):

AST (aspartate aminotransferase)
CK (creatine kinase)
LDH (lactate dehydrogenase)

A

Myocardial Infarction

54
Q

Disease associated with elevation in this enzyme(s):

GGT (glutamyl transferase)

A

*Obstructive Liver Disease (alcoholics)

55
Q

Disease associated with elevation in this enzyme(s):

*Lipase
amylase (also for mumps)

A

Acute pancreatitis

56
Q

Disease associated with elevation in this enzyme(s):

alkaline phosphatase

A

Prostate CANCER, bone disease

57
Q

Disease associated with elevation in this enzyme(s):

AST > ALT

A

hepatitis (alcoholics)

58
Q

Disease associated with elevation in this enzyme(s):

ALT > AST

A

hepatitis (viral)

59
Q

Disease associated with elevation in this enzyme(s):

CK (Creatine Kinase)

A

Duchenne muscular dystrophy

Biochemistry (15 decks)

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