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Biochem Flashcards

1
Q

What are the conditions that can cause increased LDH in the blood

A

may include liver disease, anemia, heart attack, bone fractures, muscle trauma, cancers, and infections such as encephalitis, meningitis, encephalitis, and HIV. LDH is also a non-specific marker of tissue turnover, which is a normal metabolic process.

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2
Q

Enzymes thiamine is a cofactor for:

A

Thiamine PATs your Back! (Pyruvate dehydrogenase, Alpha-ketoglutaric acid dehydrogenase, Transketolase, Branched-chain ketoacid dehydrogenase).

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3
Q

what heart condition is a/w thiamine (B1) def

A

high output cardiac failure

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4
Q

what causes chest pain in pts with MI

A

Infarcted cardiac myocytes release ATP, which is converted to adenosine extracellularly by nucleotidases. Adenosine stimulates the adenosine A1 receptors on cardiac afferent nerve endings and is responsible for chest pain in patients with myocardial infarction.

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5
Q

aromatase function

A

convert androgens to estrogens

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6
Q

Neurophysins

A

A group of carrier proteins that transport vasopressin and oxytocin from the supraoptic and paraventricular nuclei in the hypothalamus to the posterior pituitary gland for storage and release.

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7
Q

what are the neurotransmitter changes in GAD

A

increased dopamine and norepinephrine
decreased activity of inhibitory neurotransmitters like gamma-aminobutyric acid (GABA).

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8
Q

what diseases are specifically a/w Interleukin-1

A

Interleukin-1 is an inflammatory cytokine that is important in innate immune responses and is implicated in many diseases such as breast cancer, metabolic syndrome, diabetes mellitus, and Alzheimer disease.

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9
Q

what does cytotrohoblast secrete vs syncitiotrophoblast?

A

cytotrophoblasts secrete hyperglycoslyated HCG

Syncitiotrophoblasts secrete beta HCG

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10
Q

Calcitonin MOA

A

Calcitonin decreases calcium levels by blocking the breakdown of bone calcium and by preventing your kidneys from reabsorbing calcium.

it opposes the effects of PTH

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11
Q

endothelin is a vasodilator or vasoconstrictor?

A

vasoconstrictor

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12
Q

cholesterol is a precursor for:

A

steroid hormones (by extension sex hormones), bile acids, and vit D

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13
Q

diseases caused by germline mutations in the Rb gene include

A

osteosarcoma and retinoblastoma

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14
Q

Arginine is a nonessential amino acid and a precursor of …

A

nitric oxide, urea, ornithine, and agmatine

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15
Q

pellagra is caused by a deficiency in what micronutrient

A

niacin or vit 3

Niacin can be obtained through dietary intake or synthesized endogenously from tryptophan.

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16
Q

components of tight junctions

A

transmembrane proteins (eg, claudins and occludins) that associate with actin filaments, forming a beltlike seal around the apical intercellular space. This seal only permits the passage of substances from the blood to the brain via transcellular movement.

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17
Q

what does Glucose-6-phosphatase do

A

catalyzes the hydrolysis of glucose-6-phosphate to glucose during gluconeogenesis, thereby helping to maintain glucose levels in the fasting state; increased activity would improve hypoglycemic symptoms by increasing circulating glucose levels.

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18
Q

Which glucose transporter is insulin dependent

A

GLUT4

insulin binds a tyrosine kinase receptor that results in GLUT4 being transported to the plasma membrane to allow for passive diffusion of glucose.

it is insulin dependent, *EXCEPT* for when a muscle is contracting, that stimulates translocation of GLUT4 too

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19
Q

what are the main NTs of pain in the peripheral nervous system

A

glutamate and substance P

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20
Q

what substances are commonly mixed in with lidocaine injections and why?

A
  1. sodium bicarb to decrease acidity and keep the lidocaine molecules in uncharged (lipophilic) form
  2. epinephrine to cause vasoconstriction, keeping the med at the active site for longer and to decrease local bleeding.
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21
Q

what is lyonization

A

In females, however, only one X chromosome gets expressed, and the other X chromosome forms a transcriptionally inactive Barr body. This process is called X-inactivation or lyonization. If the inactivation is random, about half of the female’s cells will be affected in the case of an X linked mutation

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22
Q

BMPR2 mutation causes

A

idiopathic pulmonary HTN

sx: progressive dyspnea and fatigue without cough, or wheezing

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23
Q

HMG-CoA Reductase

what does it do

A

cholesterol synthesis (upregulated by estrogen)

24
Q

cholesterol 7alpha-hydroxylase

what does it do?

A

rate limiting enzyme in bile acid synthesis (inhibited by fibrates)

25
Q

Ferrochelatase vs ferrireductase

A

Ferrochelatase = terminal enzyme of the heme biosynthetic pathway in all cells. It catalyzes the insertion of ferrous iron into protoporphyrin IX, yielding heme.

ferrireductase = duodenal enz. that converts Fe3+ to Fe2+ for iron absorption

26
Q

V1 receptor

A

A class of vasopressin receptors that are coupled to a Gq-protein. Activation mediates smooth muscle contraction (e.g., vasoconstriction and uterine contractions).

27
Q

____________ is caused by autosomal recessive mutations in the ATP7B gene,

(impaired copper transport/excretion)

A

Wilson disease

28
Q

mutation in the HFE gene causes what condition

A

hemachromatosis

HFE codes for a membrane protein that facilitates interaction of transferrin and its bound iron with its receptors

29
Q

clinical utility of monitoring AFP

A

AFP can be used as a marker for yolk sac tumors (endodermal sinus tumors), mixed germ cell tumors, ataxia telangiectasia, and hepatocellular carcinoma

30
Q

Li Fraumeni syndrome (aka SBLA syndrome) is d/t what mutation

A

Mutation in TP53

causes tumors:

  1. Sarcoma
  2. Breast Cancer
  3. Leukemia
  4. Adrenal Gland Carcinoma
31
Q

p-ANCA meaning

A

containing antibodies against neutrophil myeloperoxidase –> perineuclear

32
Q

c-ANCA meaning

A

containing autoantibodies against neutrophil proteinase 3 –> cytoplasic

strongly a/w granulomatosis with polyangiitis (GPA)

33
Q

what microbes activate adenylate cyclase?

A

Overactivated by heat-labile toxin from enterotoxigenic E. coli (ETEC), cholera toxin from Vibrio cholerae, and pertussis toxin from Bordetella pertussis. Mimicked by edema toxin from Bacillus anthracis.

34
Q

what is α-glucosidase .

A

The enzyme α-glucosidase facilitates glucose absorption at the small intestine brush border membrane. Inhibition of α-glucosidase would decrease intestinal sugar absorption, meaning it would decrease blood glucose concentration.

35
Q

what’s this mnemonic for

Tisk Tisk (TSC 1 and 2), MEN discontinue (D/C) BRides to watch SMut on VHs and CDs then WaiT TEN minutes at an RBs (for a hooker), Never Fearing that their home, APartment C will be TPd

A

the tumor suppressor genes

Mn: TiSk - Tumor Suppressor

36
Q

what molecule signals via serine kinase/threonine kinase

A

TGF-beta

37
Q

where are each of the collagen types found

A

I –> bone

II –> cartilage, joint articulation

III –> blood vessels

IV –> basement membrane (GBM, cochlear BM, and in the lens of the eye (mn: can’t see in the basement))

38
Q

cofactors required for alpha-keto-glutarate-dehydrogenase

A
39
Q

what are the antibodies in limited vs diffuse scleroderma (aka systemic sclerosis)

A

limited: anti-Centromere
diffuse: anti-Scl-70 (anti-DNAtopoisomerase-Iantibody) and anti-RNA polymerase III.

40
Q

a glycoprotein hormone produced by peritubular fibroblast cells in the renal cortex

what is this?

A

erythropoietin (EPO)

41
Q

which receptor type uses Zinc finger motif

A

Zinc-finger motifs are composed of chains of amino acids bound together around a zinc atom via linkages with cysteine and histidine residues. They recognize specific DNA sequences and are used by many transcription factors to bind DNA and alter activity of target genes. Intracellular receptors that bind steroids, thyroid hormone, and fat-soluble vitamins act directly as transcription factors and contain zinc-finger binding domains.

42
Q

pt with hx of alcoholism, bleeding gums, echymosis, nosebleeds, and ulcurs

what’s the dx?

A

The only thing that can explain all these sx is scurvy d/t vit C def, which can happen in any nutrient deprived state such as in a chronic alcoholic

n.b. This may present similarly to pancytopenia or thrombocytopenia, but alcoholism isn’t a/w with that. it’s only a/w macrocytic megaloblastic anemia d/t folate or b12 def.

43
Q

for what biochemical process is Thiamine (B1) a cofactor

A

decarboxylation of alpha keto acids via its active form thiamine pyrophosphate

  • Enzymes thiamine is a cofactor for: Thiamine PATs your Back! (Pyruvate dehydrogenase, Alpha-ketoglutaric acid dehydrogenase, Transketolase, Branched-chain ketoacid dehydrogenase).
    def. a/w: Beriberi and Wenicke Korsakoff syndrome (pathogenesis: Thiamine deficiency → impaired glucose breakdown → ATP depletion → tissue damage that primarily affects highly aerobic tissues (e.g., brain, heart)

strongly a/w alcoholism

44
Q

for what biochemical process is riboflavin (B2) a cofactor

A

mitochondrial redox reactions via its active forms flavin mononucleotide (FMN) and flavin adenin dinucleotide (FAD)

Enzymes affected: Succinate dehydrogenase (TCA cycle) and glutathione reductase in erythrocytes

def. is a/w corneal vascularization, Cheilosis/cheilitis (cracking of corners of mouth), stomatitis (inflamed, sore, mouth ), glossitis (enlarged tongue)

45
Q

for what biochemical process is niacin (B3) a cofactor

A

redox reactions via its active forms Nicotinamide adenine dinucleotide (NAD+/NADH)

processes affected: synthesis of fatty acids and steroid, the respiratory burst, the cytochrome P450 system, and glutathione reductase

def. is a/w pellagra (dermatitis (in C3-C4 distribution), dementia, diarrhea (mn: the 3 Ds)

a/w tryptophan deficiency dzs: Hartnup, Carcinoid

46
Q

for what biochemical process is pantothenic acid (B5) a cofactor

A

Essential component of coenzyme A (CoA = B5 + ADP + cysteine)

Cofactor for the transfer of acyl groups → activation of carboxylic acids (e.g., pyruvate dehydrogenase, α-ketoglutarate dehydrogenase)

Cofactor for fatty acid, cholesterol, and acetylcholine synthesis

def. A/W: adrenal insufficiency, paresthesias, alopecia, dermatitis (but deficiency is rare)

47
Q

for what biochemical process is biotin (B7) a cofactor

A

carboxylase reactions (adds a 1-carbon group)

Acetyl-CoA → malonyl-CoA (fatty acid synthesis)

Pyruvate → oxaloacetate (gluconeogenesis)

Propionyl-CoA → methylmalonyl-CoA (fatty acid reduction)

def. is rare but a/w hair loss

48
Q

for what biochemcial process is pyridoxine B6 a cofactor

A

active form is pyridoxal phosphate (PLP). involved in: Transamination (e.g., AST and ALT), Decarboxylation, Glycogenolysis (glycogen phosphorylase)

Involved in the synthesis of Heme –> def. A/w sideroblastic anemia

can aslo cause Cheilosis, glossitis, stomatitis

49
Q

for what biochemical process is folate (B9) a cofactor

A

active form: tetrahydrofolic acid (THF)

involved in hydroxymethyl/formyl carrier (purine and thymine synthesis)

def. A/w neural tube defects and megaloblastic anemia

50
Q

active form = methylcobalamin

cofactor for methionine synthase (DNA synthesis) and methylmalonyl-CoA mutase (fatty acid metabolism)

A
51
Q

for what biochemical processes is Vit C (ascorbic acid) a cofactor

A
  • chelates and redoxes iron –> both increase iron solubility and therefore absorption
  • hydroxylation of proline and lysine –> collagen synthesis
  • noradrenaline synthesis (req. for dopamine beta hydroxylase)
52
Q

what are the clinical manifestations of vit E deficiency

A

aka tocopherol

Neurologic dysfunction

Demyelination of the posterior column and spinocerebellar tract → ↓ proprioception and vibration sensation; ataxia

Neurologic symptoms are similar to vitamin B12 deficiency, except that vitamin E deficiency does not lead to hypersegmented neutrophils, megaloblastic anemia, and increased methylmalonic acid levels.

53
Q

what happens to homocysteine and methionine levels after folate supplementation?

A

homocysteine decreases (used up)

methionine increases

54
Q

what happens with methylmalonic acid, homocysteine, and methionine levels during B12 deficiency

A

increased methylmalonic acid*, increased homocysteine, decreased methionine

*this is used as a biomarker for B12 levels in special tests

55
Q

what is the mechanism of nerve injury in B12 deficiency

A

Methylmalonic acid can’t be converted to succinyl CoA → accumulation of methylmalonyl CoA and its precursor propionyl CoA → Propionyl CoA replaces acetyl CoA in neuronal membranes → demyelination

56
Q

DNA Pol III vs DNA pol I

A
57
Q

Given phenotypically normal parents, the probability that a female sibling of a male affected by an X-linked recessive disease will give birth to an affected child is __________

A

1/8.

Boards High Yield (28 decks)

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