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MS1 - MCBD > Week 4 Review > Flashcards

Week 4 Review Flashcards

1
Q

What is the difference between Marasmus and Kwashiorkor?

A

Marasmus is insufficient calorie and protein intake.

Kwashiorkor is sufficient calorie intake but insufficient protein intake.

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2
Q

Aminotransferase enzymes need which cofactor?

A

PLP (B6)

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3
Q

What do you get when you add a nitrogen to alpha-KG?

A

glutamate

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4
Q

What do you get when you add a nitrogen to glutamate?

A

glutamine

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5
Q

What do you get when you take a nitrogen off of alanine?

A

pyruvate

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6
Q

What do you get when you take a nitrogen off aspartate?

A

oxaloacetate

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7
Q

Zone 1 hepatocytes are found near the ______ ______. Name three prominent reactions involving nitrogen that these hepatocytes carry out.

A

Zone 1 is near the portal triad (incoming blood).

They use 1) glutaminase to take a nitrogen off glutamine and 2) glutamate DH to take a nitrogen off glutamate. The nitrogens go to the urea cycle for 3) conversion to carbamoyl phosphate with CPS I.

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8
Q

Which amino acid is the major carrier of nitrogen in the blood?

A

glutamine

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9
Q

What does it mean if serum levels of AST and ALT are high?

A

Indicative of liver damage. Hepatocytes are dying and spilling out enzymes

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10
Q

Zone 3 hepatocytes are found near the ______ ______. Name one reaction involving nitrogen that these cells carry out.

A

Zone 3 hepatocytes are near the central vein. They use glutamine synthetase to stick NH4+ on glutamate –> glutamine; glutamine goes back into the bloodstream.

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11
Q

Can non-alcoholic fatty liver disease (NAFLD), alcoholic hepatitis, and viral hepatitis all cause elevated levels of serum AST and ALT?

A

Yeah

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12
Q

What are the two most common urea cycle enzyme deficiencies and what do these enzymes do?

A
  1. Carbamoyl phosphate synthetase I (CPS I): takes HCO3- and NH4+ to make carbamoyl phosphate.
  2. Ornithine transcarbamylase (OTC): takes carbamoyl phosphate and ornithine to make citrulline.
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13
Q

Which AA is histamine made from?

What receptor class does it bind to?

What physiologic responses does it elicit?

A

Made from histidine

Binds to GPCRs

Mediates allergic responses and promotes gastric acid secretion.

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14
Q

Which AA is GABA made from?

Which cofactor is needed for its synthesis?

What does it do?

A

Made from glutamate, needs PLP (B6).

It is an inhibitory neurotransmitter.

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15
Q

Which AA is serotonin made from?

Which cofactor is needed for its synthesis?

What does it do?

A

Made from tryptophan, needs PLP (B6).

It contributes to feelings of happiness.

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16
Q

Which AA is nitric oxide (NO) made from? What does it do?

A

Arginine

Vasodilation and smooth muscle relaxation.

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17
Q

Thyroid hormones are made from ________ (an AA). _____ is the active form and it acts to _________ metabolic rate.

A

Made from tyrosine. T3 is the active form, it increases metabolic rate

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18
Q

Why do doomsday preppers own potassium iodide?

A

KI inhibits the Na+/I- symporter that brings iodide into thyroid follicular cells so in the event of nuclear war during a Trump presidency their thyroids won’t take up radioactive iodide. Sad!

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19
Q

Melanocytes in the skin give melanin granules to keratinocytes to shield their nuclei from UV damage. Melanin is made from…?

A

melanin is made from tyrosine

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20
Q

What degrades serotonin and catecholamines?

A

MAO

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21
Q

What is the synthetic pathway of the catecholamines?

A

tyrosine –> dopa –> dopamine –> norepinephrine –> epinephrine

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22
Q

Enzymatic defects in one of which two enzymes results in homocystinuria? What do these enzymes do?

A

Cystathione synthase (most common) converts homocysteine to cystathione.

Methionine synthase (B12 cofactor) converts homocysteine to methionine and needs folate.

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23
Q

Which major enzyme is deficient in people with phenylketonuria?

What are the biochemical and physiological consequences of this?

A

Phenylalanine hydroxylase converts phenylalanine to tyrosine.

Inability to make tyrosine means there’s an inability to make all the stuff that is made from tyrosine (melanin, thyroid hormones, catecholamines).

Excess phenylalanine is converted to acids that can cause brain damage.

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24
Q

Creatinine is often used to measure _______ function because it is freely filtered and neither reabsorbed or secreted.

A

kidney

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25
Q

What two starting materials are needed for heme synthesis? Which enzymes are disrupted by lead poisoning in the synthetic pathway?

A

glycine + succinyl coA

delta-ALA dehydratase and ferrochetalase are disrupted by lead poisoning

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26
Q

Which enzymes are deficient in acute intermittent porphyria and cutanea tarda?

A

acute intermittent porphyria: PBG deaminase

cutanea tarda: uroporphyrinogen decarboxylase

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27
Q

Why is hyperbilirubinemia dangerous for newborns?

A

It can cross the BBB cuz its not developed yet

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28
Q

Describe the breakdown pathway of hemoglobin.

A

hemoglobin –> biliverdin –> unconjugated bilirubin –> conjugation in liver –> excretion in urine

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29
Q

PRPP and glutamine are needed for _______ synthesis.

A

purine

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30
Q

______ is the branch-point in purine synthesis where either AMP or GMP can be produced.

A

IMP (inosine monophosphate)

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31
Q

Tetrahydrofolate is needed for synthesis of ________ (purines or pyrimidines).

A

purines

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32
Q

Which enzyme is deficient in Lesch-Nyhan syndrome and what pathway is it involved in?

A

HGPRT: needed for purine salvage (XMP and GMP)

note that AMP is salvaged with APRT enzyme

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33
Q

What are the starting materials for pyrimidine synthesis?

A

HCO3- and glutamine

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34
Q

Orotic aciduria is a result of a deficiency of ________ (enzyme) in the _________ biosynthetic pathway.

A

UMP synthase in the pyrimidine synthesis pathway

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35
Q

Describe the biochemical mechanisms by which severe combined immunodeficiency (SCID) inhibits lymphocyte expansion.

A

Deficient adenosine deaminase (involved in the breakdown of nucleic acids) leads to a build-up of adenosine, which is enzymatically converted to ATP and dATP, which in turn inhibit ribonucleotide reductase, so no deoxynucleotides can be made. No DNA = no cell division, no lymphocyte expansion.

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36
Q

Gout is characterized by an accumulation of ______ _______ crystals in joints.

A

uric acid

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37
Q

_____ _____ is produced by parietal cells in the stomach and is necessary for the absorption of B12 in the distal ileum.

A

Intrinsic factor is needed for B12 absorption in the distal ileum

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38
Q

Explain how a B12 deficiency can cause megaloblastic anemia.

A

B12 is needed for methionine synthase (homocysteine –> methionine). This reaction also needs N5-methyl THF. If there is no B12 to run the methionine synthase reaction, there is no way to regenerate THF from N5-methyl THF, so the folate is “trapped.” THF is needed for purine synthesis. No purines = no DNA synthesis = no erythroid cell differentiation

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39
Q

Sulfonamides inhibit ______ synthesis in bacteria.

A

folate

40
Q

What does an increase in neuronal diameter do to internal resistance?

A

It lowers internal resistance

41
Q

What does myelin do to membrane capacitance?

A

It lowers capacitance

42
Q

What does myelin do to membrane resistance?

A

It increases membrane resistance

43
Q

What is the role of calcium in neurotransmitter release?

A

When an AP reaches the bouton, voltage-gated Ca2+ channels open and calcium flows into the cell, which causes neurotransmitter vesicle fusion (mediated by SNAREs) and release into the synaptic cleft.

44
Q

Fast EPSPs are mediated by which neurotransmitter(s)?

A

glutamate (CNS) and ACh

45
Q

Fast IPSPs are mediated by which neurotransmitter(s)?

A

GABA and glycine

46
Q

Slow EPSPs are mediated by which neurotransmitter(s)?

A

ACh

47
Q

Slow IPSPs are mediated by which neurotransmitter(s)?

A

GABA

ACh

48
Q

What is the difference between ionotropic and metabotropic receptors?

A

Ionotropic receptors also act as ion channels (fast!)

Metabotropic receptors work through GPCRs (slow).

49
Q

Nicotonic ACh receptors are _______ (ionotropic or metabotropic) and muscarinic receptors are ________ (ionotropic or metabotropic).

A

Nicotinic - ionotropic

Muscarinic - metabotropic

50
Q

Neurotransmitters are cleared from the synaptic cleft by which two major mechanisms?

A

enzymatic degradation and endocytotic reuptake (with clathrin)

51
Q

Electrical synapses between cells use ______ ______.

A

gap junctions

52
Q

The liver expresses ________ glucose receptors, which are not sensitive to insulin levels.

A

GLUT2

53
Q

Which tissues express GLUT4 receptors (insulin sensitive)?

A

Muscle, adipose

54
Q

Describe the glucose-alanine (Cahill) cycle.

A

Muscle protein is broken down for energy, nitrogens are plopped onto pyruvate to make alanine, alanine is sent in bloodstream to the liver. Liver takes nitrogen off alanine to make pyruvate again, and does gluconeogenesis to make glucose, which is sent back to muscle for use.

55
Q

Does the brain rely on blood glucose or ketone bodies for energy?

A

Yeah

56
Q

Is the liver the major regulator of blood glucose?

A

Yeah

57
Q

Does epinephrine promote glucose mobilization?

A

Yeah

58
Q

From which root (ventral or dorsal) do all motor neurons (somatic and autonomic) exit the spinal cord?

A

ventral

59
Q

Where would you find cell bodies of sensory neurons? What morphological type of neurons are they?

A

Dorsal root ganglia. They’re pseudounipolar neurons.

60
Q

How many cervical nerves are there? How many cervical vertebrae are there?

A

8 nerves, 7 vertebrae

61
Q

If you have a disc herniation at the C5-C6 disc that compresses the spinal cord, which levels will be affected?

A

C7 and distal nerves will be affected

62
Q

At which level does the spinal cord end?

A

L1/L2

63
Q

The filum terminale is an extension of the ______ ______ that anchors the spinal cord to the coccyx.

A

dura mater

64
Q

Which neurotransmitter is used at all autonomic presynaptic synapses?

A

ACh

65
Q

Which neurotransmitter is used at parasympathetic postsynaptic synapses?

A

ACh

66
Q

Which neurotransmitter is used at sympathetic postsynaptic synapses?

A

Norepinephrine (except for sweat glands use ACh)

67
Q

The sympathetic nervous system is called the “thoracolumbar” system because its nerve cell bodies live in the ______ horns from spinal segments ____ to ____.

A

lateral horns from T1 to L2

68
Q

For organs in the abdominal cavity, sympathetic preganglionic synapses occur in the ________ ganglia.

A

prevertebral (preaortic)

69
Q

For organs in the thoracic cavity, sympathetic preganglionic synapses occur in the ________ ganglia.

A

paravertebral ganglia (chain ganglia/sympathetic trunk)

70
Q

Where do parasympathetic nerve cell bodies live?

A

CN III, VII, IX, and X, and in sacral segments S2, 3, 4 (craniosacral)

71
Q

How do visceral afferents cause referred pain?

A

Pain from organs is carried to the spinal cord, and synapses occur in the spinal cord at levels that also synapse with pain receptors from other body parts, so you think the pain is coming from the other body parts.

72
Q

Primary curvatures are kyphoses of the _______ and ______ spine, while secondary curvatures are lordoses of the _______ and ______ spine.

A

primary: kyphoses of the thoracic and sacral spine
secondary: lordoses of the cervical and lumbar spine

73
Q

What is the difference between a bulging disc and a herniated disc?

A

Bulging is when the annulus fibrosus bulges into the spinal canal. Herniation is when the nucleus pulposus herniates into the spinal canal.

74
Q

The main function of HDL is to take up excess ________.

A

cholesterol

75
Q

How do statins work?

A

They inhibit HMG-CoA reductase, which converts HMG-CoA to mevalonic acid (regulated step in cholesterol synthesis)

76
Q

Which apoprotein is needed for LDL binding to LDL-R?

A

B100

77
Q

After LDL binds LDL-R, what happens?

A

The LDL is endocytosed –> lysosome –> cholesterol liberation

78
Q

Can cholesterol in a cell inhibit synthesis of LDL-R, promote LDL-R endocytosis, and inhibit HMG-CoA reductase?

A

Yeah

79
Q

Familial hypercholesterolemia is characterized by inability to endocytose LDL. Name three mechanisms by which this problem can occur.

A
  1. Defective/missing LDL receptor (misfolded and degraded, or present but broken)
  2. Mutated Apo-B100
  3. Problem with endocytosis (ex. PCSK9: LDL-R binds LDL but can’t endocytose it)
80
Q

What is the equation for prevalence?

A

Prevalence = # of people with disease / # of people in population

81
Q

What is the equation for incidence proportion?

A

Incidence proportion = # of new cases / # of people initially free of disease

82
Q

What is the equation for incidence rate?

A

Incidence rate = # of new cases / person-time

83
Q

What is the relationship between prevalence and incidence?

A

Prevalence = incidence x duration

84
Q

Where are astrocytes found? Name three things that they do.

A

Found in the CNS

  1. Give nutrients to CNS neurons from blood vessels
  2. Provide structural rigidity
  3. Regulate the ECM
85
Q

What cytoskeletal protein is used by astrocytes? Why is this clinically important?

A

Glial-fibrillary acidic protein (GFAP). Expression is increased when neurons are under stress; can be a tumor marker.

86
Q

What cell type makes CSF and lines the ventricles of the brain?

A

Ependymal cells

87
Q

What are the small, thorny macrophages that live in the CNS called?

A

Microglia

88
Q

Degeneration of an axon distal to the damage site is called…?

A

Wallerian degeneration

89
Q

What is chromatolysis and when is it seen?

A

Dispersal of ribosomes (no more Nissl bodies) seen when neurons are under stress/damaged.

90
Q

Bone is mostly made up of what type of collagen?

A

type I

91
Q

_______ fibers connect periosteum to bone.

A

Sharpey’s

92
Q

Describe the two layers of the periosteum.

A

Outer layer is fibrous, inner layer is cellular and responsible for appositional growth.

93
Q

What is the difference between Haversian canals and Volkmann’s canals?

A

Haversian canals run longitudinally and Volkmann’s canals run transversely to the bone

94
Q

What does parathyroid hormone do regarding calcium and bone homeostasis?

A

It tells osteoblasts to make RANKL, RANKL tells osteoclasts to resorb bone and increase blood [Ca2+]

95
Q

Long bones grow in length via _______ growth.

A

Interstitial

96
Q

Increase in bone girth occurs via _______ growth.

A

appositional

97
Q

What is the difference between endochondral and intramembranous ossification?

A

Endochondral is when a cartilage model is formed first - happens for the long bones.

Intramembranous is when osteoid is laid down - no cartilage first. Flat bones.

MS1 - MCBD (17 decks)

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