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MS1 - MCBD > Week 3 Review > Flashcards

Week 3 Review Flashcards

1
Q

You made a drug that is a weak acid with a pKa of 6.9. You designed it to be absorbed by GI epithelial cells in the duodenum, where the pH is ~7.5. Will your drug easily cross the cell membrane?

A

Nope. Your drug has a lower pKa than the environment; it therefore is a stronger acid than the environment and will donate a proton –> A- + H+. Charged ions don’t like to cross membranes.

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2
Q

If a drug is in an environment where its pKa = pH of the environment, what proportion of drug is ionized?

A

50%!

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3
Q

What is LogP?

A

It indicates how lipid-soluble a drug is. High LogP = high solubility.

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4
Q

What are the two phases of drug metabolism?

A

Phase I and II

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5
Q

What enzymes are involved in Phase I drug metabolism? What do they do?

A

Cytochrome P450 enzymes add/unmask a polar functional group such as -OH, -SH, or -NH2 to increase reactivity.

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6
Q

What enzymes are involved in Phase II drug metabolism? What do they do?

A

Transferases conjugate the reactive group from Phase I with a large polar group. This increases water solubility and reduces the chance of drug reabsorption in the renal tubule.

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7
Q

Howard wants to be able to drink more beer without getting hungover. But since he is half asian, he underexpresses aldehyde dehydrogenase, which converts acetaldehyde (hangover molecule) to acetate –> acetyl coA. Howard would benefit from a(n) _________, which would increase his expression of this enzyme.

A

An inducer.

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8
Q

Cytochrome P450 enzymes are most commonly found in which organ? Specifically where in the cell are they?

A

Liver - on smooth ER

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9
Q

Name three specific CYP450 enzymes that play a role in drug metabolism.

A
  1. CYP2C9
  2. CYP2D6
  3. CYP3A4
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10
Q

What does p-glycoprotein do? What is the clinical significance of this?

A

It pumps drugs out of cells using ATP.

Inhibition of this –> more drug in cells.

Cancer cells may overexpress P-gp –> drug resistance

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11
Q

Drugs that are eliminated following zero-order kinetics are eliminated at a ________ rate.

A

constant rate (ie 2mg/L/hr)

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12
Q

Describe first-order drug elimination.

A

First-order kinetics = half life process; drug concentration is cut in half per unit time.

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13
Q

Intravenous, intramuscular, interosseous, and subcutaneous drug injection are all examples of the _________ route of administration.

A

parenteral

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14
Q

Oral, rectal, and buccal drug administration are all examples of the __________ route of drug administration.

A

enteral

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15
Q

What will have higher bioavailability: a drug administered parenterally or enterally?

A

A drug administered parenterally because it bypasses the liver (no first-pass metabolism) and goes straight into circulation.

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16
Q

What are the five pharmacokinetic equations we need to memorize?

A
  1. t 1/2 = .693 • Vd / CL
  2. CL = dose rate/Cp (steady state)
  3. Vd = dose / Cp
  4. loading dose = Vd • Cp / F
  5. maintenance dose = Cl • t • Cp / F
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17
Q

How many half lives does it take to eliminate a drug from a system and/or reach steady-state?

A

4-5

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18
Q

Amylase breaks down ________ and is made by the ________ and _______ ______.

A

breaks down carbohydrates, made by the pancreas and salivary glands

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19
Q

Describe how intestinal epithelial cells absorb glucose.

A

They use a Na+/glucose cotransporter. Na+ travels down its conc. gradient while glucose travels against its conc. gradient.

The Na+/K+ ATPase on the basolateral side of the cell is required to keep Na+ in the cell low so the Na+/glucose cotransporter can do its thing.

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20
Q

In a muscle that is undergoing anaerobic metabolism, glucose is converted to ________, which is further oxidized to ________.

A

glucose –> pyruvate –> lactate

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21
Q

In the Cori cycle, lactate produced by muscle goes in the bloodstream to the _______ for conversion back to _______.

A

liver takes lactate and converts it back to glucose (acetyl CoA is an intermediate)

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22
Q

What is the net ATP yield from glycolysis alone?

A

2

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23
Q

What product of glycolysis is used in the electron transport chain to ultimately build up a proton gradient?

A

NADH

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24
Q

Name three organs that store glycogen.

A

Liver, muscle, kidneys

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25
Glycogen stores are depleted after roughly ____ hours of fasting.
30
26
The first step in glycogen synthesis is glucose-1-P. The second step is...?
2nd step is a glucosyltransferase reaction (addition of a UDP to glucose) to activate the glucose
27
Name the two major enzymes in glycogen synthesis (after UDP addition).
glycogen synthase and branching enzyme
28
Which two enzymes are involved in glycogen breakdown? What does each one do?
glycogen phosphorylase-a breaks alpha-1,4 linkages up until 5 units away from a branching point. Note that it is active when phosphorylated (fasting state - glucagon present - glucagon phosphorylates everything) debranching enzyme breaks alpha-1,6 linkages (the branches)
29
Glucokinase is found primarily in the _______ (an organ). Describe its kinetic properties (Km, Vmax) with respect to hexokinase.
glucokinase is in the liver it has a much lower affinity (higher Km) than hexokinase but has a much higher Vmax than hexokinase.
30
What does glucose-6-phosphatase do? What is the disease called when you don't have it?
It converts glucose-6-P to glucose (last step in gluconeogenesis). Disease is called Von Gierke's/glucose-6-phosphatase deficiency
31
Name 5 symptoms of Von Gierke's disease and explain the physiological/biochemical basis for each.
1. Hypoglycemia: glucose is unable to enter the bloodstream 2. Hyperuremia: high glucose-6-P concentrations increase the forward reaction of the pentose phosphate pathway, resulting in lots of purines. Purine degradation --> high uric acid concentrations. 3. Lactic acidosis: high glucose-6-P concentrations increase the forward reaction of glycolysis. However, glycolysis is “over-run” causing a buildup of pyruvate and NADH. To continue glycolysis, NADH reduces pyruvate to lactic acid. 4. Hyperlipidemia: high glucose-6-P concentrations increase the forward reaction of glycolysis, which ultimately resulting in an increase of acetyl-CoA concentration. The backed up Krebs cycle forces triglyceride synthesis --> doll face (chubby cheeks from excess fat storage) and xanthomas. 5. Hepatomegaly: high glucose-6-P concentrations increase the forward reaction of glycogenesis.
32
How does neutralization of reactive oxygen species relate to the pentose-phosphate pathway?
The PPP generates NADPH, which is used to reduce oxidized glutathione --> reduced glutathione. Reduced glutathione is used to convert peroxides to water.
33
What does superoxide dismutase do?
Turns O2- into H2O2 (hydrogen peroxide) for subsequent reaction by glutathione reductase --> H20
34
What type of glucose transporters are found on muscle and adipose cells?
GLUT4
35
Are GLUT4 transporters found in the liver?
Nope
36
Explain the correlation between glucose-6-phosphate DH deficiency and increased RBC susceptibility to oxidative stress.
No G-6-P DH means that the PP pathway can't run --> no NADPH to deal with ROS --> denaturation of cytoskeletal proteins in RBCs --> loss of cell shape --> lysis in microvasculature --> Heinz bodies on blood smear
37
Name four things that can cause oxidative stress.
1. Infection 2. Fava beans 3. Sulfa drugs 4. Antimalarial drugs
38
Irreversible, non-enzymatic addition of a sugar on the N-terminal end of a protein is called ________.
glycation
39
What is HbA1c and what is its clinical significance?
HbA1c is glycated hemoglobin. Used clinically to measure a person's glycemic status over the long-term (~4 months)
40
If someone has recently had dialysis or a blood transfusion, would taking their HbA1c level be a good idea?
Nope
41
How are you going to remember the Ras/ERK pathway for tyrosine kinase receptor activation?
After ligand binding and tyrosine residue auto-phosphorylation... Grab (Grb2) help (SOS guanine exchange factor) Ras, Ras goes and gets his twin brother Raf and they both go get Dr. MekErk.
42
What does ERK 1/2 do?
It is a master cell cycle regulator
43
What type of receptor are growth factor receptors? Which signaling pathway do they use?
Tyrosine kinase --> Ras/ERK pathway
44
Name three different type of G-proteins involved in GPCR signaling.
1. Gαs 2. Gαi/o 3. Gαq
45
Describe the events that occur in GPCR signaling from activation to termination of a Gαsβγ-coupled receptor.
1. Ligand binds to receptor 2. Gαs-GDPβγ comes over so the receptor can do a nucleotide exchange (GDP for GTP) 3. Gαs-GTP dissociates from βγ 4. Gαs-GTP activates adenylate cyclase. 5. cAMP concentration increases 6. cAMP activates PKA 7. PKA phosphorylates -OH groups on serine and threonine residues 8. GTPase on the Gαs hydrolyzes GTP --> GDP to turn off.
46
What does Gαi/o do?
Inhibits adenylate cyclase --> decrease in cAMP
47
What does Gαq do?
Activates PLCβ --> PIP2 cleavage --> IP3 and DAG. IP3 binds to IP3 receptors on SER --> Ca2+ release. DAG activates PKC.
48
What do arrestins do to GPCRs?
They bind to phosphorylated GPCRs (GRKs phosphorylate them) to keep the receptor from activating G proteins or trigger endocytosis of the receptor.
49
How does Gαs turn off?
It has intrinsic GTPase activity that will hydrolyze GTP --> GDP to turn off
50
What kind of receptor is the insulin receptor? Outline the steps in the receptor pathway.
RTK Ligand binds --> autophosphorylation --> IRS1 binds to phosphorylated tyrosine residues and activates/phosphorylates PI3K --> PIP2 phosphorylation --> PIP3 --> AKT phosphorylation and activation
51
Phosphotyrosine residues of some RTKs can bind and activate ________, which also cleaves PIP2 to IP3 and DAG --> increase in Ca2+ and PKC activation. This is an example of _________.
PLCgamma this is convergence
52
Some Gαi and Gαq subunits can activate ADAM17, which can cleave EGFR ligands from cell membranes → activation of ________. This is called _________.
EGFR ligands bind to and activate RTKs. This is called transactivation
53
Where are steroid hormone receptors located in the cell?
Nucleus (stuck on promoter sequences on DNA) or in the cytoplasm.
54
Hormone receptors are _________ (monomers or dimers) that upregulate transcription after binding their hormone. Nuclear hormone receptors __________ transcription when they are not hormone-bound, and upregulate transcription once they bind their hormone.
Hormone receptors are dimers (or the cytoplasmic ones dimerize after binding hormone) Nuclear hormone receptors repress/downregulate transcription when not bound to hormone
55
Chylomicrons that are formed in intestinal epithelial cells enter the lymphatic system through ________.
lacteals
56
Which organ makes bile? What precursor molecule is used to make bile? What does it do?
Liver makes it from cholesterol. It emulsifies fats --> micelles
57
After chylomicrons enter the bloodstream, ______ (an enzyme) breaks TAGs down to FFAs and glycerol for uptake by cells like muscle cells and adipocytes.
LPL (lipoprotein lipase)
58
When the body needs to get some FFAs into the blood, ______ (an enzyme) in adipocytes breaks down TAGs into FFAs and glycerol for release into the blood. What does inulin do to this enzyme?
Hormone sensitive lipase. Insulin inhibits it
59
In the first step of ketone body synthesis, two ________ are combined to form acetoacetyl coA.
two acetyl coAs
60
Name two ketone bodies.
β-hydroxbutyrate and acetoacetate
61
Name the four cellular responses to stress.
1. Hypertrophy 2. Hyperplasia 3. Atrophy 4. Metaplasia
62
Loss of innervation can cause ________. The mechanism for this is self-degradation by lysosomal enzymes in a process called ________.
atrophy autophagy
63
The substitution of columnar epithelium for the stratified squamous epithelium at the squamocolumnar junction in the esophagus is an example of _________.
metaplasia
64
Name four morphological changes that occur during reversible cell injury.
1. ER dilation with detachment of polysomes 2. Plasma membrane swelling 3. Plasma membrane blebbing 4. Loss of microvilli
65
Name three bad things that reactive oxygen species can do to cells.
1. Lipid peroxidation 2. DNA fragmentation 3. Protein crosslinking
66
What does catalase do?
Turns hydrogen peroxide into water
67
What does superoxide dismutase do?
Turns O2- into hydrogen peroxide
68
Can vitamins somehow deal with ROS?
Yeah
69
What are the three fancy words for nuclear changes seen during irreversible cell damage? Briefly describe each.
1. Pyknosis: chromatin condensation 2. Karyorrhexis: fragmentation of nucleus (chocolate chip cookie) 3. Karyolysis: no more nucleus
70
Cells shrink during ________, whereas during ________ cells will swell.
apoptosis - cells shrink necrosis - cells swell
71
_________ necrosis results from ischemia/infarction in most tissues except in the CNS.
Coagulative
72
Preservation of the structural outline of dead cells is characteristic of which type of necrosis?
Coagulative
73
Coagulative necrosis in the lungs is called a "wet pulmonary infarct" because the lungs have a dual ______ _______.
blood supply
74
What tissues in the body predominantly undergo liquefactive necrosis?
Brain/CNS
75
Liquefactive necrosis is characterized by the release of lysosomal enzymes by _______ and ______ ______that digest the tissue.
neutrophils and dead cells
76
Can a bacterial abscess result in liquefactive necrosis? Why?
Yeah, cuz neutrophils come and try to eat everything.
77
Dry gangrene occurs is a type of _______ necrosis that occurs when peripheral tissue is infarcted. Superimposition of gangrene with an anaerobic bacterial infection results in...?
type of coagulative necrosis wet gangrene = dry gangrene + anaerobic infection
78
Why do TB/fungal infections result in caseous necrosis?
When macrophages eat M. Tuberculosis and fungi there is a release of lipids from bacterial cell walls.
79
Necrotizing granuloma is often seen with what type of infection? What are multinucleated giant cells often associated with?
TB! TB!
80
_________ necrosis is characterized by deposition of proteins like fibrin into blood vessel walls.
Fibrinoid
81
Malignant hypertension and immune vasculitis can lead to _______ necrosis.
fibrinoid
82
Fat necrosis typically occurs in the ________ (an organ) and is a result of digestive enzymes that liquefy fat membranes, leading to saponification and ________.
pancreas saponification and calcification
83
Briefly describe the sequence of events that occur during the intrinsic pathway of apoptosis.
1. Cell stress leads to leakage of cytochrome C from mitochondria. 2. Initiator caspases are activated. 3. p53 arrests cell cycle and activates Bax. 4. Bax is pro-apoptotic and inactivates Bcl2 (anti-apoptotic). 5. Without Bcl2, cytochrome C leaks out of mitochondria like crazy and binds to Apaf-1, forming the apoptosome. 6. Apoptosome activates executioner caspases.
84
Bax, Bak, Bid, and Bim are _________, whereas Bcl2 is ________.
pro-apoptotic Bcl2 is the only one we learned about that is anti-apoptotic
85
In the extrinsic apoptotic pathway, _____ or _____ bind to extracellular "death" receptors, leading to a signaling cascade that ultimately activates _________ for apoptosis.
Fas or TNF bind to receptors ultimately leads to activation of caspases
86
Arachidonate is released from _________ in cell membranes by the enzyme _________ for eventual use as signaling molecules.
glycerophospholipids/membrane lipids --> arachidonate phospholipase A2 is the enzyme
87
What are eicosanoids?
Eicosanoids are the signaling molecules that originate from arachidonate - prosgaglandins, lipoxins, and leukotrienes
88
Cyclooxygenase enzymes form which two major families of signaling molecules?
Prostaglandins and thromboxanes
89
True or false: COX-1 is constitutively expressed for homeostatic functions, while COX-2 expression is induced by inflammatory cytokines.
tru dat
90
What specific enzyme do corticosteroids inhibit?
Phospholipase A2
91
Lipoxygenases convert arachidonate to ________ and ________.
leukotrienes and lipoxins
92
NSAIDs inhibit which enzymes?
COX enzymes
93
Which two classes of eicosanoids generally have antagonistic effects?
Thromboxanes and prostaglandins
94
Which specific eicosanoid promotes vasodilation and decreases platelet aggregation?
PGI2 (prostacyclin)
95
Which specific eicosanoid causes histamine release from mast cells to induce bronchoconstriction and vasodilation?
PGD2
96
Which specific eicosanoid causes pain via sensitization of neurons, Na+ resporbtion in kidneys, and promotes house-keeping functions in gastric mucosa?
PGE2
97
Why can chronic NSAID use potentially cause gastric ulcers?
NSAIDs block COX enzymes --> no PGE2 production (PGE2 stimulates production of gastric mucosa)

MS1 - MCBD (17 decks)

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