Lecture 3: Ion Flux Flashcards Preview

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Flashcards in Lecture 3: Ion Flux Deck (44):
1

A small biotech company in Boston recently created a more potent version of digoxin for treating patients with CHF. Which of the following is the direct protein target to which this drug binds to in order to exert its effect on cardiomyocytes?
A) Sodium calcium exchanger
B) Sodium potassium ATPase
C) Sodium channel
D) Calcium ATPase
E) Calcium channel

B) Sodium potassium ATPase

2

A 16 year old boy was brought to the emergency room by his mother due to severe abdominal pain. She told the physician that the pain seemed to come in waves. Ultrasound of the abdomen revealed kidney stones. After further testing a diagnosis of cystinuria was made. Transport of which AA is defective in this condition?
A) Cysteine
B) Cystine
C) Glycine
D) Histidine
E) Methionine

B) Cystine

3

The plasma membrane is semi-permeable. What is it permeable to?

Lipophilic molecules, move easily

Ex. Steroid hormones

4

What is the PM impermeable to?

Hydrophilic/polar molecules

- Needs a specific transport mechanism

5

What ions are high inside the cell?

Potassium

6

What ions are high outside the cell?

Na+, Cl-, Ca2+

7

____________ transport is energy-independent, where molecules move down their concentration gradients

Passive

8

__________ transport is energy-dependent where molecules move against their concentration gradient

Active

9

Where do P type ATPases phosphorylate a protein?

On conserved aspartate residue

10

The difference between ABC transporters and P-type ATPases is in the phosphorylation. What is the difference?

The phosphate covalently attaches to the protein when a P-type ATPase is used but never covalently attaches in an ABC transporter

11

Sodium calcium exchanger is an example of what type of secondary transporter?

Antiporter

12

Lactose permease is an example of what type of secondary active transporter?

Symporter

13

Mito calcium transporter is an example of what type of secondary active transporter?

Uniporter

14

The ________ _________ transporter is present n the epithelial cells that line the small ntestine and renal tubules and mediates UNIdirectional movement. Across small intestine and renal tubules

Sodium glucose transporter (SGLT1)


- Movement of Na+ occurs down its gradient, this provides energy to move glucose against its gradient

**The Na+ gradient is reset by the Na+/K+ATPase

15

What does the Na+/Ca2+ exchanger function to do?

Maintain low levels of intracellular calcium levels

16

The Na+/Ca2+ exchanger imports ________ down their gradient and exports _____ against the gradient

3 Na+; 1 Ca2+

- Uses the energy stored in the Na+ gradient

17

Where is SGLT1 located on an enterocyte?

Apical side

18

What molecules does SGLT1 facilitate the movement of and what type of transport is this?

Glc, Gal, Na+

Secondary active

19

What part of the enterocyte is GLUT5 located on>

Apical side

20

What molecules does GLUT5 facilitate the movement of and what type of transport is this?

Fru

Facilitated diffusion

21

Where is GLUT2 located on an enterocyte?

Basolateral side

22

What molecules does GLUT2 facilitate the movement of and what type of transport is this?

Glc, Gal, Fru

Facilitated diffusion

23

Where is Na+/K+ ATPase located on an enterocyte?

Basolateral side

24

What is the movement of Na+ and K+ through the Na+/K+ ATPase located on an enterocyte

3 Na+ out of enterocyte to the bloodstream and 2K+ into enterocyte from the bloodstream

25

Where do monosaccharides derived from the digestion of polysaccharides such as starch and disaccharides such as sucrose and lactose in the diet need to be transported from?

From the intestinal lumen, across the enterocyte into the blood stream

26

The process of transporting monosaccharides from the intestinal lumen, across the enterocyte and into the blood stream is facilitated by what types of transport?

Facilitated diffusion and active transport

27

What is the first step in neurotransmission?

Sodium channel on presynaptic neuron opens and begins the AP

28

What happens after the sodium channel opens on a presynaptic neuron and an AP has been initiated?

The potassium channel opens on the presynaptic neuron to allow calcium to leave the cell

29

What happens after the potassium channel opens on the presynaptic neuron during neurotransmission?

Voltage gated Ca2+ channel on presynaptic neuron opens causing the formation of vesicles and the release of them into the synapse

30

What happens after the voltage-gated calcium channels open on the presynaptic neuron during neurotransmission?

Ligand-gated ion channels on postsynaptic neuron opens

31

What happens after ligand gated ion channels open on post synaptic neurons during neurotransmission?

Na+/K+ ATPase on postsynaptic neuron is actiated

32

What happens after the Na+/K+ ATPase on the postsynaptic neuron is activated during neurotransmission?

The sodium calcium exchanger is activated on the post synaptic neuron

33

What happens after the sodium calcium exchanger is activated on the postsynaptic neuron durng neurotransmission?

The plasma membrane Ca2+ ATPase on the presynaptic membrane is activated

34

Cystic fibrosis is caused by a mutation in what?

CF transmembrane conductance regulator (CFTR) gene -> Results in defective CFTR protein

**CF is an autosomal recessive disorder

35

What is CFTR?

A chloride channel that mediates the active transport of Cl- from inside the cells to the outside in airways and sweat ducts

36

Defective CFTR causes a buildup of what?

Cl- and salt inside the airway epithelial cells creating a thick mucous secretion in lungs that interferes with breathing and leads to secondary microbial infections

37

What is cystinuria caused by?

A defect in the transport responsible for uptake of dimeric AA cystine and other dibasic AAs Arg, Lys, and Ornithine

**Cystinuria is an autosomal recessive disorder

38

What is the result (buildup) of Cystinuria?

Results n formation of cystine crystals or stones in the kidney -> patients present with renal cholic (abdominal pain that comes in waves and is linked to kidney stones)

39

What causes Hartnup disease?

A defect in transporter for nonpolar or neutral AAs (Ala, Val, Thr, Leu, Trp, etc.)

**Hartnup disease is autosomal recessive!

40

Where is the transporter that is responsible for Hartnup disease located?

Found primarily in kidneys and intestine

41

_____________ deficiency leads to deficiency of serotonin

Tryptophan

- This is found in Hartnup disease

42

What are the symptoms of Hartnup disease?

Cerebellar ataxia (lack of muscle coordination), photodermatitis and photosensitivity

43

____________ ___________ such as ouabain and the more lipophilic drug digoxin act as cardiotonic (contraction inducing) drugs

Cardiac glycosides

44

What do cardiac glycosides (such as digoxin) inhibit?

The Na+/K+. ATPase on cardiac myocytes

- This leads to increase in intracellular Na+ and a secondary increase in Ca2+ due to slowing of the exchanger -> increased sarcoplasmic Ca2+ results in stronger excitation contraction of heart muscle with each AP