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Sem 1 Flashcards

1
Q

What temperature is classed as hypo and hyperthermia, and what are the consequences?

A

Below 35 - impaired temp regulation, cardiac fibrillation

Above 38.3- fever , disorientation and febrile convulsion, coma and death

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2
Q

What are the three common types of hormones and their roles?

A

Amines- fast, short half life, PM receptor, alter 2nd messengers
Peptides/proteins- half life minutes, act for hours, trigger 2nd messengers
Steroids- hours half life, days action, cytosolic and nuclear, control transcription and mRNA stability

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3
Q

What is the role of anticonvulgants?

A

Block Na current in VG Na channels. Treat epilepsy

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4
Q

How does reuptake of Nor, glutamate, serotonin occur?

A

Use NA gradient as secondary active transport

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5
Q

What is fluoxetine?

A

SSRI an antidepressant . Get elation and sticky platelets.

Block sodium symport , less K leaves cell.

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6
Q

What is the structure of a G protein and where does ligand bind?

A

Single polypeptide , 7TM spanning regions, n terminal extracellular , c intra. Binds between 2/3 and at the N terminal region. Interaction leads to binding of GTP to alpha subunit causing dissociation. Interacts with second messenger. Intrinsic gtpase activity reverses.

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7
Q

How does cholera toxin interfere with G protein function?

A

Modifies Galpha s so unable to hydrolyse GTP, constant activation and high cAMP, high pKa activation. Phosphorylation of CFTR, efflux of cl. Loss of water and dehydration and diarrhoea in stools.

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8
Q

How does pertussis toxin affect the body?

A

Interacts with Gi , prevents GDP to GTP, no dissociation. No inhibition. Leads to hypoglycaemia and immune system inhibition. Increase camp affects signalling

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9
Q

What are the calcium concentrations in cells , extracellular and ER?

A 
Extra = 10-3
Intra = 10-7
ER = 10-4

Calcium released from PLC pathway and Ip3 R but need PKC activation by calcium to maintain contraction

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10
Q

Where do adrenaline and noradrenaline bind in vasculature an what does Ach bind in lungs ?

A

Noradrenaline alpha 1
Adrenaline higher affinity for B2, but at high conc activate alpha 1
B2 is dilation alpha 1 is constriction
Ach para bing M3 bronchoconstriction

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11
Q

How does morphine work?

A

Binds mew opioid receptor Gi G protein. YB subunit blocks VOCC

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12
Q

How is net rate of molecule movement through a membrane calculated?

A

J=Permeability coefficient x (C1-C2) concentration gradient

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13
Q

What does the NA/K ATPase work?

A

Alpha subunit binds ATP and Ion
Beta directs protein to membrane
3NA in 2K out

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14
Q

How does glucose increase lead to potassium release?

A

Glucose enters through 2NA glucose symport. Increased NA less NAKATPase activity , higher intra K , depolarisation , insulin release.

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15
Q

What acid extruders do we have?

A

NA/H antiport exchanged NHE. Regulates cell volume too. Responds to growth factor.

Na/H/HCO3-/Cl- . H+ and Cl- leave. This is the NA dependent CL/HCO3 exchanger

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16
Q

What base extruders do we have?

A

HCO3-/ CL- exchanger or anion exchanger

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17
Q

How do cells resist swelling?

A

Conductive system of K+ and Cl- channels , amino acids

Cotransport (cl-/HCO3 in) (K+out/ H+ in ) , H+ and HCO3 make H2CO3 which leaves cell as co2 and water follows

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18
Q

How does cell resist shrinking?

A

Conductive : Na Ca channels but not good as very charged
Contransport: CO2 in reverse of swelling but instead Na exchanges not K but H+
Pump glucose in with NA

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19
Q

What are the stages of kidney nephron filtration?

A

Proximal tube
Thick ascending limb
Distal convoluted tubule
Cortical collecting duct

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20
Q

What happens in the proximal tube?

A

Bicarbonate reabsorption to maintain buffer
Na and water retention
Renal control of Na is treatment for mild hypertension

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21
Q

What happens in the thick ascending limb?

A

Na reuptake
NKCC2 channels uptake into cells than NA/K atpase into blood. Loop diuretic block this
Renal outer medullary K channel move k back into TAL to maintain NKCC2

22
Q

What happens in the distal convoluting tubule?

A

ENaC (Na) moves Na into cells and so does NCCT(NA/Cl symport)
Thiazides block NCCT
Amiloride blocks enac
Both diuretics

23
Q

What happens in the cortical collecting ducts?

A

Aquaporin moves water directly 5x faster
Spironolactone inhibits Romk ,enac, Na pump, k pump
Aldosterone activates ADH which increases Romk, enac, aquaporin, na and k pump water retention.
Alcohol prevents ADH production

24
Q

What do we give to treat lactate acidosis?

A

Sodium bicarbonate

25
What are the membrane potentials if they are only permeable to K, Cl-, Ca, Na?
K -95 Cl -95 Ca +122 Na +70 K dominates
26
What is the Goldman Hodgkin equation?
Calculates the membrane potential based on multi ions and their permeability
27
What are slow and fast synaptic transmission mechanisms ?
Slow- G protein and intracellular messengers Fast- excitatory or inhibitory , transmitter opens ion channels and leads to depolarisation and hyperpolarisation. Excitatory and inhibitory post synaptic potential
28
What determines the amount of charge needed for action potential?
Capacitance of membrane
29
What is the structure of the VGNA channel?
One polypeptide 1 alpha subunit, 6 transmembrane regions, 4 is voltage sensor. Positive charge against positive amino acid causes 5/6 pore region to open. 6/1 inactivation loop acts as a Na plug and hyperpolarisation to release. KVG channel is 4 alpha subunit , but same structure as NA. Quarter in size, four times as much.
30
What order do local anaesthetics block?
Small myelinated Unmyelinated Large myelinated Blocks in use dependent manner VGNA channels hydrophilic and use independent hydrophobic through membrane
31
What is the length constant for an current?
The distance for action potential to fall by 1/e 37% of original value
32
What is myelin and what produces it?
Oligodendrocytes and Schwann cells. Fatty white substance , protein cholesterol, water and lipid. Optimum conductance velocity d/D= 0.7
33
What disease involves myelin?
MS in CNS Guillian barre in PNS Charcot Marie tooth disease in PNS
34
What is used to block l type calcium channels?
Nifedipine
35
Discuss competitive and depolarising blockers of nAChR?
Competitive - d-tubocurarine, binds but can be overcome | Depolarising- succinylcholine - maintains depolarisation and leads to inactivation
36
What is myasthenia graves?
Autoimmune abs target of nAChR in skeletal muscle .Patient weak muscles. EPP fail to reach amplitude. machr in parasympathetic system
37
What is the equation for molarity?
G/L divided by Mwt. Even when conc the same number of molecules around a receptor can very a lot
38
Why might we use a partial agonist opioid drug?
Full agonist causes respiratory depression. Buprenorphine has high affinity and low efficacy but less side effects.
39
What do we use to treat heroin addiction?
Diamorphine is heroin a full agonist of opioid receptor. Buprenorphine is a partial agonist lower efficacy but acts as a antagonist to heroin. Referee to as mixed. Used in gradual withdrawal, still gives some withdrawal effects.
40
What are the measures of agonism and antagonism?
ECa50 and IC50
41
What do we use to reverse respiratory depression caused by opioids ?
Naloxone, antagonist high affinity competes
42
What irreversible antagonist is used to treat pheochromocytoma?
Phenoxybenzamine alpha 1 antagonist treats hypertension prevents adrenaline binding
43
What are the main methods of drug absorption?
Passive diffusion- lipophilic drugs, weak acids and bases Facilitated drugs- organic anion and cation transporters. Have a net charge, move based on electrochemical gradient. Secondary active- transported with Na+ or H+ ions
44
What factors affect drug absorption?
``` Gi length Drug lipophilicity PKa Solute Carrie proteins OAT OCT secondary active Blood flow Gi motility Food ph, low ph can destroy some drugs ```
45
What is first pass metabolism?
Phase 1 enzyme- cytochrome p450, increase ionic charge, activate prodrugs like codeine, genetic polymorphism, 6 isozymes metabolise 90% of drugs. Increased translation or decreased degredation can reduce plasma levels of drugs. Concurrent drug administration can inhibit p450 Phase 11 enzyme - conjugated, cystolic enzymes, increase ionic charge enhance renal elimination Products most go to kidney , heavy go to gallbladder Reduces systemic availability F oral (oral availability)- =AUCoral/AUCIV, loser than 1 is better
46
How do we calculate the apparent volume distribution of a drug?
Drug dose divided by plasma drug concentration at T=0. In litres or litres per kg
47
How are drugs eliminated in the kidney?
Glomerula filtration- 20% blood drug enter via bowmans capsule Proximal tubular secretion- 80% blood, high OAT, OCT and active, water reabsorbed Distal tubular reabsorption - passive reabsorption from intraluminal space of lipophilic and ionised drugs, enters urine through collecting duct
48
What is drug clearance?
Volume of plasma that is cleared of drug per unit time. CAnt ever be completely , referenced to hepatic and renal
49
How do we calculate drug half life?
0.7 x vd / CL (ml per minute) . Linear on a log scale as long as less drug molecules than active sights. Get zero order kinetics if high dose of drug, not enough active sites rate doesn't increase. Drugs whose therapeutic dose are near zero order kinetics can be dangerous as more adverse effects, toxicity, hard to calculate half life, more drug interactions. A problem in infants and elderly and those with organ failure or cancer. Examples alcohol mdma Prozac.
50
How are adrenaline and noradrenaline made?
Tyrosine dopa dopamine noradrenaline, adrenaline (adrenaline only in adrenal medulla Noradrenaline not taken into vesicle metabolised by MAO and COMT

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