Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FunMed Random > :))))))) > Flashcards

:))))))) Flashcards

1
Q

what are DEXA scans?

A

= two different, low energy x-ray sources; more precise and accurate calculation of density

a) the denser the bone the fewer the x-rays get to detector
b) used for diagnosis of osteoperosis (health condition that weakens bones)
c) can measure BMI and fat (more precise soft tissue measurements)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the different types of x-ray contrast media?

which makes tissue denser / less denser?

A

contrast media

  • use air to reduce density of hollow organ soft tissue (esp. GI system): creates negative contrast
  • e.g. can see large intestine more

OR
- can make tissue denser: liquid contrast media used are barium and iodine. non-toxic substances that contain elements of high atomic number - increased atomic number

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is method and what does barium sulphate and iodine highlight when used as contrast media?

A

1. barium sulphate:

  • highlight: GI system
  • method: swallow barium meal / enema

2. iodine - angiography

highlights: blood vessels
method: injection of iodine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does MRI show what are the two types?

A
  • v high soft tissue contrast
  • get two views: T1: normal anatomical structure and T2: good for pathology - can see water in bone (oedema)
  • *T1:**
    a) in brain: good gray/white matter contrast (fat: white = myelin, yellow = bone marrow etc)
    b) white is fat
  • *T2: pathology.**
    a) white is fluid (water)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the contrast medium for MRI?

which scan does it give more detail in?

A

gadolinium contrast

  • changes relaxation time of H ion spin
  • gives more detail in T2
  • gadolinium highlights breakdowns of blood brain barrier (normally cant go through them)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is doppler ultrsound?

A

shows blood flow direction:

- red = towards transducer

- blue = away from transducer

can measure blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which ducts drain into the duodenum?

A

pancreatic and bile ducts drain into duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how do you describe the different organs that located with the peritoneum?

A
  • organs stuck to the posterior abdomen wall: peritoneum covers the anterior surface of the organ (these organs = retroperiotneal organs)
  • organs that are full covered: intraperitoneal organs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the intraperitoneal folds?

A

GO: greater omentum fold

LO: lesser omentum fold

M: mesentery folds

MC: mesocolon fold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the epiploic foramen?

A

The epiploic foramen (also called the foramen of Winslow) is a passage between the greater sac (peritoneal cavity proper) and the lesser sac (omental bursa), allowing communication between these two spaces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is a drug?

A

any substance that interacts with a molecule or protein that plays a reg. role in living systems:

  • hormones: endogenous drugs
  • poisons
  • toxins are poisons of biological origins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which systems do inverse agonists work in?

A
  • only work on systems that are constitutively active: autonomic NS and histomine systems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which type of pharmocological antagonists:

  1. reduces agonist efficacy?
  2. reduces agonist potency?
A
  1. reduces agonist efficacy: non-competitive antagonist
  2. reduces agonist potency: competitive antagonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is a physiological antagonist? e.g.?

A

physiological antagonist: two drugs that have exactly opposite actions via different pathways

  • e.g. adrenaline when have allergic reaction (oppposite effect and pathways to histamines)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what type of drug is heparin?

A

chemical antagonist

  • binds to thrombin and inactivates it: stops thrombin to going to clotting cascade
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what do most drugs tend to be?

what are their properties?

A

weak acid or weak base (incomplete dissociation in water)

  • less H and negative charges (than strong acid)
  • undissociated form of acid / base
  • lipid soluble
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

a protonated (less dissociated / proton still there) weak acid is more X soluble?

an un-protonated (more dissociated / proton left) strong acid is more X soluble?

what happens to a protonated drug in the kidney?

A
  1. lipid soluble (liphophilic)
  2. water soluble (hydrophilic)
  3. almost all drugs are filtered by kidneys
    - protonated drug in kidney: reabsorbed back into blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what can affect the action of a drug?

what are the three sub categories of ^?

A

other drugs
- allosteric interactions: indirectly affect receptor -> affect efficacy or binding affinity

  • allosteric activators; increase activation of receptor
  • allosteric inhibitors: decrease activity of the receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is EC50?

A

Half maximal effective concentration (EC50) refers to the concentration of a drug, antibody or toxicant which induces a response halfway between the baseline and maximum after a specified exposure time.[1]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

where do drugs with large / small VD distributed to?

A

Large VD: distributed to tissues (fat / bones)

Small VD: distributed to blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

why may drugs stay in the blood as opposed to going to tissues? (2)

A
  1. molecule is too large to leave
  2. molecule binds preferably to v (albumin) / less to tissue proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the relationship between drugs working and proteins in the blood?

A
  • drugs are only active when unbound to proteins: unbound drugs are excreted quickly
  • drug bound to protein: pharmacologically inactive. non-diffusable, non-metabolised and non excreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what can happen to other drugs in body if you stop / start a drug that binds to proteins?

explain using warfarin (anticoagulant) and phenytoin (anti seizure) drugs

A

changes the level of the other protein bound drugs

e.g. warfarin (anticoagulant) and phenytoin (anti-seizure):

  • both normally bind to albumin (low VD)
  • for surgery: stop warfarin = more sites on albumin for phenytoin to bind
  • patient may have seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what also can effect the distribution of drugs? (for unbound drugs)

A
  • *unbound:**
  • capillary structure (blood brain barrier)
  • chemical nature of drug
  • blood flow through tissues (hydrophobic drugs0
  • presences of non active binding drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

name 4 clinically important receptors for each main type of receptors

A
  • ligand gated ion channel: GABAA receptor
  • g-protein coupled receptors: B-adrenoreceptor
  • kinase-linked receptors (like tyrosine): VEGF receptor
  • nuclear receptors: Oestrogen receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what type of molecules bind to intracellular receptor proteins?

how work?

give 4 e.g.s of these signal molecules

A
  1. steriod hormones
  2. thryoid hormones
  3. retinoids
  4. vitamin D

all hydrophobic signal molecules (hydrophilic drugs cant pass through cell membrane)

work by:

a) activating nuclear receptors: can bind to DNA regions
b) regulate gene transcription

28
Q

what is a) tolerance? b) tachyphylaxis?

how do ^ occur?

A

. tachyphylaxis: acute tolerance from rapid and repeated admin of drugs in short intervals (the image)

  1. tolerance: chronic longer term admin can reduce drug effect (e.g. alchohol)

mechanisms for tolerance or tachyphylaxis:

  1. receptor desensitized or loss of receptors
  2. receptor internalisation (degraded in lysosome)
  3. increased metaboloic degradation of drug
29
Q

how can we regulate amount of receptor on membrane?

A

via process of B Arrestin mediated internalisation:

  • B-arrestin binds to gcpr
  • B-arrestin desensitised
  • B-arrestin internalised
  • B-arrestin recyled
    OR
    -B-arrestin degraded
30
Q

what protein regulates the amount B-adrenoceptor at the membrane?

A

B-arrestin

31
Q

which method of administration of drugs goes straight into the CSF?

A

intrathecal (into CSF )

32
Q

which family of enzymes undergoes oxidation reaction in biotransformation?

A

cytochrome P450 family enzymes

33
Q

what happens to drugs if reabsorbed back into bile?

if phase 1 drug? phase 2 drug?

A

if goes back via bile:

  • goes back into GI system:

i) phase 1 drug: reabsorbed from GI system and goes back to liver 4 further met.
ii) phase 2 drug: exits via defecation

34
Q

what is clearance?

how calculate?

A

clearance: rate of elimination in relation to the drug concentration

clearance = rate of elimination (through urine) / concentration remaining (in blood plasma)

35
Q

how do u work out 1/2 life of a drug?

A
36
Q

what are two different types of dosing?

A
  • *loading dose:**
  • larger than normal dose
  • gets to therapeutic range quicker (emergencies)
  • mainly for drugs with large vol. of distribution
  • *maintenance dose:**
  • small fixed dose
  • maintains drug in therapeutic range
37
Q

what are NANC neurons?

where found?

what are the NTs used ? (probs dont need to know exact)

A
  • NANC = non-adrenergic non cholinergic neurons (NTs aren’t adreneric or cholinergic class)
  • location: peripheral tissues - smooth muscle in GI, airways and reproductive tracts
  • NTs: nitric oxide, ATP, 5HTP, neuropeptide Y
38
Q

explain structure of nicotinic receptor

where are the different a subunits found (awareness)?

A

- pentameric sodium ion channel

  • *- 2 alpha subunits:**
  • alpha 3 found on autonomic ganglia
  • alpha 1 found on neuromuscular junction
  • alpha 4 & 7 found in CNS

- 3 beta subuits

39
Q

which receptors do both acetylcholine & carbachol work on? what does this mean as a consq?

what is carbachol used to treat?

A
  • work at both nicotinic and muscarinic receptors: have an effect on both para and sympathetic NS
  • carbachol: treats glaucoma
40
Q

how many types of muscarinic receptors are there? which ones are inhib/ excitatory? - what are second messengers for inhibit / excitatory?

A

5 types:

  • M1 = excitatory: 2nd messenger = IP3 & DAG
  • M2 = inhibitory: 2nd messenger = cAMP
  • M3 = excitatory: 2nd messenger = IP3 & DAG
  • M4 and M5 in CNS (dont need to know)
41
Q

what does clostridium botulinum bacteria do?

how effect?

A

botulinium toxin (botox)

  • prevents ACh release: stops synapse signalling
  • irreversble
  • can be used for XS sweating, overactive bladder or muscle spasms
42
Q

what do sympathomimetics do?

what are two important classes?

A

produces a similar response as noradrenaline and adrenaline on the sympathetic NS

classes:

  • *i) monoamines
    ii) catecholamines (e.g. noradrenaline, adrenoline)**
43
Q

what type of receptors are adrenoreceptors? what does that mean ?

A

GCPR - can have excitatory or inhibitory response (depending on 2nd messenger system)

44
Q

what do cholinesterase inhbitors do?

A
  • stimulate GI function
  • cognitive enhancers (given to AD patients)
  • skeletal muscle activity
45
Q

what variants of adrenoreceptors are there? which are pre / post synaptic? excitatory or inhbitor?

A
  • *alpha**:
  • alpha 1: postsynaptic excitatory
  • alpha 2: presynaptic. inhbits further release of noradrenaline
  • *beta**:
  • beta 1: postsynaptic excitatory
  • beta 2: postsynaptic excitatory
  • beta 3: postsynaptic excitatory
46
Q

which muscarinic receptor is found in the eye, lung and gut? what is agonist / antagonist drug for thAT has effects on them

A

M3:

  • *i) eye:**
  • pilocarpine: pupil constrict (agonist)
  • tropicamide: pupil dilates (antagonist)
  • *ii) lungs:**
  • ipatroprium: lungs conflate (antagonist)
  • *iii) gut:**
  • neostgimine: gut more moveable (antagonist)
  • scopolamine: inhibits peristalsis - antispasmodic (agonist)
47
Q

what is thalidomide? how was it involved in tragedy?

A
  • prescribed as sedative or hypnotic:
  • S-thalidamide = effective sedative
  • *- R-thalidamide** = teratogenic (an agent that can disturb the development of the embryo or fetus​)

both given - made disformities

48
Q

what is ECM made from?

A

▪ Collagens: Major protein of the body (25%) and The ECM

▪Elastin: Provides elasticity and resilience to tissues such as the arteries, lungs, tendons, skin, and ligaments

▪Glycoproteins:
Molecules made up of proteins and carbohydrates e.g., laminin and fibronectin
Found on the surface of the lipid bilayer of cell membranes (cell surface)

▪Proteoglycans:
Molecules made up of a core protein attached to glycosaminoglycans (GAGs)
Found in connective tissues

49
Q

what does integrin do?

A

it is a adhesion protein, found in lipid bilayer of cells. helps to hold up the cell on the ECM

50
Q

what do actin filaments do? where found?

A

found in cytoplasm, part of cytoskeleton:

  1. cause the cell to be held in place
  2. structural support
51
Q
A
52
Q

can you give two examples of when cells migrate?

A
  1. embryo development
  2. cancer development
53
Q

what is structure of collagen like?

A

Triple helical structure formed by 3 peptide chains

: ▪every 3rd amino acid is glycine

▪Gly-X-Y (proline-hydroxyproline)

54
Q

what do changes in ECM characteristics show?

what is fibrosis?

A

too much ECM - assocaited with chronic disease

fibrosis: too much ECM - becomes tough

55
Q

explain difference between fibrillar and non-fibrillar collagen

A
  • *non-fibrillar collagen:**
  • *-**forms microfibrils or mesh-like structures.
  • therefore is used for anchorage of cells and filtration
  • major structural components of basement membranes - relatively thin layers of ECM
  • *fibrillar collagen:**
  • forms well-organised banded fibrils, with provide high tensile strength. therefore is used for major components in tendons, ligaments, skin etc
56
Q
A
57
Q

what is Osteogenesis imperfecta?

how is Osteogenesis imperfecta formed?

A

brittle bone disorder

in type 1 collagen: single base mutations cause Gly to convert to bulky amino acid. this prevents the corrected triple helix formation of collagen into fibrils. therefore is loose triple helix

58
Q

what are the two types ofOsteogenesis imperfecta?

A
  • *Type 1:**
    a) autosomal dominant
    b) most common - 50% of cases
    c) mildest type
    d) COL1A1 & A2 genes are mutated on chr. 17 and 7 respectively. causes an amino acid change - looser collagen chain and looser triple helix.
  • *Type 2:**
  • more severe - babies born with so many broken bones they die.
  • usually new mutation
  • dominant if affected individuals survive
59
Q
A
60
Q

what is structure of elastin like?

A
  • rich in glycine and proline - like collagen, but has more valine which interacts with hydrophobic domains, therefore makes it elastic.
  • elastin fibres are normally covered by the glycoprotein fibrillin.
  • can stretch in 2D.
  • when in relaxed state, fibres are jumbled. when stretch - stretches out and gives flex.
61
Q
A
62
Q

what is Marfan syndrome?

A

-rare genetic disease (1/10000)

- fibrillin protein is mutated and usually absent:

characteristics:
tall stature, long arms and legs, arachnodactyly (spider fingers), loose joints, floppy cardiac valves, eye problems, aortic aneurysms

63
Q

what are roles of glycoproteins in ECM?

A

receptors of cell surfaces for:
- bacteria, viruses and toxins. START immune response

hormones

strength and support to ECM

slime layer of bacteria and flagella

64
Q
A
65
Q

what are laminin and fibronectin and what are their roles?

A

both glycoproteins

1. laminin:

  • cell adhesion to the ECM.
  • cell migration
  • cytoskeleton organisation

2. fibronectin
cell adhesion to the ECM.
cell migration
cell shape
cell differentiation
cytoskeleton organisation

66
Q

what are proteoglycans?

how do proteoglycans change with age?

A
  • *proteoglycans:**
  • Proteoglycans form large aggregates within tissues made up of lots of side chains of negatively charged GAGs
  • peptide chain with covalently bound sugars. - mainly made of GAGs (glycosaminoglycans)
  • 95% carb, 5% protein
  • GAG side chains have sulphate group - gives a negative charge. this attracts water and so water moves into ECM
  • gel forming components of ECM.

with age:
decrease with age
- shorter core and fewer side chains
- draw and hold less water in tissue
- more likely to be damaged
e.g. in vertebral discs lose water - THIS IS WHY YOU GET SMALLER IN AGE

  • *with healing:**
  • They are upregulated in damaged areas
  • They cause oedema associated with the original injury
  • They provide nutrients and growth
67
Q
A

FunMed Random (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions