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EOYS > FunMedEOYS3 > Flashcards

FunMedEOYS3 Flashcards

1
Q

what property do intracellular receptor proteins have? [1]

give 4 examples [4]

how do they cause change in body? [1]

A

what property do intracellular receptor proteins have? [1] hydrophobic

give 4 examples [4]
steroid H
thyroid H
vitamin D
retinoids

​how do they cause change in body? [1]
bind to nuclear receptor
change gene transcription

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2
Q

define drug

a) tachyphylaxis [1]
b) tolerance [1]

A

define drug

a) tachyphylaxis [1] acute tolerance from rapid and repeated admin of drugs in short intervals
b) tolerance [1] chronic longer term admin can reduce drug effect (e.g. alchohol)

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3
Q

give 3 mechanisms that tachyphylaxis can occur [3]

A

mechanisms for tolerance or tachyphylaxis:

  1. receptor desensitized or loss of receptors
  2. receptor internalisation (degraded in lysosome)
  3. increased metaboloic degradation of drug
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4
Q

where do you find glycoproteins? [1]
where do you find proteoglycans? [1]

A

▪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

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5
Q

which molecule causes receptor modulation? [1]

A

B arrestin

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6
Q

which method of administration of drugs goes straight into the CSF? [1]

A

intrathecal​

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7
Q

which family of enzymes undergoes oxidation reaction in biotransformation? [1]

A

cytochrome P450 enzymes

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8
Q

what happens to drugs if reabsorbed back into bile?

phase 1 drug? [1]
phase 2 drug? [1]

A

what happens to drugs if reabsorbed back into bile?

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

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9
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)

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10
Q

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

A
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11
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)
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12
Q

what type of receptors are adrenergic receptors? what does this mean with regards to their action?

A

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

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13
Q

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

autonomic NS that doesnt use Ach, adrenaline or noradrenaline !!

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14
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
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15
Q

what are the components of ECM? [4] (MESS)

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

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16
Q

describe the structure of collagen [3]

A

Triple helical structure formed by 3 peptide chains

: ▪every 3rd amino acid is glycine

▪Gly-X-Y (proline-hydroxyproline)

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17
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
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18
Q

describe pathophysiology of osteogenesis impefecta [2]

what are the two types ofOsteogenesis imperfecta? [2]

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

  • *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
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19
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.
20
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

21
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

22
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

23
Q

describe structure of proteoglycan [2]

what gives proteoglycans their negative charge? [1]

A
  • 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.
24
Q

structure of antibody?

A
  • antigen binding site is combination of light chain and heavy chain
  • Fragment antigen binding is at the top
  • Fc is at the bottom: determines role of antibody (if IgE / IgM etc)
26
Q

what are the receptors found on lymphocytes? - explain basic overview of adaptive immune system

what receptors found in innate immune system? on which cells/

A
  • *adaptive immunity:**
  • lymphocytes are covered in receptors:
  • *- antigen specific T cell receptor (TcR):** two types - αβ and γδ (gamma delta)
  • antigen specific B cell receptor (BcR): immunglobin on B cell surface
    1. once B or T cells is activated by recognising antigen: resting cell -> activated cell. massive cell division. makes cytokines, come killer cells and make antibodies
  • *innate immunity:**
  • phagocytes, macrophages & neutrophils receptors:
  • *- pattern recognition receptors (PRR)
  • Fc receptors**
  • response immediately
27
Q

what happens when B cells become activated? [2]
what happens when T cells become activated? [2]

A

when B cell activated:
- divide lots (aka clonal expansion)
- B cells can become:
- plasma cells (make antibodies)
- memory cells

  • *when T cell activated:**
  • clonal expansion (due to IL-2)
  • become CD4 or CD8 cells
28
Q

what controls T cell clonal expansion?

A

IL-2

29
Q

what is inflammation?

A

when white cells leave the blood and move into the tissues - in process of gettting rid of pathogens, kill normal tissue too

30
Q

how do B cells regonise antigens? [2]

A
  • B-cells have recognition molecules called immunoglobins (Ig): often the eptiope is conformational
  • *- without help of other cells !!**
31
Q

how is the great number of receptor diversity generated on antibodies?

A
  • each developing B cells expresses a distinct receptor
  • not different genes for millions of different receptors
  • INSTEAD: diversity is generated by mixing and matching gene segements within the heavy and light chain loci:

- Immunglobin heavy chain has:

a) V segments (40); b) D segments (25); c) J segments (6)
- get splicing of each of ^ to make lots of different genes: combinatorial diversity
- also: additional nucleotides can be added at the joints of ^^ to make more variation: junctional diversity

THEN:
any of immunoheavy chain stuff can associate with any of the light chains: more diversity: combinatorial diversity

32
Q

whats the 9 regions of abdo?

A
33
Q

label these structures :)

A
34
Q
A
37
Q

how many layers of elastin are in muscular arteries?

A

arteries further from the heart: muscular arteries (normally named arteries) - less elastin, more connective tissue. ONLY 2 layers of elastin - external and internal elastic lamina. rest = smooth muscle

38
Q
A
39
Q

which vertebral levels are:

a) paravertebral ganglia[1]
b) prevertebral ganglia [1]

A

which vertebral levels are:

a) paravertebral ganglia: T1-T4
b) prevertebral ganglia: T5-L2

40
Q

Folding of newly synthesized polypeptides in the crowded cellular environment requires the assistance of so-called molecular WHAT proteins [1]

A

Folding of newly synthesized polypeptides in the crowded cellular environment requires the assistance of so-called molecular chaperone proteins

41
Q

draw structure of a a.a.

A
42
Q

name 4 derivatives from cholesterol [4]

A
  • steroid hormones
  • sex hormones
  • vitamin D
  • bile salts
43
Q

what is the warburg effect?

A

Modification of metabolism to support neoplastic proliferation – Warburg effect:

cancer exhibit glucose fermentation even when enough oxygen - allows proliferating cells to convert nutrients such as glucose more efficiently into biomass promoting anabolism.

44
Q

name three ways in which cancer cells can evade apoptosis [3]

A
  1. eliminating the internal sensors the trigger apoptosis e.g. hypoxia, lack of nutrients,
  2. upregulating anti-apoptotic factors (e.g. bcl-2)
  3. Downregulation pro-apoptotic factors (e.g. bax)
45
Q

name a receptor, when overexpressed causes cancer? [1]

A

HER2

46
Q

what class of pathogen is malaria? [1]

A

protozoa

47
Q

what are the three shapes of bacteria? [3]

A

Spherical (cocci)

Cylindrical rod (bacilli)

Curved/spiral (spirochetes)

48
Q
A
49
Q

what colour does ziehl-neelosn stain turn mycobacteria? [1]

A

red

50
Q

name 2 complement blood proteins used in innate immunity [2]

A

Uses complement blood proteins that

  • opsonise (act as markers for phagocytes)
  • cytolyse (directly attack via membrane attack complex (MAC))
  • enhance inflammation

EOYS (39 decks)

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