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EOYS > FunMed EOYS2 > Flashcards

FunMed EOYS2 Flashcards

1
Q

which two types of receptors could detect changes that would induce thirst? [2]

A
  1. osmoreceptors: in hypothalamus
  2. baroreceptors: detect when there is decreased blood volume (in great veins, right atrium of heart -> relied to vasomoto center) -> relayed to hypothalamus
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2
Q

what are ways you can test blood glucose? (3)

A

fasting glucose test - (not eating / drinking anything other than water for 8hrs)

glucose tolerance test - after fasting and again after 2 hours after being given a glucose drink

glycated haemoglobin test (HbA1C) - measure of average blood sugar level over past 3 months.

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3
Q

state the components of ECF [3] & ICF x

A

ECF:
high Na+
low K+
HCO3-

ICF:
low Na+
high K+
PO43-
protein anions

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4
Q

what are the 3 mechanisms of regulating H+ levels? [3]

A
  1. chemical buffer system in blood and ICF (HCO3-): immediate action.
    * *H20 + CO2 ⇌ H2CO3 + HCO3- + H+**
  2. Respiratory centre in brain stem:acts within 1-3 minutes.
  3. kidneys : hours to days
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5
Q

define anion gap

what is the equation to work out anion gap?

what is normal anion gap?

what does it indicate if you have greater than normal anion gap?

A

anion gap: quantity difference between cations (positively charged ions) and anions (negatively charged ions) in serum, plasma, or urine. measure of Na+, Cl- & HC03 in blood

[Na+] - ([Cl-] + [HCO3-]) = 8 to 12 mEq/L

what is normal anion gap: 8-12

high anion gap = acidosis,

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6
Q

how does the kidney produce bicarbonate?

A
  • Glutamine -> glucose, HCO3-, NH4+
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7
Q

how does body keep H+ in renal lumen when in acidosis? [2]

A

when the body is acidosis:

@ distal proximal tubule:

H+ get secreted out of renal tubule cell into lumen. BUT want to stay here. SO, use NH4+ and H2PO4 buffes to keep the H+ in the filtrate

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8
Q

how do you test to determine if patient has metabolic acidosis? [1]

A

check anion gap: values greater than 12 = metabolic acidosis

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9
Q

why are biofilm bacterial infections problematic [2]

A
  • extreme resistance to antiobiotics and other anti-microbrial agents
  • high resistance to host immune defences
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10
Q

name two bacterial spreading factors and briefly state how they work

A

1. hyaluronidase: breaks down hyaluronic acid (intracellular cement of CT)

2. collagenase: breaks down collagen network - gives access to deeper tissues. E.g. Clostridium spp.

both allow further spreading into tissues

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11
Q

what are the two invasion techniques for bacteria entering cells? [2]

A
  • *1. triggered invasion:**
  • bacteria inject virulence factors into host cell cytoplasms to activate uptake by cell
  • bacteria force the cell to extend local protrusion that engulf the bacterium
  • = type 3 secretion system-dependent
  • Salmnoella spp, Shigella flexneri
  • *2. Zippered invasion:**
  • bacteria produce outer membrane protein, with extracellular part exposed
  • recognises receptor on target cell
  • taken up by the cell
  • specifc high affinity interaction between bacteria molecule and host cell receptor.
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12
Q

what is the role of phosphocreatine? [1]
under which conditions is it made? [1]

A

what is the role of phosphocreatine? [1] ATP buffer (in muscle & nerve cells)
under which conditions is it made? [1] anaerobic conditions

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13
Q

how can some pathogens resist toxic oxygen derived substances from host? [2]

A

detoxifcation of oxygen derived harmful substances from the host:

e.g. some microbes have:

  • *- superoxide dismutase (SOD):** neutralises free radicals such as O2
  • *- catalase** (breaks down H2O2): e.g. Staph. aureas
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14
Q

how can some bacteria destroy IgA? [1]

A

using IgA proteases

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15
Q

what is the basic structure of gram +ve bacteria? [3]

what does interaction with host cell cause?

A

structure: lipid A, core polysaccharide, O antigen

production of cytokines: results in septic shock, ferver, intravascular coagulation = haemorrage and endotoxin shock

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16
Q

which type of immune cell do superantigens cause expansion of?

A

superantigens:

  • induces non-specific class II MHC and T cell receptor binding: widespread binding stimulation of T cells.
  • Excessive cytokine release: fever, vomiting, diarrhea, organ failure
  • *- 20 / 30% T cells activated**
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17
Q

which cytokines causes the differentation of ThO into:

a) Th1
b) Th2?

A

a) Th1: IL-12
b) Th2: IL-4

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18
Q

which antibiotics do you use on:

  • gram +ve? [1]
  • gram -ve ? [1]
A

glycopeptide antibiotics: gram postive

polymyxins: gram negative

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19
Q

name 4 methods that are acquired antiobiotic resitance mechanisms [4]

A
  • *1. drug inactivation
    2. activation of drug pumps**(pump out)
  • *3. modification of target**: e.g. acquire new gene that methylates Rb, so is resistant to drugs that target Rb.
  • *4. alternative metabolic pathways:** e.g. with FA production, get mutations which mean that enzymes change structure so cant be targeted
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20
Q

name 3 ways that biofilm adherence can occur to bacteria

A

specific:

  • Proteins on microbe cell surface binds to host cells e.g. Hemagglutinin
  • Fimbriae interact with cell surface receptors
  • Pili transfers DNA between Bacteria
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21
Q

which bacteria class have high priority antibacterial resistance? [1]

A

gram negative: have multi drug resistance.

22
Q

what is the role of the following RNA?

Reverse transcriptase

Integrase

Protease

RNA polymerase

A

Reverse transcriptase – turns +ssRNA into DNA

Integrase – integrates viral DNA with host genome

Protease – help create viral building blocks

RNA polymerase – forms mRNA before going to ribosome

23
Q

what are 4 ways that viruses can evade host? (not drugs)

A
  • *Latency**: Dormancy that reactivates when host is immunocompromised e.g. HIV, Herpes
  • *Phagocyte evasion**: Prevention of phagosome and lysosome fusion e.g. HIV
  • *Antigenic shift and drift**: Genetic shuffling and random mutation makes immune system naïve again
  • *Hiding**: Within cells: HSV, VZV, malaria
24
Q

give two ways the bacteria can evade drug action [2]

A

1. gram-negative bacteria: outer membrane forms a permability barrier - drugs cannot cross

2. efflux pumps: active transporter. Efflux systems function via an energy-dependent mechanism (active transport) to pump out unwanted toxic substances through specific efflux pumps.

25
Q

what are beta lactamases? [1]

A

B-lactamases (aka penicillinase): Beta-lactamases are enzymes (EC 3.5. 2.6) produced by bacteria that provide multi- resistance to β-lactam antibiotics such as penicillins.

MoA: hydrolyse the b-lactam antibiotics and make it ineffective

can treat with beta lactamase inhibitors

26
Q

what are the different types of viral mutations that occur? [2]

A

Antigenic shift: combination of different viral RNA in the host cell to produce a new variant

Antigenic drift: accumulation of random mutations during viral replication

27
Q

what are the two mechanisms for cartilage production? [2]

A

a) Interstitial growth: chondrocytes grow and divide and lay down more matrix inside the existing cartilage f
b) appositional growth: undiff. cells at the surface of the cartilage (perichondrium)

28
Q

name a location that you would find hyaline, fibro and elastic cartilage [3]

A

Hyaline - most common, found in the ribs, nose, larynx, trachea. Is a precursor of bone.

Fibro- is found in invertebral discs, joint capsules, ligaments.

Elastic - is found in the external ear, epiglottis and larynx.

29
Q

how do cells get over asymmetrical ionic charge distribution caused by proteins not being permeable? [2]

A
  • *1. Active Na/K diffusion**
  • 3Na+ from intracellular to extracellular
  • 2K+ from extracellular to intracelluar

effects:
- high Na+ conc in extracellular space, low intracellular
- high K+ conc in intracellular space, low extracellular
32- results in +ve extraceullar space c.f. intracellluar space: sets up resting membrane potential

  • *2. membrane permeability:**
    • K+ (50:1 difference): more +ve charged ions move out of the cell: sets up more -ve charge inside cell. neuron plasma membrane is 50-100 times more permeable to K+ than Na=
  • resting membrane potential of cell: approx. -70mV
30
Q

describe the intra and extracellular ion concentrations that sets up the cells resting membrane potential. [3]

A

- Na+ greater outside cell

- K+ greater inside cell

- A- (proteins) greater inside cell

= creates a resting membreane potential: +ve outside, -ve inside = -70mV

31
Q

which part of AP is postive feedback and whch is negative feedback? [2]

A
  • *depolarisation** = postive feedback
  • *repolarisation** = negative feedback
32
Q

how do local anaesthetics work? [2]

A

- bind to open Na+ channel: become inactivated

  • physically prevent Na+ reopening and generating AP: drugs stablises inactive state

- cant depolarise cell

  • pain fibres cant send pain to brain
33
Q

what is temporal summation? [1]

what is spatial summation? [1]

A
  • *temporal summation**
  • post synaptic potentials at same syanpse (A&A) occur in rapid succession
  • first potential doesnt have time to dissipate: next potentials add to previous once
  • *spatial summation**
  • multiple postsynaptic potentials from different synapses (A+B) occur same time and add
  • alone, EPSP not strong enough to cause AP. reinforce each other = AP.
34
Q

what are 2 mechanisms that inhib signals occur? [1]

give an example of a direct and indirecct inhib signal [2]

A

- K+ permeability increased OR increased Cl- perm.

  • *indirect: Muscarinic ACh receptor:**
  • G-protein activated
  • acts via 2nd messenger
  • indirectly opens K+ channel
  • *direct: GABAA receptor:**
  • opens Cl- channel

BOTH: = hyperpolarisation

35
Q

explain what receptor modulation is and how it occurs

A

receptor modulation by other NTs:

  • NTs influence accumulation of opposite NTs on post-synaptic membrane
    e. g. ionotropic glutamate receptor fires excitatory response BUT also feedback to GABA receptor and causes to disperse (and vice versa)

causes a balance of inhib and excitatory systems.

36
Q

what do enteric neurons use as their major NT? [3]

A

Ach, NO & seratonin

37
Q

describe the structure of Na ion gated channel
how does it work?

A

2 channels:

  • *activation gate: (in middle of channel)**
    a) closed in resting state
    b) bridge in middle of channel stops Na+ being able to enter cell
  • *inactivation gate: (located intracellularly)**
    a) open in resting state

works by:

open in response to depolarisation:

activation gate
v fast opens due to depol

inactivation gate
closes due to depol

38
Q

what are the names and vert. roots of the sympathetic nerves that innervate:

a) foregut [2]
b) hindgut [2]

A

what are the names and vert. roots of the sympathetic nerves that innervate:

a) foregut [2]: greater splachnic nerve; T5- T9
b) hindgut [2] **lesser splachnic nerve; T10 - T12

both synapse at coeliac ganglion**

39
Q

what are the origins of the PNS? **** [2]

A

Craniosacral outflow:

a) Cranial nerves: III, VII, IX, X: organs in head
b) Sacral nerves: S2-S4: rectum, bladder and genitals

40
Q

where do you find the plexi of the enteric NS? [2]

A

organisation: two major plexuses:

  • *a) Myenteric plexus:**
    located: between circular and long. muscle layers
    function: motility
  • *b) submucosal plexus:**
    located: between submucosal and circular muscle layer
    function: controls secretion and muscle function in the mucosal layer
41
Q

what is the name for C1 and C2 vert? [2]

A

C1 is atlas

C2 is axis

42
Q

where do the frontal, sphenoidal, temporal and parietal bones join together? [1]

A

pterion

43
Q
A
44
Q

what can be used for MRI contrast medium? [1]

A

gadoilinium

45
Q

what are DEXA scans specifically good at showing? [2]

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)

46
Q

which type of pharmocological antagonists:

  1. reduces agonist efficacy? [1]
  2. reduces agonist potency? [1]
A
  1. reduces agonist efficacy: non-competitive antagonist
  2. reduces agonist potency: competitive antagonist
47
Q

what is a physiological antagonist? [1]

A

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

48
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]

49
Q

define what a drug is [1]

give 3 examples

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
50
Q

where do drugs with large / small VD distributed to?

A

Large VD: distributed to tissues (fat / bones)

Small VD: distributed to blood

51
Q
A

EOYS (39 decks)

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