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:)))) Flashcards

1
Q

which channels let water through membranes?

A

aquaporins

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2
Q

what are similar or differences between them?

difference between ECF and ICF?

A

-Plasma and interstitial fluid: same electrolyte components BUT plasma has proteins - e.g. albumin and anions c.f. interstitial fluid

Intracellular fluid c.f. extracellular fluid: ICF has very little Na+. Lots of K+ and PO43- - (buffers acid / base situation), protein anions (think - sea with Na+ is ECF, banana tree: ICF). ECF has high Na+ and Cl-

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3
Q

what characteristics do osmoreceptors have?

A

(in the Subfornical organ: in the hypothalumus. (Organum Vasculosum of the lamina terminalis (OVLT) - dont need to know)

  • characterised by: a) extensive vasculature b) lack of normal blood brain barrier
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4
Q
  1. where are the osmoreceptors found in brain?
  2. what is another stimuli that triggers sensation to drink?
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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5
Q

Q

what is the main stimulus for the thirst sensation?

A

increase in plasma osmolality

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6
Q

describe mechanism of aldosterone working

(where made? released from? what does it cause to do? result?)

A

aldosterone:

released from: adrenal cortex

released when: reduced Na+ or increased K+

function: increases reabsorbtion of Na or increased K secretion
result: homeostatic plasma levels of Na+ and K+.

aldosterone binds to kidney cells:

a) ENAC (Na channel) - can reabsorb more Na
b) Na/K pump ( pumps Na in / K out)

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7
Q

how does atrial natruiretic peptide work? released from? releaed when?

A

Atrial natriuretic peptide (ANP)

released from: cardiac Atria

released when: increased blood volume (stretches atria)

function: promotes excretion of Na+ and Cl-, in turn decreases water reabsorbtion (brings blood volume back towards normal)(acts on hypothalamus and adrenal cortex up the mechanism.)

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8
Q

what horomone does same role as aldoesterone (i think)

A

angiotension II

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9
Q

which channels in the kindey, controlled by ADH and aldosterone, controls the variable reabsorbtion of water?

A
  • *-aquaporins
  • ENAC
  • Na/K pumps**
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10
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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11
Q

state and say use of each type of blood test pls

A
  • complete blood count:

- arterial blood gas: CO2 and O2 levels

- blood smear: represents a snapshot of cells in blood at the time. size, shape and colour of RBC and WBC can be measured - can determine diagnosis

- blood cultures: suspect a pathogen

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12
Q

what is hematocrit a measure of ?

A

Hematocrit, the proportion of red blood cells to the fluid component, or plasma, in your blood

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13
Q

the concentation of hydrogen ions is regualted by which systems?

how long does it take for each system to regulate?

A

1. chemical buffer system in blood and ICF: immediate action

2. Respiratory centre in brain stem:acts within 1-3 minutes

3. kidneys : hours to days

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14
Q

what are the three major chemical buffer systems in the body?

A

Bicarbonate (HCO3-) buffer system: H20 + CO2 ⇌ H2CO3 + HCO3- + H+

Proteins (Hb and albumin) buffer system

Phosphate buffer system

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15
Q

what is anion gap?

what happens if have high anion gap?

A
  • measure the conc of Na, Cl and HCO3- in blood. - cations should be greater by anions by 8 to 12 mEq/L.

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

If your results show a high anion gap, you may have acidosis, which means higher than normal levels of acid in the blood

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16
Q

which part of brain controls for difference in breathing rate due to acid / alkaline blood lvels?

A
  • change incurred by Pons and medulla
  • expelling more co2 lowers the acid levels
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17
Q

how does the kidney produce bicarbonate?

A
  • Glutamine -> glucose, HCO3-, NH4+ (excreted out and used to combine with H+ ions to make sure excreted into urine)
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18
Q

when the body is in acidosis, how do we ensure H+ stay out of renal tubule cells?

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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19
Q

what do you look for when get results from arterial blood gas? what does each one mean

A
  1. pH low (acidosis) or high (alkalosis)?
  2. what is PaCO2 value? (resp. indicator)
  3. what is HCO3- value? (metabolic indicator)
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20
Q

what test do you if have a metabolic acidosis?

A

check anion gap

Therefore, values greater than 12 define an anion gap metabolic acidosis.

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21
Q

describe briefly synthesis of phosphocreatine

what is it used for?

location?

A

phosphocreatine synthesis:

  • transfer of phosphate group from ATP
  • enzyme used: creatine kinase
  • anaerobic conditions

function: ATP buffer (can restore ATP when needed)

Location: in tissues that have high, fluctuating energy demands - muscle and brain

-

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22
Q

explain proton motive force

A
  • making a gradient to keep out of equilibrium.
  • get an electrochemical gradient (gradient of BOTH electrical potential and chemical concentration across a membrane)
  • transfer of H+ via proton pumps across membrane creates a source of energy (PMF): get a proton electrochemical gradient of proteins: proton motive force

can use thise electrochemical conc. gradient of protons across a membrane to power the synthase of ATP

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23
Q

which are the energy conversion pathways that occur in cellular resp?

A
  1. glycolysis
  2. krebs cycle
  3. electron transport chain
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24
Q

why / how is cyanide a poison?

A

- binds to cyctochrome c oxidase (4th complex in ECT)

  • cyanide attaches to iorn within protein complex and inhibits activity of the complex system

- ECT can’t pump H+ into intermembrane space = pH of intermembrane space increases -> pH gradient decreases.

- ATP synthesis stops

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25
Q

describe the structure of two motors in ATP synthase

what are they used for?

A

function: converting ion gradients to ATP

in ATP synthase:

  • 2 motors - one electrical, one chemical
  • one motor location: membrane - powered by flow of protons
  • one motor location: intermembrane space: powered by ATP

WHEN ONE TURNS, CAUSES THE OTHER TO TURN

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26
Q

how does muscle contraction work with ATP?

A
  • myosin has two heads: one binds to ATP, one binds to actin.
  • when ATP binds to myosin. ATP is hydrolysed as a result.
  • change in 3D shape of myosin.
  • changes the position between actin and myosin filaments
  • = muscle contracts
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27
Q

how is energy used in heat?

how does this process work with ATP synthase?

A
  • thermogenin (uncoupling protein): found in the mitochondria of Brown adipose tissue
  • allows passage of protons back into mt matrix
  • generates HEAT
  • do not have enzyme activity to catalyse production of ATP - so H+ move down energy gradient without using this energy for synthesis of ATP

= NON SHIVERING HEAT PRODUCTION

with ATP synthase:

  • ATP synthase and thermogenin / uncoupling protein work in parrallel
  • both in mitochondria membrane
  • uncoupling protein generates HEAT
  • ATP synthase generates ATP
  • last step in ox. phosphorylation
28
Q

what are three stores of biological energy?

What are 4 general uses of biological energy?

A
  • *stores:**
  • ATP
  • Phosphate
  • PMF
  • *uses:**
  • anabolism (synthesis of x)
  • transport (primary / secondary AT)
  • motility
  • heat
29
Q

why are biofilm associated infections really problematic? (2)

A
  • extreme resistance to antiobiotics and other anti-microbrial agents
  • high resistance to host immune defences
30
Q

how do microbes undergo local spread and invasion through degredative enzymes / spreading factors ?

explain 2 pls

A

bacterial patogens often produce degradative enzymes - aka spreading factors: facilitate growth and spread of pathogen (dont kill host cells)

  • *1. hyaluronidase:**
  • breaks down hyaluronic acid (intracellular cement of CT). e.g. Strept. spp, Staph aureas. allows invasion further into tissues
  • *2. collagenase:**
  • breaks down collagen network - gives access to deeper tissues. E.g. Clostridium spp.
31
Q

how does invasion of host cell oocur by bacterial invasion of host cells?

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.
32
Q

whats hypersensetivity? give example of type II, III and IV?

A

Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.

Type II: IgG/IgM to patients own RBCs due to M. pneumonia

Type III: complement activation causing inflammation e.g. S. pyogenes causing glomerulonephritis

Type IV: T cell mediated e.g. TB granulomas

33
Q

what are the specific (3) and non-specific ways that biofilm adherence occurs

A

non specific: Force of attraction e.g. Van der Waals forces

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

all creates a dense biofilm that protects pathogen

34
Q

natural host defences are type of which immunity?

A

innate immune response

35
Q

which specific proteins from complement system cause: opsonisation, membrane attack complex (MAC) and inflammation

A

opsonisation: (C3b and IGG):
membrane attack complex (MAC): (C5b)
inflammation: (C5a & C3a)

36
Q

what are ways that microbibes can evade host defences when INSIDE the host? (4)

A

microbiocidal effects

  1. escape from endosome-phagosome and grow in cytoplasm: Listeria / Shigella
  2. inhibition of phagosome-lysosome fusion: Leigonella pneumophilia
  3. survive within phagolysosome
  4. replicate within phagolysosome: Salmonella
37
Q

how can some microbes survive detoxifcation of oxygen derived harmful substances?

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
38
Q

how do some microbes destory antibodies?

A
  • create IgA proteases
  • these destroy IgA (IgA coat foreign microbes with mucous)
39
Q
A
  1. toxins that damage membranes: cytolysines and pore forming toxins. help spread of bacteria
  2. toxins that act as enzymes: A/B toxins, more diverse group of toxins
    - 2 subunits: A&B
    - A = enzymatic activity
    - B = binds to cell membrane (allows A to go into cell(
  3. toxins that activate immune response: superantigens
40
Q

which bacteria produce lipooploysaccharide (LPS)?

where located in bacteria?

made of? which part is toxic?

what happens?

A

gram negative bacteria

location: outer membrane of bacteria cell wall

structure: lipid A, core polysaccharide, O antigen

lipid A = toxic

activates complement and stimualtes producion of cytokines: results in septic shock, ferver, intravascular coagulation = haemorrage and endotoxin shock.

41
Q

how can some microbes survive detoxifcation of oxygen derived harmful substances?

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
42
Q

what do superantigens caused to be released? compared to normal antigens?

A
  • *superantigens:**
  • induces _non-specific class II MHC and T cell receptor binding: w_idespread binding stimulation of T cells.
  • Excessive cytokine release: fever, vomiting, diarrhea, organ failure
  • *- 20 / 30% T cells activated**
43
Q

How can microbes cause cancers?

A
  • some microbes can cause development of chronic inflam processes: H. pylori (stomach cancer)
  • some viruses incorp. nucleic acids into host genome: cause development of cancers
  • Hep B: hepatocellular carcinoma
  • HIV: lymphoma
  • HPV: cervical carcinoma
  • Epstein Bar - Burkitt’s lymphoma
44
Q

which cytokines causes the differentation of ThO into:

a) Th1
b) Th2?

A

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

45
Q

people with non-functional IFNy receptor are highly suscepitble to ?

A

mycobacterial infections

46
Q

which B-lactam antibiotics are used on gram postive / negative bacteria?

A

glycopeptide antibiotics: gram postive

polymyxins: gram negative

47
Q

which are the current exploited antibiotic targets?

what are the most successful?

A
  • inhibition of bacterial cell wall synthesis
  • inhibition of bacterial protein synthesis
  • inhibition of DNA transcription and replication
  • inhibition of RNA synthesis and replication

most successful hit:

  • rb
  • cell wall synthesis
  • DNA gyrase or DNA toposiomerase
48
Q

which drugs act on pathogen nucelic acid synthesis?

A

quinolones / fluoroquinolones:

  • broad spectrum
  • bind to topoisomerase II (DNA gyrase) and topoisomerase IV and inhibit DNA synthesis.

Rifampicin:

  • acts on RNA transcription: inhibits RNA polymerase on gram postive
  • treats TB
49
Q

what does susceptibility, intermediate and resistant mean?

what is a breakpoint??

A

susceptibility: bacterial strain inhibited in-vitro by a conc of an antimicrobial agent that is associated with a high likelihood of therapeutic success

intermediate: bacterial strain inhibited in-vitro by a conc of an antimicrobial agent that is associated with a uncertain therapeutic success

resistant: bacterial strain inhibited in-vitro by a conc of an antimicrobial agent that is associated with a high likelihood of therapeutic failure

breakpoint concentration: A breakpoint is a chosen concentration (mg/L) of an antibiotic which defines whether a species of bacteria is susceptible or resistant to the antibiotic. changes all the time

50
Q

how do antibacterial targeting protein synthesis work?
what do aminglycosides, tetracylines, macrolides and chloramphenicol do?

A
  • aminglycosides: change shape of 30S portion & disrupt the structure (Gentamicin, tobramycin and amikacin). Gram-negative bacteria. can cause hearing loss and renal impairment. IV drugs
  • tetracyclines: bind to 30S. interfere with attachment of tRNA to rb. oral drugs
  • macrolides: bind to 50s subunit. prevents translocation
  • chloramphenicol: bind to 50S, inhibit formation of peptide bond
51
Q

what are PD indecies for antimicrobial activity and MIC?

A

effect of drug regarding its antimicrobial activity can differ regarding PD indices:

  • *- Cmax / MIC ratio** - concentration depending killing: most importnat is getting high conc above MIC.
  • T>MIC - time dependent killing - most important is time above MIC. with minimal prolonged antibiotic effect
  • *- AUC24 / MIC ratio** - combo of above time dependent killing with prolonged antibiotic effect
52
Q

how does activation of efflux pumps work in bacteria to cause antibiotic resistance?

A

normally used to pump out metabolic waste:

  • undergo mutations - pump out drug instead
  • high level of resistance provided
  • genes for multidrug resistance efflux pumps integrate into plasmids can transfer between bacteria: can be acquired or intrinsic
53
Q

what are 4 acquired antiobiotic resitance mechanisms

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
54
Q

give an example of drug inactivation by B-lactamases

how get over this?

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

  • beta-lactamase hydrolyse the b-lactam antibiotics and make it ineffective

beat this by: use inhibitors of b-lactamases.

55
Q

which bacteria have high priority antibacterial resistance?

A

the highly cirtical ones are all gram negative: have multi drug resistance. BUT THERE ARE NO NEW DRUGS IN THE PIPELNE :(

56
Q

what are two intrinsic mechanisms of antibiotic resistance?

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.
57
Q

what do the following do with 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

58
Q

how does viral evasion of host defence occur?

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
59
Q

what is herd immunity threshold?

Ro ​= ?
1/ Ro = ?
Ro < 1 ?
Ro > 1 ?

1-1/Ro ?

A
  • *Ro =** av. number of new transmissions per case over infectious period in sus or non vaccinated pop
  • *1/ Ro** = proportion of the population sus. to virus (aka epidemic threshold)
  • *Ro < 1** infection dies out
  • *Ro > 1** infection will spread
  • *Ro = 1** infection stable

proportion of pop. that needs to be vaccinated to eliminate virus: 1-1/Ro

60
Q

how can antivirals target viruses?

A

Targets viral replication process:

• Reverse transcriptase: RNA to DNA

  • Integrase: integration of viral genetic material into host genome
  • Protease: cleave precursor proteins
61
Q

why are there so few antivirals?

A
  • the virus life cycle is tied to host cell: difficult to target virus alone
  • viruses are difficult to grow
  • most virus infections are short lived
  • compound must block virus replication compelely otherwise the virus will mutate and become resistant
62
Q

what is herpesvirus?

how work?

A
  • dsDNA viruses
  • stays latent in body after infection:
  • chickenpox infection: virus goes into dorsal root ganglia and stays latent and can reemrge later in life as shingles
63
Q

how does Aciclovir treat herpesvirus?

A

acyclovir:
- reduces symptoms but doesnt cure
- mimics one of the 4 bases for DNA (but misses OH group): terminates DNA sythesis
- prodrug mechanism:
- has to be activated by HSV enzyme thymdine kinase to add P
- cellular kinases add 2nd and 3rd P
- chain termiantes

  • can get resistance
  • need to treat IC patients
64
Q

what are the different types of viral mutations that occur?

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

65
Q

how do HIV ARV works?

A

drugs: HAART (Highly Active ART)

Uses a variety of inhibitors in from different classes of anti-viral drugs to reduce the viral load.

  • Entry inhibitors
  • Reverse transcriptase inhibitors (NRTI, NNRTI)
  • Integrase inhibitors
  • Protease inhibitors
  • Fusion inhibitors

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