FunMed EOYS2 Flashcards
which two types of receptors could detect changes that would induce thirst? [2]
- osmoreceptors: in hypothalamus
- baroreceptors: detect when there is decreased blood volume (in great veins, right atrium of heart -> relied to vasomoto center) -> relayed to hypothalamus
what are ways you can test blood glucose? (3)
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.
state the components of ECF [3] & ICF x
ECF:
high Na+
low K+
HCO3-
ICF:
low Na+
high K+
PO43-
protein anions
what are the 3 mechanisms of regulating H+ levels? [3]
- chemical buffer system in blood and ICF (HCO3-): immediate action.
* *H20 + CO2 ⇌ H2CO3 + HCO3- + H+** - Respiratory centre in brain stem:acts within 1-3 minutes.
- kidneys : hours to days
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?
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,
how does the kidney produce bicarbonate?
- Glutamine -> glucose, HCO3-, NH4+
how does body keep H+ in renal lumen when in acidosis? [2]
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
how do you test to determine if patient has metabolic acidosis? [1]
check anion gap: values greater than 12 = metabolic acidosis
why are biofilm bacterial infections problematic [2]
- extreme resistance to antiobiotics and other anti-microbrial agents
- high resistance to host immune defences
name two bacterial spreading factors and briefly state how they work
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
what are the two invasion techniques for bacteria entering cells? [2]
- *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.
what is the role of phosphocreatine? [1]
under which conditions is it made? [1]
what is the role of phosphocreatine? [1] ATP buffer (in muscle & nerve cells)
under which conditions is it made? [1] anaerobic conditions
how can some pathogens resist toxic oxygen derived substances from host? [2]
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
how can some bacteria destroy IgA? [1]
using IgA proteases
what is the basic structure of gram +ve bacteria? [3]
what does interaction with host cell cause?
structure: lipid A, core polysaccharide, O antigen
production of cytokines: results in septic shock, ferver, intravascular coagulation = haemorrage and endotoxin shock
which type of immune cell do superantigens cause expansion of?
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**
which cytokines causes the differentation of ThO into:
a) Th1
b) Th2?
a) Th1: IL-12
b) Th2: IL-4
which antibiotics do you use on:
- gram +ve? [1]
- gram -ve ? [1]
glycopeptide antibiotics: gram postive
polymyxins: gram negative
name 4 methods that are acquired antiobiotic resitance mechanisms [4]
- *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
name 3 ways that biofilm adherence can occur to bacteria
specific:
- Proteins on microbe cell surface binds to host cells e.g. Hemagglutinin
- Fimbriae interact with cell surface receptors
- Pili transfers DNA between Bacteria
which bacteria class have high priority antibacterial resistance? [1]
gram negative: have multi drug resistance.
what is the role of the following RNA?
Reverse transcriptase
Integrase
Protease
RNA polymerase
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
what are 4 ways that viruses can evade host? (not drugs)
- *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
give two ways the bacteria can evade drug action [2]
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.
what are beta lactamases? [1]
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
what are the different types of viral mutations that occur? [2]
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
what are the two mechanisms for cartilage production? [2]
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)
name a location that you would find hyaline, fibro and elastic cartilage [3]
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.
how do cells get over asymmetrical ionic charge distribution caused by proteins not being permeable? [2]
- *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
describe the intra and extracellular ion concentrations that sets up the cells resting membrane potential. [3]
- Na+ greater outside cell
- K+ greater inside cell
- A- (proteins) greater inside cell
= creates a resting membreane potential: +ve outside, -ve inside = -70mV
which part of AP is postive feedback and whch is negative feedback? [2]
- *depolarisation** = postive feedback
- *repolarisation** = negative feedback
how do local anaesthetics work? [2]
- 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
what is temporal summation? [1]
what is spatial summation? [1]
- *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.
what are 2 mechanisms that inhib signals occur? [1]
give an example of a direct and indirecct inhib signal [2]
- 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
explain what receptor modulation is and how it occurs
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.
what do enteric neurons use as their major NT? [3]
Ach, NO & seratonin
describe the structure of Na ion gated channel
how does it work?
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
what are the names and vert. roots of the sympathetic nerves that innervate:
a) foregut [2]
b) hindgut [2]
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**
what are the origins of the PNS? **** [2]
Craniosacral outflow:
a) Cranial nerves: III, VII, IX, X: organs in head
b) Sacral nerves: S2-S4: rectum, bladder and genitals
where do you find the plexi of the enteric NS? [2]
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
what is the name for C1 and C2 vert? [2]
C1 is atlas
C2 is axis
where do the frontal, sphenoidal, temporal and parietal bones join together? [1]
pterion
what can be used for MRI contrast medium? [1]
gadoilinium
what are DEXA scans specifically good at showing? [2]
= 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)
which type of pharmocological antagonists:
- reduces agonist efficacy? [1]
- reduces agonist potency? [1]
- reduces agonist efficacy: non-competitive antagonist
- reduces agonist potency: competitive antagonist
what is a physiological antagonist? [1]
physiological antagonist: two drugs that have exactly opposite actions via different pathways
what is EC50?
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]
define what a drug is [1]
give 3 examples
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
where do drugs with large / small VD distributed to?
Large VD: distributed to tissues (fat / bones)
Small VD: distributed to blood
