Blocks 2 and 3 Flashcards

1
Q

What are the relevant virulence factors for Streptococcus pneumoniae? KEY EXAM Concept - One example of impedin, aggressin, and modulin to illustrate pathophysiology of Sp Pneumoniae

A

The Capsule. Most important. Impedin as it confers resistance to phagocytosis, allowing more bacteria to survive and multiply. And 90 capsule types mean few opportunities for acquired immunity.

Capsule also generates the immune response (aggressin). Adhesin proteins mediate adherence.

Cell lysis acts as an agressin. Cell wall components peptidoglycan, techoic acid, lipotechoic acid generate vigorous local inflammatory response. Pneumolysin is cytotoxic to endothelial cells via pneumolysin. Together they eliminate the muco-cilliary escalator and disrupt alveola-capillary boundary, facilitating transfer to bloodstream.

Lysis also acts as modulin - pneumolysin is cytotoxic to immune cells, and peptidases interfere with immune signalling.

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2
Q

What are the names and gram stain appearance of the 4 most common pathogens commonly associated with respiratory infections?

A

Strep. pneumoniae - Gram positive diplococci

Haemophilus Influenzae - Gram negative coccobacilli

Moraxella Catarrhalis - Gram negative diplococci (Upper respiratory tract)

Neisseria meningitidis - Gram negative diplococci (Lower respiratory tract)

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3
Q

How can Strep. Pneumonia lead to baceraemia and meningitis?

A

Once infection established, partial cell lysis releases pneumolysin. Cytotoxic to endothelial and immune cells, breaks down barrier between alveoli and capillaries. Haematogenous spread (bacteraemia). Sp has a tropism for CNS,

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4
Q

What are the Gel and Coombes classifications of immunopathologies?

A
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5
Q

What is the Difference between sex and gender

A

sex: male and female biology; chromosomes, hormonal profiles, sex organs
gender: social and cultural construction of male and female and masculinity and femininity

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6
Q

What impact does the delineation of sex and gender have on illnesses?

A

illnesses are often distributed along gender lines for biological and social reasons
there are genuine biological differences in disease prevalences (these may be obscured by past epidemiological research, e.g. research tended to be done on men rather than men and women)
there are genuine differences in health-seeking patterns; women more likely to report

E.g. breast cancer research done on women only, but men can get breast cancer too (1% of cases are in men); “wear pink for breast cancer” - how would men feel then?

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7
Q

What are the 5 criteria for medicalisation?

A

condition must be biologically plausible
Must speak to preoccupation/anxiety in society
Must have an authority in medicine
Must have an acceptable method of diagnosis
Must have an acceptable method of treatment

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8
Q

What are the three models of disability?

A

Medical, social, biopsychosocial

medical model

disability is a medical problem
policy aids rescue of the disabled
can result in devaluing the lived experience of the disabled
Christopher Reeve was an advocate, saying living with a disability was terrible; this caused debate as not all disabled people agree

social model

“disability is in the eye of the beholder”
opposite model to the medical model
based on principle of equivalence; disabled people should have same opportunities as able-bodied
destigmatises disability
current federal government uses this model (trying to improve access for disabled people in the workplace)
e.g. Graeme Innes vs RailCorp over unintelligible announcements; if think it is ridiculous that RailCorp argued the case, then you believe in the social model

biopsychosocial model

recognises that bodies suffer in individual ways
model based on principle of respect for these differences
prepares for, recognises and responds to fluctuations in physical and emotional capacity
recognises that the internal and physical world of the person needs appropriate healthcare provision
national disability insurance scheme (NDIS) follows this policy model

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9
Q

Why are the poor sicker?

A

The poor are more likely to have a chronic illness, and are more likely to be severely disabled; possible explanations include:

lack of health services (tend to be fewer in poorer areas)
poorer health hardware (e.g. lack of refrigeration means range of health promoting choices limited)
environments conducive to ill-health (poorer quality food, more exposure to env. pollutants)

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10
Q

Why are sick people (chronic illness) more likely to be poor?

A

downward drift (happens to even the richest people that become chronically ill; people with chronic illness may find it harder to keep down a job because of the illness, and thus may lose their income earning capacity; relationships may come under threat, again reducing the income the individual has)
health care costs (it costs money to be ill and to be constantly accessing services)
need to pay ongoing attention to one’s physical self
become embroiled in health system and possible worker’s compensation
expenditure of money, loss of income
loss of many of the external attributes of self that one once had

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11
Q

Endocrine histology - Cells and function

A
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12
Q

What is Procreative autonomy? Example?

A

Definition: to have control over one’s reproductive capabilities; the freedom to choose whether or not to have children

development of the COCP:

reinforced the view of sexual pleasure as something to be enabled (prior to this, masturbation was “self-abuse” and “not biologically healthy”)
allowed sex and reproduction to be decoupled
became a tool to support the evolving autonomy of middle-class women

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13
Q

What factors do you consider when describing a tumour?

A

Site

Size

Shape

Surface

Margins

Colour

Consistency

Capsule?

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14
Q

MI at the different stages

A

One Day

Macro - Subtle changes, dark mottling

Micro - Contraction bands, coagulation necrosis, haemmhorage, scattered neutrophils

Two Days

Macro - Mottled with yellow/tan infarct centre.

Micro - Coagulation Necrosis, Neutrophils

One Week

Macro - Hyperaemic border, central yellow softening

Micro - Disintegration of myofibres (borders disapearing), dying neutrophils, macrophages.

Two Weeks

Macro - Maxmially yellow/tan and soft, depressed infarct borders

Micro - Phagocytosis, Granulation tissue (angiogenesis and ECM), early fibrosis (lots of collagen and spindle cells)

Two Months

Macro - White scarring

Micro - Dense, collagenous scar

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15
Q

Asbestos

What is it?
Modifiers?

Complications?

A

Pneumoconiosis - Restrictive lung disease caused by inhalation of dust.

Modifiers - Duration and length of exposure, amount of retained dust, small size, shape of particles (type of asbestos), solubility of particles, Additional Irritants, preexisting lung disease.

Complications - Pleural plaques, asbestosis, pleural effusions, cancer (lung, mesothelium, other)

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16
Q

What is the Pathogenesis of Atherosclerosis?

A
  1. Chronic endothelial injury/assault from risk factors, particularly LDL which then oxidises.
  2. Infiltration of endothelium by leukocytes - particularly monocytes, and platelet aggregation.
  3. Monocytes are activated, cytokines released that lead to smooth muscle recruitment.
  4. Lipid engulfed by macrophages and smooth muscle cells, leading to fatty streaks.
  5. Smooth muscles proliferate in the intima, ECM is laid down (fibrous cap), and there is significant intra- and extracellular lipid. This is a highly thrombogenic mix, should it ever again make contact with the blood.
17
Q

How can pharmacogenetics impact dosing regimes?

A

Multiple possibilities, so need multiple dosing regimes.

May have a mutation in drug target protein or pathway - if mutated gene leads to fewer functional receptors, would want to drop the dose.

May have mutation in protein that metabolises it - hang around in the system for much longer

Idiosyncratic - Interplay with another pathway that may be stressed by the drug (e.g. G6PD and ibuprofen, which stresses RBC’s).

18
Q

How does the kidney synthesise new HCO3- from glutamine?

A

Early Proximal Tubule

Glutamine enters the cell (Na-cotransport), and mitochondria.

Glutaminase strips off NH4+, leaving glutamate

Glutamate dehydrogenase strips off NH4+, leaving alpha-KG.

2x Alpha-KG enter gluconeogenesis, using 2 protons from 2xH2O

Remaining two OH- react with CAII, corming 2xHCO3-

HCO3- leaves cell with Na symporter.

2xNH4+ dissociate, NH3 diffuses, H+ pumped by proton or Na/H antiporter, recombine in the lumen.

19
Q

What is the mechanism of action of osmotic diuretics?

A

By acting in the PT and TAL, ‘binds’ water in the tubule by osmosis, and prevents the maintenance of a concentration gradient. So not only does the kidney have the extra ECF (thus RBF) to deal with, it can’t concentrate the urine properly, and due to hyper-osmolar urine, decreased H2O resorption in DT/CD.

20
Q

What are the 4 classes of antiarrhythmics? One example from each class?

A

I - Voltage-sensitive Na Channel blocker - Lidocaine

II - Beta Blockers - Metoprolol

III - Repolarisation inhibitors (K+ blockers) - Ibutilide

IV - Calcium blockers - Nifedipine/Verapamil

21
Q

What is afterload?

A

NOT diastolic OR systolic pressure - approximately equal to Mean Arterial Pressure. MAP is the driving force on perfusion.

22
Q

How do you calculate Mean Arterial Pressure in the aorta and femoral artery?

A

Aorta - MAP = (Syst+Diastol)/2

Femoral - MAP=(Syst+2*Diastol)/3

23
Q

What is clearance? How do you calculate it?

A

Clearance - virtual volume of blood that would be totally cleared of substance in a given time [mL/min].

Clearance = (Urine concentration x Urine volume mL)/

                  (Plasma concentration x 1440 (min/day))
24
Q

What is the heirarchy of control systems in volume regulation?

A

If there is competition between osmocontrol (ADH) and volume control (RAA etc), osmocontrol prevails with a stronger and faster response.

Hence why thirst is satiated by drinking H2O (osmolarity) rather than by NaCl craving.

This makes sense, as to clear it by NaCl (volume) would be robbing Peter to pay Paul, stealing it from intracellular fluid.

25
Q

What are clinical networks?

What are the models of clinical networks?

A

Multidisciplinary groups of clinicians and senior managers who work together across profession, organisational and jurisdictional boundaries in order to improve delivery of care, clinical outcomes and health service performance.

3 main types:

  • clinical network (most common in ACT; relatively flat structure (no hierarchy), commitment to common purpose; focus on building relationships, sharing information, aligning policies)
  • clinical service network (builds on model of clinical network; includes clinicians from primary, secondary and tertiary care; focus on equitable provision of high quality services; more formal than clinical network; no budget)
  • service delivery network (full responsibility and accountability; assigned an operating budget; focus on fully integrated service delivery)
26
Q

What are the alcohol recommendations?

What constitutes binge drinnking?

A

Binge drinking = more than 5 std drinks (10g alcohol) on a single occasion.

Guieline 1 - Drinking no more than 2 std on any day reduces risk of harm from alcohol-related disease or injury.

Guideline 2 - Drinking no more than 4 standard drinks on a single occasion reduces risk of alcohol-related injury arising from that occasion.

27
Q

What are the features of malignant cells?

A

Microscopic (cytological) features of malignant cells:

  • Variable cell size & shape (cellular pleomorphism)
  • Variable nuclear size & shape (nuclear pleomorphism)
  • Increased nuclear-cytoplasmic ratio ( normal is 1:4 to 1:6 – ratio may approach 1:1)
  • Hyperchromatic nuclei (increased DNA)
  • Increased mitosis and abnormal mitosis
  • Tumour giant cells
28
Q

Why is acetyl CoA the centre of metabolism?

A

Common point of many catabolic pathways (glycolysis, FA oxidation, protein degradation, ketone utilisation).

From there, can be used for:

Immediate Energy (O2 Phosphorylation)

FA production (TAGs, prostoglandins, phospholipids)

Cholesterol (steroid hormones, bile salts)

Common point that allows direction of flux to address whatever body needs.

29
Q

What is the endogenous cholesterol pathway?

A

Synthesis pathway - lipids are synthesised in liver, and moved to storage, either in liver or peripheral tissues.
In hepatocytes, dietary chylomicrons, together with HDL/LDL from periphery, are synthesised into VLDL. On release, apoproteins are exchanged with HDL, while TAGs and FAs are spun off into peripheral tissues. Eventually, this process leads to LDL, which is packed with cholesteryl esters and returns to the liver via the bloodstream (or gets stuck and forms a plaque).

30
Q

How do you calculate mid-parental height?

A

For boys - ((Mum+12.5cm)+Dad)/2

For girls -(Mum+(Dad-12.5cm))/2

31
Q

How do you calculate incident rate?

A

Number who develop the disease/number of person-time at risk.

Make you you start with writing a table - badly written question. Start jotting down years immediately. Remember they drop out of the study when they get the disease, and remember to add people who survived the whole time.

32
Q

Study Design Table

A
33
Q

How do case-control and (cohort/cross sectional) studies differ in their intepretation?

A

Case Control talks about odds of exposure among cases vs controls.

Cohort/Cross Sectional talks about the odds of having the disease among the exposed and the unexposed.

34
Q

What is the phone number of the national interpreter system?

A

13 14 50 - Plebs

1300 13 14 50 - Doctors’ priority line.

35
Q

What are the benefits of a clinical network?

A
  • quality and safety improvements (Px experience, Px access, clinical outcomes, reduced variability in care)
  • management improvements (staff engagement and satisfaction, efficient management of scarce resources)
  • relationship improvements - comms and collaboration
  • reporting improvements (data sharing, develop and monitor agreed quality measures)
  • recognised body of experts