Sc06 sanjay's malaise


Published on

Published in: Health & Medicine
  • Be the first to comment

  • Be the first to like this

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Sc06 sanjay's malaise

  1. 1. Sanjay’s MalaiseVentilation-Perfusion Relationships1. What is pulmonary blood flow in L/min?12. What is approximate ventilation of the lungs in mL/min?23. What is the normalVa/Q (ventilation-perfusion) matching for normal gasexchange?34. Why could you have a normal pulmonaryVa/Q but poor gas exchange?45. Which veins account for the 2% of venous blood which does not pass through thelungs?56. What two deformities of the heart could initially cause L to R shunt in newborns?67. How does constant high pressure in the pulmonary circulation cause right to leftshunts?78. List the four heart malformations that make up Fallot’s tetraolgy89. Does ventilation or breathing 100% oxygen help a patient with right to left shunt?910.Would an area of high perfusion low ventilation be described as dead space orshunt effect?101 5000ml/min blood2 7500ml/min air3 0.84 Ventilation/perfusion could be matched on pulmonary level but also need to be matched on alveolar level5 Bronchial veins and small veins draining the wall of the L.vent go into arterial circulation6 Atrial and septal defects7 Pulmonary vascular resistance and remodelling8 Overriding aorta (middle of heart rather than left), ventricular septal defect, R.vent hypertrophy, pulmonarystenosis (narrowing caused by hypertrophy of heart wall).9 Little, because the haemoglobin is already fully saturated, it cannot open up the unventilated/unperfusedareas or dead space10 Shunt - dead space would be a high ventilation/perfusion (because it means poor gas exchange takingplace)
  2. 2. 11.Why do highVa/Q areas not compensate for low ones?1112.What would aVa/Q of zero indicate?1213.What normal mismatch could occur due to gravity in normal lungs?1314.How is the response of pulmonary vasculature different to that of other tissues inhypoxic conditions?1415.Why does load on the right heart increase in respiratory failure?1516.What is the normal alveolar-arterial pressure gradient in mmHg for a healthyadult, why is this caused?16Respiratory Failure1. What defines respiratory failure in terms of pO2 and pCO2?172. What is the difference between type 1 (hypoxaemic) respiratory failure and type 2(hypercapnic) respiratory failure?183. What pathologies can cause right to left shunts?194. List the factors that could cause type 1 respiratory failure?2011 More blood tends to come from the low Va/Q areas as the high Va/Q areas are mostly caused by poorperfusion. High Va/Q areas do not have higher O2 content because the blood is already fully saturated. Soincreasing PO2 does little to increase O2 content.12 A completely collapsed lung or one where perfusion is completely blocked13 Gravity improves both perfusion and ventilation at the bottom of the lungs but effect on perfusion is largerthan effect on ventilation. So the Va/Q is higher at the top and lower at the bottom.14 Vasoconstriction in some areas to divert blood from poorly ventilated areas to better ventilated ones, soimproves Va/Q matching. So using vasodilators in the case of poor ventilation to certain areas of the lungmay in some cases be detrimental.15 Because of vasoconstriction in the pulmonary vasculature16 5-10mmHg, pressure difference is caused by gravity (top of lung more efficient)17 When arterial pO2 falls below 8kpa and pCO2 rises to above 618 Hypoxaemic respiratory failure = due to failure of alveolar gas exchange, Hypercapnic = ventilatory (e.g.airway) failure.19 Cyanotic (congenital) heart malformation, pulmonary emboli, pulmonary edema20 Failure of CNS, spinal cord damage, myesthenia gravis, airway obstruction, COPD, asthma, musculardystrophy
  3. 3. 5. Why does CO2 retention not occur in type 2 respiratory failure (ventilationfailure)?216. What effect would hypoventilation have on arterial pCO2 and pO2227. What are the possible causes of hypoventilation?238. What is the most important chemical factor out of plasma pH, PaO2 and PaCO2in control of ventilation?249. Where would these chemical changes be picked up?2510.Why does a change in plasma pH alone not affect the central chemoreceptors?2611.What O2 sats would you begin to notice central cyanosis?27Respiratory Tract Bacteria and Viruses1. What organisms can be found in the normal flora of the upper respiratory tractand lower respiratory tract?282. What is the difference between endogenous and exogenous respiratory infectionsand give relevant examples?293. What are the two main common cold viruses?3021 Because CO2 diffuses across the alveolar membrane 20x better than O2, so if perfusion is normal it willget across the membrane. In the case of diffusion impairment, compensatory hyperventilation can actuallyresult in a lower than normal pCO2.22 Low paCo2 and high PaCO2. Hypoventilation is the only cause of hypoxaemia that will increase paCO2,others lead to reflex hyperventilation.23 Structural - failure of adequate chest wall movement (CNS damage), Failure of breathing control (loss ofchemoreceptor sensitivity to CO2), COPD, sleep apnoea, obstructive24 PaCO225 In the central chemoreceptors in the medulla, respond to pH of the CSF which is made more acidic by ahigher presence of CO2.26 H+ cannot diffuse across the blood-brain barrier so pH of the CSF affected mostly by plasma CO2, whichcan cross the blood brain barrier27 85% or lower, may not occur in anaemic patients, blueness comes from lots of deoxygenated haemoglobin28 Commensal bacteria, strep pneumoniae, haemophilus influenzae, some viruses. Lower respiratory tract isnormally sterile.29 Exogenous = airborne from another infected patient/animal. Endogenous = inhaled from URT, sometimesgut bacteria can increase and enter lungs via stomach and esophagus (if patients are on antacids).30 Rhinovirus 30%, Coronavirus 10%
  4. 4. 4. What is the common name for pharyngitis?315. What is the bacterial (30%) cause of pharyngitis and the early and latecomplications of this kind of infection?326. What are the pathogenic effects of the C diptheriae toxin?337. What is quinsey in relation to bacterial pharyngitis?348. What is Haemophilus influenzae?359. What is sinusitis?3610.List 3 examples of lower respiratory tract infections?3711.What is the link between haemophilus influenzae and blood?3812.Why does legionella pneumophila only grow in water?39Treatment of Infection 11. What is normal blood platelet count?402. List the main classes of antibiotics4131 Sore throat (pharynx-itits), 70% viral32 Strep Pyogenes. Complications = (early) scarlet fever, local abscess, (late) glomerulonephritis, rheumaticfever33 toxaemia (toxins in blood), myocarditis (infection of myocardium), neutritis (inflammation of nervoussystem), toxin inhibits protein synthesis at the host cell ribosome34 Complication of tonsilitis consisting of a collection of pus beside the tonsil35 Life threatening swelling of epiglottis that can cause respiratory obstruction within hours especially inyoung children36 viral URTI leads to defect on mucous membrane which results in blockage of sinuses. Symptoms areheadache, facial cellulitis and purulent discharge. Caused by haemophilus influenzae which can be presentin normal URT flora.37 Any of Strep Pneumoniae, Haemophilus influenzae, mycoplasma pneumoniae, chlamydia, influenza,adenovirus, mycobacterium tuberculosis TB, legionella pneumophila38 It needs blood factors in order to grow39 It grows inside amoebae which are present in water40 150-400 x10^9/L41 Penicillins/cephalosporins, Macrolides (e.g. erythromycin, clarithromycin), chloramphenicol,aminoglycosides, metronidazole, tetracyclines, quinolones, glycopeptides
  5. 5. 3. What is the difference between an antibiotic and an antimicrobial agent?424. What is antibiotic prophylaxis?435. Which gram type of bacteria have an outer membrane?446. By what mechanism do bacteria resist penicillins and caphalosporins?457. What part of the bacteria is targeted by macrolides such as erythromycin?468. By what mechanism does MRSA resist antibiotics?479. How does vancomycin resistant enterococci resist vancomycin?4810.Why is penecillin not effective against Pseudomonas and E. coli?4911.What does the tet (A) gene do in some resistant coliforms?5012.What 3 ways are resistance genes spread between bacteria?5113.What are MIC and MBC?5214.What is the MIC in mg/L for penicillin?5342 Antibiotic is a natural substance produced by an organism, an antimicrobial agent may be synthetic ornatural43 Pre-emptive treatment with antibiotics before an invasive procedure44 Gram negative bacteria, so antibiotics used against them must contain beta lactams to penetrate this45 Penecillins depend on beta lactams which target the bacterial cell wall peptidoglycan cross-links. Bacteriathen produce beta-lactaminases which attack the 4 membered ring of the antibiotic46 prokaryotic 70S ribosome of sterptococci and staphylococci47 Alters target site by producing a new PBP that is not inhibited by methicillin/flucloxacillin48 Again by an altered target site mechanism, altered cell wall pentapepdite instead of D-alanine to whichvancomycin normally binds49 Because they have an outer membrane which it cannot penetrate50 Resists tetracycline which has penetrated the membrane by pumping it out of the bacteria51 Conjugation (transmission of DNA between two cells), Transformation (when a bacterium takes upresistant DNA from a dead organism), Transduction (when DNA is spread by bacteriophages), viruses thatinfect bacteria.52 Minimum inhibitory concentration and minimum bactericidal concentration, a measure of how easily anantibiotic inhibits or kills a bacterium53 0.25mg/L, after incubation, bugs are killed at this concentration but not below it
  6. 6. Influenza1. What is the approximate size range for viruses?542. What is the capsid?553. Name the virus that causes influenza564. Describe the structure of this virus including names of its surface proteins575. How does the influenza virus enter new host cells?586. How many subtypes are there of the surface proteins, therefore varieties ofinfluenza A?597. What genes are these based on and where are they found as a reservoir?608. What is the difference between antigenic shift and antigenic drift?619. What were the 3 major pandemics of H/N flu in the 20th century?6210.How many different types of H and N are known to exist in nature?6311.How many cases per 100,000 population do you need to see before flu isconsidered an epidemic?6454 20-300nm55 A virusesʼ protein coat containing its receptors, forms nucleocapsid together with nucleic acid core.56 orthomyxovirus57 Lipid envelope with 2 surface glycoproteins (Hemagglutinin, neuraminidase), matrix proetin on innersurface and pores composed of M2 protein58 By attachment with host proteins, endocytosis into cell, dispersal of viral DNA and budding from cell59 15 variants of haemagglutinin, 9 variants of neuraminidase60 Based on H & N genes, found as a reservoir in birds and some mammals e.g. pigs61 Antigenic drift = minor changes, seasonal outbreaks, DNA replication as error accumulation. Antigenic shift= sudden and major changes, accounts for pandemic, genetic segment of virus changes, forms completelynew virus so host is no longer resistant (not seen in influenza B or C) e.g. mixing of animal strain with humanstrain62 H1H1 Spanish flu 1918, H2N2 Asian flu 1957, H3N2 Hong Kong flu 196863 16 H, 9 N64 200 per 100,000, this is considered higher than average and therefore epidemic
  7. 7. 12.How effective as a % is the flu vaccination?6513.What may be used as an treatment against influenza A?6614.What are neuraminase inhibitors?6715.What process is blocked by Relenza and Tamiflu?68Thermoregulation1. What is the difference between a poikilotherm and a homeotherm?692. Why is an aural temperature reading relatively quick and accurate?703. The skin contains temperature receptors, where are the three deep bodytemperature receptors located?714. Which part of the brain controls temperature regulating mechanisms, includingregulation of signals from all of the areas in (3)?725. What controls the regulation of venous plexus under the skin to moderateradiative heat loss?736. What is a countercurrent exchange?7465 70% annually, varies with different strains66 M2 channel blockers such as amantadine, blocks entry of virus into nuclear envelope and secretionpathway when in high concentrations67 target the protein on the influenza and prevent it from binding to other cells to replicate. Inhibits buddingand release.68 These are neuraminidase inhibitors, inhibit budding of new virus from invaded host cells, so cannotreplicate effectively69 poikilotherms body temp varies with changes in environmental temp, homeotherms have to have a corebody temperature maintained within narrow constant range despite variations in environmental temperature70 because it is close to the brain, which has 10x the blood supply of any other area of the body, auralthermometer detects infra red radiation from the hear drum.71 Spinal cord, abdominal viscera, great veins (SVC, IVC and pulmonary veins)72 Hypothalamus73 Sympathetic outflow moderated by hypothalamus.74 Deep veins in the limbs are positioned alongside arteries so that heat lost by the arteries is conserved bythe veins. In situations where the body wants to lose heat, countercurrent deep veins are constricted and theblood is routed to the skin.
  8. 8. 7. What are arteriovenous anastemoses?758. What is the composition of sweat when it is first secreted, at the bottom of thesweat gland?769. How does the composition of sweat change as it moves up the duct towards theskin?7710.How does sweat capacity change in someone acclimatized to high temperaturesfor a week?7811.How many times over can heat production be raised by maximum shivering?7912.Why is it of crucial importance that neonates are kept (incubated) at a fixedtemperature?8013.What is the muscle mechanism responsible for shivering?8114.What things can limit shivering?8215.What is ‘brown fat’?8316.What hormones are responsible for stimulating non-shivering thermogenesis?8417.What is a pyrogen?8575 arterio-venous plexuses in the skin which can constrict or dilate to regulate temperature enabling higherblood flow to the skin than would otherwise be possible76 Essentially the same as plasma but without albumin (and other proteins)77 At low sweating rates, most of the salt and water are reabsorbed as sweat moves up the duct, at highsweating rates more salt than water is reabsorbed but salt in surface sweat is still 50% of plasma levels.78 Sweat capacity increases 2-3 fold. There is a 5 fold reduction in salt loss during sweating, mostly due toincreased aldosterone secretion resulting from lowered plasma Na+, aldosterone increases absorbtion ofNa+ from sweat glands as well as in the kidneys79 x580 They have a poorly developed reflex for increasing temperature (particularly shivering)81 Stretch reflex centres in muscle are activated, causes feedback loop responsible for shivering82 Glycogen depletion, hypoglycaemia, hypoxia and some drugs.83 Type of adipose tissue especially important in newborns. Replaces function of shivering by maintainingwarmth, it contains numerous mitochondria which make it brown.84 thyroxine and epinephrine, increase transcription of UCP1 and UCP3, release free fatty acids that activateuncoupling85 A substance which causes an increase in body temp by resetting the hypothalmic set-point, e.g. toxin