Shit you just gotta know - Foundation to Resp Flashcards

1
Q

4 types of heat loss

A

conduction (touch), convection (carried away), radiation and evaporation

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2
Q

approx how much blood do we have?

A

5L

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3
Q

a DNA virus cannot be what type of shape?

A

helical

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4
Q

4 mechanisms of cell injury

A

mitochondrial damage, membrane damage, protein misfolding/DNA damge or Ca entry

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5
Q

a helical RNA virus always has what?

A

a lipid envelope

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6
Q

when is coagulative necrosis typical?

A

infarcts (except cerebral)

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7
Q

2 significant features of apoptosis

A

cell membrane intact, inflammation usually absent

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8
Q

nerve supply of IV disc? what part of disc

A

recurrent meningeal nerve - only outer third

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9
Q

significance of posterior longitudinal ligament? where does it run? where does ligamentum flavum run?

A

branches to cover IV discs while descending. runs in anterior part of vertebral canal.

LF = run horizontally on posterior part of vertebral canal b/w lamina

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10
Q

superficial muscles of back? where do they all attach and act?

A

trapezius, deltoid, latissimus dorsi, levator scapulae. attach and act on upper limb

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11
Q

describe the types of antagonism (3)

A

competitive (at binding site), non-competitive (pathway inhibition or functional/physiological antagonism)

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12
Q

3 kinds of allosteric modulation?

A
  1. Modulation of orthosteric ligand affinity 2. Modulation of orthosteric ligand efficacy 3. Modulation of receptor activation level
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13
Q

explain surmountable antagonism (competitive antagonism)

A

antagonist will compete with available agonist for receptor binding. Sufficient antagonist will displace the agonist from the binding sites, resulting in a lower frequency of receptor activation. Conversely increased agonist will displace the antagonist

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14
Q

5 signs of inflammation

A

redness, pain, heat, swelling, LOF

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15
Q

2 roles of neutrophil

A

phagocytosis and enzymes for breakdown of damaged tissue

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16
Q

5 causes of acute inflammation

A

infection, trauma, burns, infarction, foreign material

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17
Q

causes of pain in acute inflammation

A

bradykinin and prostaglandins

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18
Q

cause of fever in acute inflammation

A

IL-1, IL-6, TNF, prostaglandins

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19
Q

causes of vasodilation in acute inflammation

A

Histamine, prostaglandins, nitric oxide

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20
Q

causes of increased vascular permeability in acute inflammation?

A

Histamine, serotonin, bradykinin, leukotrienes,

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21
Q

endothelial activation in acute inflammation?

A

TNF, IL1

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22
Q

outcomes of acute inflammation? what leads into each outcome?

A

resolution, healing by repair or chronic inflammation.
minimal tissue damage > resolution.
some tissue damage > organization through phagocytosis and granulomatous tissue formation.
persistent tissue damage > chronic

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23
Q

3 infection that cause granulomatous inflammation other than TB

A

syphillis, fungal, parasitic

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24
Q

non-infectious cause of granulomatous inflammation. give 2 examples

A

Deposition of exogenous or endogenous irritant materials e.g. suture, keratin

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25
Q

mechanism of granuloma activation

A

macrophages present antigen to CD4 T > CD4 T releases Interferon Gamma (activates macrophages) and IL-2 (T ells)

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26
Q

what actually occurs in chronic inflammation?

A
  • Ongoing inflammation and tissue damage proceed at the same time as attempts at healing
  • Will persist until the damaging stimulus is eradicated
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27
Q

describe the structure of gram + and - cell walls

A
\+ = Peptidoglycan > plasma membrane
- = Outer membrane > peptidoglycan > inner membrane
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28
Q

how do bacteria cause tissue damage (3)

A

toxins (exo and endotoxins), induction of cytokines, induce immunopathology

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29
Q
overall function of a Beta LActam? one example. MOA.
What other drug class have same function - give example
A

inhibit cell wall synthesis. Penicillin
Bind cell wall at the d-ala, d-ala terminal >inhibit cell wall synthesis.> abnormal synthesis induces autolytic enzymes > weakens the cell wall > allows water in >bacteria will rupture.

Glycopeptides - vancomycin

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30
Q

2 types of resistance to beta lactams? MOA

A
  1. β-lactamases. destroy penicillins (and cephalosporins) by opening the β-lactam ring.
  2. Altered Penicillin Binding protein (PBP). Some bacteria have altered the protein to which penicillin binds. As such the Beta lactams cannot bind as well and the disruption of cell wall synthesis is less effective.
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31
Q

what is coamoxyclav?

A

amoxycillin (beta-lactam) and clavulinic acid (beta-lactamse inhibitor).

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32
Q

what is vancomycin and when/how is it used?

A

glycopeptide - used IV only on Gram Positive bacteria in penicillin allergic patients or MRSA

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33
Q

function MOA of aminoglycosides

A

cause the bacteria to misread the genetic code.
binds to the 30S subunit of bacterial ribosomes > cause distortion of the region where mRNA is translated > incorporation of incorrect amino acids or the premature termination of protein synthesis

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34
Q

3 resistance methods to aminoglycosides

A

modified outer membrane leading to reduced entry, enzymatic modification in cytoplasm leading to reduced entry, ribosomal mutation leading to reduced binding and efflux

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35
Q

how can bacteria acquire resistance? (2)

A

mutation and horizontal gene transfer

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36
Q

explain the 3 types of horizontal gene transfer. why is the 3rd type worrying?

A
  1. Transformation - DNA fragments of a lysed cell are taken up by a competent bacteria and incorporated into its genome
  2. Phage mediated - infection of bacteria by abnormal bacteriophage
  3. Plasmid mediated - 2 bacteria form cytoplasmic bridge>
    plasmid DNA replicates> is taken up by new bacteria> cells seperate.
    Worrying because bacteria don’t need to be related to receive plasmids
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37
Q

to commence replication what must viruses ultimately produce irrespective of its genome

A

mRNA

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38
Q

name 4 virus induced changes to a cell

A
  1. tumour induction.
  2. accumulate to cause cell lysis
  3. chronic infection - slowly release virus while keeping cell alive.
  4. latent infection - remains inactive in cell until change in circumstances (eg immunosupression)
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39
Q

apart from the plasma how else may virus spread. give example

A

cell-mediated - HIV through T cells

40
Q

T/F if false why? An essential step in the replication of all viruses is production of minus sense RNA

A

F - positive strand

41
Q

why is influenza limited to resp tract?

A

cleavage of the haemagglutinin can only be done by enzymes secreted by Clara cells

42
Q

with regard to seasonal influenza Cleavage of the viral haemagglutinin is necessary for what? Release is due to what?

A

escape the endosome. neuraminidase

43
Q

what are the 3 main receptors. which type is each?

A

Nicotinic is ligand. Adrerno + muscurinic are G-coupled

44
Q

what does SLUD stand for? which drug class activates this.

A

Salivation, Lacrimation, Urination, Defecation.

Muscurinic Agonist

45
Q

most common autonomic neurotransmitter exception?

A

sympathetic release AcH for sweat glands and adrenals

46
Q

how is histamine released?

A

released from mast cell degranulation if an antigen binds to an IgE antibody

47
Q

function of bradykinin(3)? what degrades it

A

dilates vessels, increases vascular permeability, stimulates nerve endings.
Degraded by ACE

48
Q

name 3 molecules that relax the endothelium and 1 that contracts it

A

NO, prostacyclin & EDRF (endo derived relaxing factor) relax.
Endothelin contracts

49
Q

distribution of blood in CVS

A

65% veins, 13% arteries, 5% capillaries, 10% lungs, 7% heart

50
Q

where are the baroreceptors? how do they work?

A

aortic arch and carotid sinus (internal carotid). Thin walled and highly innervated. More stretch = more firing

51
Q

where is the cardiovascular control centre?

A

medulla

52
Q

where can sympathetic and parasym nerves respectively act to alter BP

A
symp = SA node, Ventricles, Arterioles and Veins.
Para = SA node
53
Q

where are the chemoreceptors and what do they respond to?

A

aortic and carotid bodies. respond to low O2, low pH and high CO2

54
Q

what gets coagulation going?

A

TF (tissue factor) is exposed after damage to vessel wall

55
Q

what is key to the clotting system

A

thrombin. Too much = trombosis, too little = excessive bleeding

56
Q

what does thrombomodulin do?

A

inactivates thrombin

57
Q

how do glucocorticoids act on arachidonic acid pathway

A

block phospholipase A2

58
Q

what does prostacyclin do? what its its code

A

PGI2 inhibits platelets and vasodilates

59
Q

what does thromboxane do? what is its code

A

TXA2 activates platelets and vasocontricts

60
Q

how does the sino-atrial action potential differ from the ventricular?

A

Ca is the main depolarizer

61
Q

name the 4 major classes of antidysrhythmics.

A

Na channel block. Beta adrenoceptor antagonist. K channel blocker. Calcium Channel Blocker

62
Q

name the 4 classes of antihypertensive drugs?

A

ABCD.

A = angiotensin renin-system. B = beta antagonists. C = calcium channel blockers. D = diuretics

63
Q

what is a pericyte?

A

contractile cells that wrap around the endothelial cells of capillaries and venules throughout the body

64
Q

which part of the vascular system contributes most to changes in BP?

A

arterioles

65
Q

cardiac thrombi mainly caused by what? (2)?

A

infarction or LV aneurysm

66
Q

describe the 4 drug classes used in stable angina. where do they act

A

ivabridine decreases HR. Olols decrease HR, SV and afterload. Calcium channel blockers decreaes HR, SV and afterload. Nitrate decrease preload and afterload (dilate arterioles)

67
Q

name a counter-intutitve therapy of cardiac failure

A

Beta antagonists - SV actually increases coz of slower HRq

68
Q

causes of valve regurgitation (2)?

A

rheumatic fever or endocarditis

69
Q

causes of stenosis

A

rheumatic fever or degeneration

70
Q

main oral and injectable anticoagulants

A

warfarin and heparin

71
Q

what is heparin

A

injectable anti-coagulant

72
Q

what factors need vitamin K to activate them

A

2,7,9,10 (TV stations)

73
Q

streptokinase and alteplase are which type of drugs

A

thrombolytic

74
Q

what is dif about feotal Hb

A

have gamma instead of beta subunit (B for big person)

75
Q

name 4 things cholesterol forms

A

cell membranes, vitamin D, steroids and bile

76
Q

what carries cholesterol in blood. Name 4

A

lipoproteins - chylomicrons, VLDL, LDL and HDL

77
Q

grapefruit juice shouldn’t be combined with which drug. why?

A

statins - common pathway will increase statin toxcity

78
Q

r/ship with costal cartilage 1-3 and SVC

A

1st. braciocephalics meet.2nd. azygous joins.3rd. enter RA.

79
Q

the vagas nerve and phrenic run together which is more medial? which runs anterior to lung root?

A

vagas (does more things so needs to be closer to midline). phernic anterior to lung root

80
Q

how do the left and right bronchi differ? consequences

A

Right is shorter wider and more vertical - stuff will go down here

81
Q

structure of pericardium

A

outer fibrous layer. Inner serous layer which is split into parietal(fused to fibrous) and visceral (part of epicardium). Pericardial cavity is b/w the serous layers and contains serous fluid to lubricate

82
Q

describe how the ribs attach to the vertebral column

A

2 joints. Costoverterbral joint:Head of rib 4 articulates with inferior demi-facet on body of vertebra 3 and superior demi-process of 4.Costo-transverse joint:Tubercle of rib articulates with transverse process of vertebra above

83
Q

a bronchus becomes a bronchiole after the disappearance of what?

A

cartilage

84
Q

what and where is a clara cell?

A

secretes surfactant - appears in bronchioles replacing cilliated and goblet cells

85
Q

describe the cells of the alveoli

A

Type 1 pnuemocytes line the alveoli, are squamous epthiellium and take up 95% of surface area

Type 2 are more numerous and cuboidal epthelium. Usually located between alveoli.
Lamellar bodies secrete surfactant.

Alveoli Macros reside - when full the migrate up airways

86
Q

what is a triple Whammy

A

diuretic, ACE and NSAID can cause acute renal failure.

87
Q

most common cause of atypical (walking) pneumonia

A

mycoplasma

88
Q

when sore throat isnt viral, what is most likely

A

Strep. Pyogenes

89
Q

what is cor pulmonale?

A

the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or high blood pressure in the lungs

90
Q

definition of athsma

A

increased responsiveness of airways to stimuli leading to bronchoconstriction which is at least partly reversible

91
Q

definition of chronic bronchitis

A

persistent productive cough for at least 3 consecutive months in at least 2 consecutive years.

92
Q

2 main types of pneumonia. difference in CXR

A

alveolar (consolidation) and interstitial(atypical) (dots and dashes)

93
Q

what is the A-a gradient?

A

Alveolar-arterial is a measure of the overall efficiency of gas exchange across all A-C units

94
Q

where is the central Chemorecptor for resp? what does it respond to?

A

medulla. respond to CSF[H+]

95
Q

where are the peripheral chemoreceptors for resp? what do they respond to

A

carotid and aortic bodies. respond to low PaO2, low PH and high PaCO2