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phase 2 cardiovascular and respiratory block > week 4 > Flashcards

week 4 Flashcards

1
Q

H+ donator

A

acid

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2
Q

H+ acceptor

A

base

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3
Q

why is regulation of [H+] important

A

proteins eg enzymes are influenced by pH
at physiological pH most biosynthetic and metabolic pathways involve precursors which are ionised - degree of ionisation determines location of molecules in cells and organelles
deviation of pH hugely impairs cellular and metabolic function

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4
Q

acid-base disorder examples

A 
cardiovascular - BP, cardiac rhythm
respiratory - ventilation, resp rate
metabolic - protein wasting, bone
renal - electrolytes
GI
neurological - confusion, seizures
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5
Q

what can alter homeostasis and the acid-base balance

A

generation of CO2 from aerobic respiration
metabolism of foods generating acid or alkali
incomplete respiration producing lactic acid or keto-acids
loss of alkali in stool or loss of acid in vomiting

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6
Q

3 major components of acid-base regulation

A

buffering
ventilation - control of CO2
renal regulation of HCO3 and H+ secretion and reabsorption

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7
Q

how could [H+] be normal in an acid-base disturbance

A

happens at the expense of other blood chemistry eg [HCO3-] or pCO2

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8
Q

what are buffers and how do they work

A

buffers are weak acids, partially dissociated in solution

buffers react poorly with water and are available to react with either H+ or OH-

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9
Q

CO2 - HCO3 equation

A

CO2 + H2O H2CO3 HCO3 + H+
can simplify
CO2 + H2O HCO3 + H+

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10
Q

CO2 - HCO3 system

A

CO2 + H2O H2CO3 HCO3 + H+
CO2 is highly diffusible and is regulated by respiration so [CO2] is held constant
addition of H+ consumes HCO3 which generates CO2 and water - CO2 exhaled - little free H+
loss of H+ leads to the opposite
at physiological pH, [HCO3-]:[H2CO3] = 20:1 so the system effectively buffers H+
does not buffer CO2a

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11
Q

buffers other than HCO3

A

haemoglobin - buffers CO2 in blood
proteins - important intracellular buffer
bone - long term buffer
PO4 - intracellular and urinary buffer

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12
Q

volatile acid v fixed acid

A

volatile acid can be eliminated from the body as a gas

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13
Q

buffering a fixed acid

A

consumes HCO3
although CO2 will be ventilated, this will be at the expense of lowered [HCO3] - to remove the H+ effectively more HCO3 must be generated

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14
Q

how do the kidneys regulated acid-base balance

A

reabsorb filtered HCO3
secrete fixed acid: (two below - these remove volatile acid from body)
titrate non-HCO3 buffer in urine - primarily PO4
secrete NH4 into urine
all achieved by using selective permeability of the luminal and baso-lateral cell membranes to match transport of H+ and HCO3 in opposite directions

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15
Q

describe the reabsorption of filtered HCO3

A

active process largely in PCT with small contributions from TALH and DCT - consumes large amount of energy
maintaining acid-base homeostasis requires that virtually all filtered HCO3 is reabsorbed
inability to reabsorb filtered HCO3 is a cause of metabolic acidosis
no net loss of H+ or gain of HCO3

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16
Q

excretion of acid in kidneys

A

require to eliminate fixed acid
tubular cells generate a new HCO3 which is absorbed along with a H+ that binds to a base other than HCO3 - or is fixed with NH3
this takes form of either titration of filtered PO4 or secretion of NH4 into urine
titration of PO4 is dependent on delivery of filtered buffer and is relatively fixed
mechanism of NH4 excretion is complex but is able to be up-regulated in acidosis
failure to secrete H+ is a cause of acidosis

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17
Q

titration of phosphate in the excretion of acid

A

PO4 is the major non-HCO3 buffer in urine
delivery of PO4 is not amenable to much regulation but completeness of titration depends on urine pH
accounts for excretion of ~40mmol H+/day

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18
Q

excretion of ammonium in the excretion of acid

A

regulated by metabolism of glutamine
acidosis stimulates glutamine transport and oxidation
in normal conditions, generation of NH4+ accounts for 50-100mmol H+/day but can be increased

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19
Q

[H+] in acid-base disorders

A

primary disturbance which tends to make [H+] abnormal
acute change will be buffered - compensatory response so that [H+] remains in the normal range but will be at the expense of HCO3 or CO2

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20
Q

how do metabolic disorders alter [HCO3]

A

metabolic acidosis - decrease in [HCO3] and so a decrease in pH
metabolic alkalosis - increase in [HCO3] and so an increase in pH

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21
Q

how do respiratory disorders alter [CO2]

A

respiratory acidosis - increase in [CO2] so decrease in pH

respiratory alkalosis - decrease in [CO2] so an increase in pH

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22
Q

which disorders can increase H+

A

metabolic acidosis and respiratory acidosis

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23
Q

which disorders can decrease H+

A

metabolic alkalosis and respiratory alkalosis

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24
Q

approach to diagnose an acid-base disorder

A

initial clinical assessment - from history and examination and initial investigations make a clinical decision on what it is most likely to be
acid-base diagnosis - systemic evaluation of the blood gas and other results and make an acid-base diagnosis
synthesise info to make overall diagnosis

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25
Q

respiratory acidosis and link to COPD

A

condition where pCO2 rises due to increased generation of CO2 and reduced ventilation of CO2
in COPD;
reduced central sensitivity to hypoxia and hypercapnia
destruction of lung tissue causes ventilation/perfusion mismatch
respiratory muscle fatigue

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26
Q

how does the body compensate in respiratory acidosis

A

cause is respiratory so compensatory response is metabolic
acute phase - buffering
chronic phase - compensation

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27
Q

buffering respiratory acidosis

A

CO2 + H2O H2CO3 HCO3 + H+
addition of CO2 drive reaction to right generating H+
acute rise in H+ is buffered by protein (Hb and phosphate) leaving behind HCO3 which rises slightly

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28
Q

Compensating respiratory acidosis

A

effect of increased arterial pCO2 is to promote renal retention of HCO3
increase in ammonium excretion

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29
Q

causes of metabolic acidosis

A 
addition of extra acid:
generation of organic acid through metabolism eg lactic acidosis or keto-acidosis
ingestion of acid
failure to excrete acid:
renal tubular acidosis
loss of HCO3:
in stool (diarrhoea) or urine
compensatory response is fall in pCO2 due to respiratory drive
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30
Q

systemic effects of metabolic acidosis

A

specific symptoms relating to cause
CVS - arrythmias, increased cardiac contractility, vasodilation
respiratory - increased ventilation
metabolic - protein wasting, resorption of Ca from bone

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31
Q

lactic acidosis

A

lactic acid produced through glycolytic metabolism of pyruvate
buffered by HCO3 to lactate and then metabolised in liver (and kidney)
production of lactic acid is vastly greater than renal excretion of H+
acidosis usually results results from hypoperfusion and reduced hepatic clearance - occurs in sepsis
can occur due to drugs, liver failure, poisoning

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32
Q

acidosis of chronic renal failure

A

as renal function declines most patients become acidotic
intially - normal-AG acidosis due to reduced renal ammonium excretion
titratable acid excretion initially preserved due to increased PO4 excretion and decreased PO4 reabsorption in PCT
eventually patients may develop high AG as PO4 and other anions accumulate

33
Q

metabolic alkalosis

A

primary abnormality is decreased H+ and increased HCO3

compensatory response is hypoventilation thus increased pCO2

34
Q

causes of metabolic alkalosis

A

gastric acid loss in vomiting

hyperaldosteronism

35
Q

factors contributing to metabolic alkalosis

A

HCO3 is reabsorbed with Na when there is a deficiency of Cl
volume depletion:
Na reabsorption drives HCO3 reabsorption - promoted by aldosterone
chloride depletion:
HCO3 reabsorption in DCT requires Cl secretion - if tubular Cl reduced, gradient to reabsorb HCO3 increases
potassium depletion - not clear why

36
Q

2 mechanisms for secreting H+

A

titration of phosphate

excretion of ammonium

37
Q

two main types of drug and their differences

A

small molecules - chemically synthesised, cheap, common, usually oral
biologics - newer, expensive, more carefully designed for specific targets, derived from human proteins

38
Q

drug target examples

A 
usually a protein
regulatory - change the activity of cellular enzymes (receptor)
enzymes - may be inhibited or activated
transport - sodium potassium pump
structural
39
Q

types of drug target

A

enzyme linked
ion channel linked
g-protein linked
nuclear (gene) linked

40
Q

adrenoreceptors

A

g-protein coupled receptors
activation leads to activation of signalling cascades within cells which can have wide ranging effects on cellular function

41
Q

stimulation of alpha adrenoceptors

A

predominantly vascular smooth muscle contraction

42
Q

stimulation of beta adrenoceptors

A

increased cardiac contractility and heart rate

43
Q

efficacy

A

ability of a bound drug to change the receptor in a way that produces an effect - some drugs possess affinity but not efficacy

44
Q

potency of a drug

A

absolute conc of a drug needed for a particular effect

high potency - low conc needed for effect

45
Q

types of angonists

A

these are drugs that interact with and activate receptors - posses both affinity and efficacy
full - an agonist with maximal efficacy
partial - an agonist with less than maximal efficacy

46
Q

types of anatgonists

A

these interact with but do not change the receptor
competitive
non-competitive

47
Q

how competitive antagonists work

A

competes with agonist for receptor
surmountable with increasing agonist concentration
displaces agonist dose response curve to the right (dextral shift)
reduces the apparent affinity of the agonist

48
Q

how non-competitive antagonists work

A

drug binds irreversibly to receptor
produces slight dextral shift in the agonist drug response curve in the low concentration range
looks like competitive antagonist but as more receptors are bound, agonist becomes incapable of eliciting a maximal effect

49
Q

what is a drug adverse effect

A

a response to a drug which is noxious and unintended and which occurs at doses normally used in man for the prophylaxis, diagnosis or therapy of disease or for the modifications of physiological function

50
Q

types of drug adverse effect

A 
type a - related to the intended pharmacological action of a drug:
common 
predictable
usually dose related
not normally life threatening
type b  - adverse effects are unrelated to the known pharmacological action:
uncommon
unpredictable
usually not dose related
often life threatening
51
Q

median effective dose 50

A

ED50 - dose at which 50% of the population or sample manifests a given effect

52
Q

median toxic dose 50

A

TD50 - dose at which 50% of the population manifests a given toxic effect

53
Q

median lethal dose 50

A

LD50 - dose which kills 50% of the subjects

54
Q

equation for therapeutic index of a drug

A

TD50 or LD50 / ED50

55
Q

how therapeutic index is used

A

the higher the TI the better the drug

drugs acting on the same receptor or enzyme system often have the same TI

56
Q

conducting portion of the respiratory system

A

nasal cavities to the terminal bronchioles

57
Q

respiratory portion of the respiratory system

A

respiratory bronchioles to alveoli

58
Q

structure, function and location of respiratory epithelium

A

nasal cavities to the bronchi are lined by respiratory epithelium
consists of ciliated pseudostratified epithelial cells and goblet cells
warms, humidifies and filters incoming air

59
Q

location of goblet cells in respiratory tract

A

number decreases going down the respiratory tree and they are eventually replaced by clara cells which produce surfactant

60
Q

describe the mucocilliary escalator

A

has a protective function
goblet cells produce 2 layers of mucous - water layer and viscous layer
hair-like cilia project into the watery layer and move mucous away from the lungs
swallowed mucous is destroyed by stomach acid

61
Q

structure of the trachea

A

supported by 10-12 c-shaped hyaline cartilages
chondrocytes can be seen embedded in the matrix of the cartilage
posteriorly SM joins the ends of the c-shaped cartilage
lumen is lined by respiratory epithelium - deep to this is the submucosa which is rich on seromucous glands
these glands produce water and mucous secretions which hare delivered to the luminal surface by ducts
adds to the mucous being produced by goblet cells in RE

62
Q

structure of bronchi

A

walls have a similar composition to the trachea except that the cartilage is arranged as irregular plates
as bronchi divide from primary to tertiary they decrease in size and cartilage plates become smaller and fewer
number of submucosal glands and goblet cells also decreases

63
Q

structure of bronchioles

A

no cartilage or submucosal glands
smooth muscle makes up majority of the bronchiole wall
larger bronchioles lined by simple ciliated columnar epithelium with few goblet cells
as bronchioles decrease in size the epithelium becomes simple cuboidal with few ciliated cells and increasing number of clara/club cells

64
Q

type I pneumocyte structure and function

A

flattened/squamous with flat, dark oval nuclei and very thin cytoplasm
cells that are primarily involved in gas exchange
make up 40% of the number of cells in alveoli but 95% of the alveolar surface
also help to form blood-air barrier with BVs

65
Q

type II pneumocyte structure and function

A

cuboidal cells that bulge into the alveolar space to produce surfactant
surfactant acts like a detergent to reduce surface tension of the alveoli and prevent them collapsing on expiration
they are also progenitor cells that can proliferate to replace both type of pneumocytes
60% of cells in the alveoli but only cover 5% of alveolar surface

66
Q

components of the blood-air barrier

A

type I pneumocytes
endothelial cells of the capillaries
the fused BM of these cells in the middle

67
Q

how does a fibrotic lung effect gas diffusion

A

less efficient gas exchange due to the greater distance

68
Q

symptoms of a fibrotic lung

A 
shortness of breath
cough
finger clubbing
tiredness
reduced appetite and weight loss
69
Q

cardiovascular histology

A

inner layer - endothelium and subendothelial connective tissue
middle layer - contains muscle tissue
outer layer - adventitia (vessels) or serosa (heart)

70
Q

pericardium structure

A

pericardium is the serous membrane which lines the pericardial cavity
consists of a visceral (epicardium) and parietal layer
parietal sac is a network of collagen fibres which anchors heart in place within mediastinum
pericardial cavity contains pericardial fluid to lubricate contracting heart

71
Q

structure of the heart layers

A

epicardium - mesothelium and thick connective tissue - contains abundant adipose tissue which surrounds larger vessels
myocardium - cardiac muscle, connective tissue and abundant capillaries
endocardium - endothelium and thin connective tissue layer

72
Q

structure of the endocardium

A

simple squamous epithelium (protects valves) and underlying connective tissue which provides a smooth lining that helps prevent friction and aids blood flow
CT contains purkinje fibres and small blood vessels

73
Q

structure of myocardium

A

thickest layer
consists of cardiac muscle cells which are striated and branching in appearance with a central nucleus
intercalated discs contain gap junctions which help synchronise contractions of the cells

74
Q

structure of the epicardium

A

mesothelial cells are the visceral layer of the serous pericardium and these produce pericardial fluid
abundant adipose tissue surrounds larger coronary vessels and nerves

75
Q

structure and location of purkinje fibres

A

these are specialised cardiomyocytes
in endocardium
appear paler than cardiomyocytes as they have less myofibrils

76
Q

structure of blood vessel layers

A

tunica intima - endothelial lining provides a smooth luminal surface to minimise friction for blood
tunica media - smooth muscle
tunica adventitia - connective tissue and vaso vasorum

77
Q

structure and function of elastic arteries

A

characterised by numerous bundles of elastic fibres (elastic laminae) in the tunica media
conduct high pressure blood flow out of the heart eg pulmonary artery, aorta
enable the walls to resist pressure and recoil to maintain arterial pressure during diastole

78
Q

structure and function of muscular arteries

A

distribute blood to small arteries in the organs of body
thick tunica media dominated by SM, little elastic tissue - enables them to contract to maintain BP further away from the heart
internal elastic lamina forms a clear boundary between the tunica intima and tunica media
external elastic lamina forms a boundary between the tunica media and tunica adventitia

79
Q

structure of veins

A

tunica intima, media and adventitia are less obvious than in arteries
tunica media is thinner than the adventitia and the SMCs are not as well organised as in arteries
valves can be present

phase 2 cardiovascular and respiratory block (5 decks)

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