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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
respiratory acidosis and link to COPD
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
26
how does the body compensate in respiratory acidosis
cause is respiratory so compensatory response is metabolic acute phase - buffering chronic phase - compensation
27
buffering respiratory acidosis
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
28
Compensating respiratory acidosis
effect of increased arterial pCO2 is to promote renal retention of HCO3 increase in ammonium excretion
29
causes of metabolic acidosis
``` 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 ```
30
systemic effects of metabolic acidosis
specific symptoms relating to cause CVS - arrythmias, increased cardiac contractility, vasodilation respiratory - increased ventilation metabolic - protein wasting, resorption of Ca from bone
31
lactic acidosis
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
32
acidosis of chronic renal failure
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
metabolic alkalosis
primary abnormality is decreased H+ and increased HCO3 | compensatory response is hypoventilation thus increased pCO2
34
causes of metabolic alkalosis
gastric acid loss in vomiting | hyperaldosteronism
35
factors contributing to metabolic alkalosis
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
2 mechanisms for secreting H+
titration of phosphate | excretion of ammonium
37
two main types of drug and their differences
small molecules - chemically synthesised, cheap, common, usually oral biologics - newer, expensive, more carefully designed for specific targets, derived from human proteins
38
drug target examples
``` usually a protein regulatory - change the activity of cellular enzymes (receptor) enzymes - may be inhibited or activated transport - sodium potassium pump structural ```
39
types of drug target
enzyme linked ion channel linked g-protein linked nuclear (gene) linked
40
adrenoreceptors
g-protein coupled receptors activation leads to activation of signalling cascades within cells which can have wide ranging effects on cellular function
41
stimulation of alpha adrenoceptors
predominantly vascular smooth muscle contraction
42
stimulation of beta adrenoceptors
increased cardiac contractility and heart rate
43
efficacy
ability of a bound drug to change the receptor in a way that produces an effect - some drugs possess affinity but not efficacy
44
potency of a drug
absolute conc of a drug needed for a particular effect | high potency - low conc needed for effect
45
types of angonists
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
types of anatgonists
these interact with but do not change the receptor competitive non-competitive
47
how competitive antagonists work
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
how non-competitive antagonists work
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
what is a drug adverse effect
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
types of drug adverse effect
``` 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
median effective dose 50
ED50 - dose at which 50% of the population or sample manifests a given effect
52
median toxic dose 50
TD50 - dose at which 50% of the population manifests a given toxic effect
53
median lethal dose 50
LD50 - dose which kills 50% of the subjects
54
equation for therapeutic index of a drug
TD50 or LD50 / ED50
55
how therapeutic index is used
the higher the TI the better the drug | drugs acting on the same receptor or enzyme system often have the same TI
56
conducting portion of the respiratory system
nasal cavities to the terminal bronchioles
57
respiratory portion of the respiratory system
respiratory bronchioles to alveoli
58
structure, function and location of respiratory epithelium
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
location of goblet cells in respiratory tract
number decreases going down the respiratory tree and they are eventually replaced by clara cells which produce surfactant
60
describe the mucocilliary escalator
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
structure of the trachea
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
structure of bronchi
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
structure of bronchioles
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
type I pneumocyte structure and function
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
type II pneumocyte structure and function
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
components of the blood-air barrier
type I pneumocytes endothelial cells of the capillaries the fused BM of these cells in the middle
67
how does a fibrotic lung effect gas diffusion
less efficient gas exchange due to the greater distance
68
symptoms of a fibrotic lung
``` shortness of breath cough finger clubbing tiredness reduced appetite and weight loss ```
69
cardiovascular histology
inner layer - endothelium and subendothelial connective tissue middle layer - contains muscle tissue outer layer - adventitia (vessels) or serosa (heart)
70
pericardium structure
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
structure of the heart layers
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
structure of the endocardium
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
structure of myocardium
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
structure of the epicardium
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
structure and location of purkinje fibres
these are specialised cardiomyocytes in endocardium appear paler than cardiomyocytes as they have less myofibrils
76
structure of blood vessel layers
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
structure and function of elastic arteries
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
structure and function of muscular arteries
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
structure of veins
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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