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PP2131 end of semester exam (guided)
Terms in this set (134)
has stable set points (minutes/hours/days); assumes one set point
adjusts homeostasis for conditions
homeostasis with a lifespan trajectory (changes with age); continued development changes 'normal' homeostasis
in the brainstem
a. Location of control centres
fight or flight
a. Sympathetic responses
rest and digest
a. Parasympathetic responses
increased breathing, O2 in blood, heart rate, blood in muscles; decreased blood in stomach, abstract thinking, pupils dilate, skeletal muscles brace
Discuss the concept of stress in terms of physiology
alarm stage = response, resistance stage = removal of response or adaptation, a new set point; exhaustion stage = stressor or response overwhelms
Define the stages of the general adaptation syndrome
short = prepare for increased activity, fight or flight response, rapidly remove stress; long = reinforces catecholamine response, longer term response, expect stressor to be more persistent
Examine short and long term stress responses
tissue = increased pulse, BP, respiration, muscle tension, nausea, vomiting, diarrhoea, sweat, fatigue; behavioural = anxiety, irritability, reduced concentration, altered sleeping/eating patterns, increases substance abuse
Briefly examine some tissue and behavioural responses to stress
vascular = vasodilation, increased permeability; cellular = platelets, mast cells, later, neutrophil infiltration, macrophages, eosinophils, basophils
Describe the vascular and cellular events in acute inflammation and the key chemical mediators
due to persistent acute inflammation, repeated bouts of acute inflammation, long acting and never showing acute inflammation
Describe chronic inflammation
serous (mild inflammation, fluid, watery), fibrinous (sticky, contains fibrin), purulent (from infection, neutrophils, debris, pus, icky), haemorrhagic (severe, leakage of blood vessels)
Characterise exudates from inflammation
a) re-epithelialisation, collagen and wound formation, contraction and remodelling
b) initial injury, osteoblast invasion, osteoclasts digest dead bone, remodelling
c) cardiac muscle = no regenerative capacity; smooth muscle = much regenerative capacity; skeletal muscle = has some regenerative capacity
Describe wound healing in:
a. Skin (epithelium)
ischaemia, nutritional, infectious and immunological, chemical, physical
Describe the 5 causes of cellular injury
hyperplasia, metaplasia, hypertrophy, dysplasia, atrophy
Describe the 5 cellular adaptations to injury and environmental challenge
necrosis = coagulative, liquefactive, fat, caseous; gangrene = gas, wet, dry
Describe the characteristics of the 4 types of necrosis and 4 types of gangrene
programmed cell death
Describe the processes of apoptosis
progressive narrowing of the arterial lumen obstructs blood flow; thrombus formation, coronary vasospasm, and endothelial dysfunction may also cause ischaemia; ischaemia may lead to myocardial infarction
Describe atherosclerosis and how to contributes to coronary heart disease:
asymptomatic until the person is stressed, as with exercise
may rupture or erode, evoking thrombus formation and acute coronary occlusion, commonly associated with ACS & sudden cardiac death, has a thin fibrous cap
failure of the heart to pump blood effectively leading to congestion in the systemic or pulmonary circulations
Define congestive heart failure
slow progression due to obstruction by atherosclerotic plaque, ischaemia is intermittent, conditions include stable angina pectoris & ischaemic cardiomyopathy, treatment is rest &/or nitroglycerin
Chronic coronary syndrome
sudden, unpredictable of severe and prolonged angina, plaque rupture and acute thrombus formation believed to underlie angina, conditions include unstable angina pectoris and myocardial infarction.
Treatment is repercussion therapy (if there is ischaemia) and anti platelets (if there is no ischaemia)
Acute coronary syndrome
the inability of muscle to contract; <50% of LV blood pumped
the inability of muscle to relax; >50% of LV blood pumped
atrial or ventricular cells which should lack automaticity become able to spontaneously depolarise and produce action potentials, producing new pacemakers
inappropriate automaticity (mechanisms of abnormal sites of impulse initiation)
an extra action potential is triggered spontaneously during or immediately following repolarisation (includes EADs and DADs)
triggered activity (mechanisms of abnormal sites of impulse initiation)
two types, functional - occurs when part of the electrical conduction in the heart is abnormally slow, and anatomical - occurs when part of the electrical conduction in the heart is through an unusually long pathway
re-entry (mechanisms of abnormal sites of impulse initiation)
growths formed by colonies contained in fibrin deposits occur on the valves
people with healthy hearts develop endocarditis secondary to an acute bacterial infection, IV drug users and people with gum disease are especially vulnerable
generally affects people with pre-existing susceptibility for bacteria colonising in their valves
'congestive', the dilation of all 4 chambers where the muscle becomes thin and mild fibrosis is observed;
ventricle (left is more likely) becomes thickened and hyperkinetic, may impair filling or obstruct ejection, and reduce end-diastolic volume and compliance, resulting in diastolic dysfunction
the myocardium becomes stiff and fibrotic, with fibrosis found on both ventricles, impairs diastolic filling and low stroke volume, and can lead to LHS congestive heart failure
allows oxygenated blood to flow back to the right side of the heart, to be sent to the lungs again, oxygenation of the systemic system isn't compromised (acyanotic defect) but the heart must work harder to pump the extra volume to the lungs
left to right shunts
allows deoxygenated blood to flow from the right side of the heart into the left and the systemic circulation, causing cyanosis
right to left shunts
restricted openings obstruct blood flow, workload is greatly increased and heart failure may occur
if the atrial septum doesn't shut, blood can shunt from LA to RA (high to low pressure), may lead to pulmonary hypertension, RV hypertrophy and a right-to-left shunt (cyanosis) and heart failure), repaired by surgery
atril septal defect
shunt is at first left-to-right, increasing RHS workload and potentially leading to pulmonary hypertension, RV hypertrophy and shift to right-to-left shunt, surgical repair of large defects
ventricular septal defect
in utero, allows blood to bypass the lungs by flowing from the pulmonary artery to the aorta, may not have any clinical significance if shunt remains left-to-right, without surgical correction may develop into right-to-left shunt
Patent ductus arteriosus
abnormal fusion of the cusps causes obstruction, afterload is increased and RV hypertrophies, corrected by surgery
Pulmonary artery stenosis
abnormal function of cusps or abnormal development of subvalvular fibrous ring, high LV afterload due to resistance to blood ejection, LV hypertrophy, surgical replacement
narrowing of the aorta in any position, but is more common before (preductal) and after (postductal) the ductus arteriosus, preductal is more severe as can compromise blood flow to the lower extremities, the resistance offered by severe preductal coarction increases LV workload, leading to
Coarction of the aorta
severity relates to the degree of pulmonary stenosis, the overriding aorta receives the deoxygenated blood, producing cyanosis, 4 things go wrong (pulmonary stenosis, overriding aorta, valvular septal defect, and right ventricular hypertrophy)
Tetralogy of Fallot
the structure of the great arteries (pulmonary artery and aorta) are moved as they go straight down instead of crossing over resulting in being attached to the wrong ventricle
Transposition of the great arteries
where the pulmonary artery and the aorta 'fuse' into one, creating one single blood vessel connected to both ventricles, pulmonary vs. systemic pressure profiles determine how much blood flows down each artery
caused by insufficient blood flow and oxygen to the muscle of the heart; supply does not meet demand
Describe the pathology of angina
Occlusion of artery secondary to plaque rupturing and thrombus formation (complete of major artery
What is a STEMI
partial blockage of major artery/complete blockage of minor artery
What is a NSTEMI
reduce platelet aggregation and activation, reduce the blood cells clumping together
what do anti platelets do?
reduce the body's ability to form clots, lengthens the time it takes to form a clot, also known as blood thinners
what do anticoagulants do?
dissolves clots in vessels, increases blood flow
what do thrombolytics do?
heparin, warfarin, rivaroxaban
drug management of VTE?
acts on proximal convoluted tubule & descending loop of Henle, inhibits fluid absorption
acts on the ascending loop of Henle, 20-25% of fluid reabsorption here
acts on the distal convoluted tubule, inhibits the absorption of sodium and chloride in the proximal segment of DCT
acts on the ascending loop of Henle & the collecting tubule
potassium sparing diuretics
acts on phases 4 & 0, it blocks the voltage-dependent sodium channels
what part of the action potential do class 1 work on?
acts on phase 4, extends the refractory period
what part of the action potential do class 2 work on?
acts on phase 3, prolongs cardiac action potential duration (increased Q-T) and decreases the rate of action potential
what part of the action potential do class 3 work on?
acts on phase 2, shortens phase 2 therefore shortening the action potential
what part of the action potential do class 4 work on?
vasodilator at low dose, vasoconstrictor at high dose, ionotropic and chronotropic at high dose, may trigger angina due to high cardiac workload
stabilises mast cells, product of noradrenaline, reduces bleeding via vasoconstriction
vasodilator and inotrope, product of isoprenaline, increases myocardial O2 demand so may exacerbate ischaemic heart disease
alpha agonist activity, manly vasoconstrictor effects, mild inotropic and chronotropic effects, product of dopamine
positive inotropic and chronotropic effects, reduces peripheral resistance, improves coronary blood flow, increases automaticity and AV nodal conduction
40% ICF, 18% fat, 22% solids, 15% ISF, 5% plasma volume
Examine the ionic composition of body fluid compartments and ion movement
EC ions and buffer effect - increased ECF
only expands plasma, isotonic
cortex (outside, features the glomerulus, proximal tubule, distal tubule); medulla (middle, features the nephron loop, collecting ducts); pelvis (inside)
Revise the structure of the kidney
reabsorption in proximal tubule, regulated reabsorption in distal tubule
where is sodium reabsorbed?
reabsorption in proximal tubule, regulated absorption in collecting duct
where is water reabsorbed?
reabsorbed in proximal tubule and nephron loop, regulated in distal tubule by aldosterone
where is potassium reabsorbed?
most reabsorbed in proximal tubule, regulated in the distal tubule by parathyroid hormone
where is calcium reabsorbed?
bicarbonate produced in proximal tubule, secreted into urine and distal tubule
where is acid produced/secreted?
formed in HCO3 formation and acid excretion
where is ammonia produced/secreted?
produced by liver, filtered in glomerulus
where is urea produced/secreted?
waste product of creatine metabolism, produced in muscle, not absorbed nor secreted
where is creatinine produced/secreted?
recycled in blood by production in kidneys, extra bicarbonate is produced by the metabolism of glutamine
how do the kidneys regulate bicarbonate?
excreted via urine with ammonia
how do the kidneys excrete acid?
damage to the glomerulus leading to protein losses due to inflammation
what is glomerulonephritis?
excessive protein losses
what is nephrotic syndrome?
sudden loss of renal function
define acute renal injury
Inadequate blood supply (pre-renal), damage to nephron (renal), ureter blockage (post-renal)
what are the 3 causes of acute renal injury?
Looks at creatinine and urine output criteria
what does the RIFLE scale look at?
reduced blood flow to nephrons, causes include absolute ECF volume decrease & decreased renal blood flow, high osmolarity of urine, and normal ratio of urine: plasma osmolality
what is pre-renal injury?
damage to nephrons - they start to die leading to reduced absorption capacity and cannot process electrolytes properly, has high sodium in urine & high sodium clearance rate
what is intra-renal injury?
death of tubular epithelial cells that form the renal tubules of the kidneys, presenting with acute kidney injury caused by ischaemia and nephrotoxin
what is acute tubular necrosis?
nephron damage/death, reduced removal of waste, regulation of volume and regulation of ions (RIFLE scale)
what is the oliguric phase?
recovery, increased urine, sodium & electrolyte output
what is the post-oliguric phase?
an obstruction of renal outflow and can be due to occlusion of ureter/urethra, or drugs inhibiting bladder constriction, sphincter relaxation
what is post-renal failure/injury?
some form of kidney damage GFR>90
what is stage 1 of chronic kidney disease?
reduction in GFR but no other symptoms GFR 60-89
what is stage 2 of chronic kidney disease?
other symptoms start developing hypertension, further decrease in GFR 40-59
what is stage 3a of chronic kidney disease?
other symptoms start to develop, further decrease in GFR 30-44
what is stage 3b of chronic kidney disease?
symptoms progressing, further reduction in GFR 15-29
what is stage 4 of chronic kidney disease?
end stage, <15
what is stage 5 of chronic kidney disease?
Pressure change required to alveolar volume change
what is compliance?
minimal volume of air in lungs that you can never exhale
volume of air that never gets near respiratory surface
dead space volume
usual amount of air you exchange
air held in lungs that you never breathe out
amount of air you usually breathe out
inspiratory reserve + tidal volume
the amount of air you can physically move in and out, approx. 8-% of lung volume
when the usual amount of air you exchange (TV) includes the ventilation of dead space so not all the tidal volume gets to the alveoli
the air taken into the respiratory system every minute
Defines what is important in the diffusion of gas from the alveoli into the blood & vice versa
what does ficks law do?
what is the driving pressure of CO2
what is the driving pressure of O2?
high arterial CO2
low arterial CO2
low O2 in the tissue
low O2 in the arterial blood
Neuromuscular, vascular, trauma, respiratory and body shape
what are the 5 causes of acute respiratory failure?
anything that increases resistance
define obstructive lung disorders
decreased lung compliance - alveoli hard to inflate
define restrictive lung disorders
infections, secretions (post op or excessive) or foreign material
what are the 3 types of pathology which can lead to airway obstruction?
what is the diagnostic test for asthma?
have to relieve bronchoconstriction & reduce inflammation; mild/moderate = low dosed inhaled corticosteroids (ICS); severe = SABA with LABA and ICS
therapeutic regimes for asthma
is an excessive mucus production which is common in smokers, hypertrophy in mucus glands
describe chronic bronchitis
Centriacinar (damage of the central lobule); panacinar (distention of the whole lobule); paraseptal = peripheral lobes
postural changes, physio, mucolytics to expect sputum
chronic bronchitis treatments
essation of smoking, inhaled bronchodilators, anti-tussives, expectorants, O2 therapy (late stages)
progressively, partially reversible airway obstruction and hyperinflation
emphysema = rises at .25, decreases at .5 & 7, goes under x axis at 4.5; bronchitis = rises at .25, drops at .5 & 8, drops under x axis at 5.5; pulmonary fibrosis = rises at 4.25, drops at 5.25, drops under the x axis at 7.
Describe flow volume loops for defining lung disease
anti-muscarinic agents, SABA sued for acute events, but LABA can be added as severity increases; in extreme cases use corticosteroids
treatments for COPD
damage to the alveolar-capillary membrane, which leads to hypoxemia despite oxygen therapy
define acute respiratory distress
air in the pleural cavity which restricts its capacity to inflate; treatment is chest tube, suction and supplementary oxygen
define pneumothorax & treatment
Spontaneous (rupture of the alveoli), open (open hole in the chest wall) and tertiary (air enters but doesn't leave)
what are the 3 different types of pneumothorax?
The escape of fluid from a vessel via rupture or exudation; treatment is drainage, treatment of the underlying cause & surgery
define effusion & treatments
Pleural, transudative (fluid has little protein), exudative (from leaky capillaries, has high protein), empyema (infection of the intrapleural space, haemothorax (blood in pleural space) and chylothorax (damage to the lymphatics)
what are the different types of effusion?
administer a vasodilator drug to reduce afterload
A patient comes to the clinic complaining of crushing chest pain. She is diagnosed as having acute myocardial infarction. Which of the following manipulations would be the best choice to immediately ease her pain?
systemic venous congestion
Right-sided congestive heart failure produces both forward and backward effects. Which of the following effects are included in the backward effects of right-sided congestive heart failure
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