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Water Dysbalance. Edema.

Case 1 (N 57)
Examination of a 32-year-old patient revealed various signs of pathology,
including excessive body mass: his height is 168 cm, and eight 8!"# $g" %he
patient also has a pasty face, periorbital puffiness, pale s$in& he had slo
rebound of tissue to its original contour after pressing the feet or shin ith the
fingertip" %he patient told the physician about tightness of a ring and shoes in
the evening" 'n investigation of the cardiovascular system revealed the
folloing: minor arterial hypotension, areas of cardiac dullness are slightly
increased& other parameters are unremar$able" %he daily urine volume is
ithin the normal range"
(uestions:
1" )hat is the possible cause of the patient*s excess of body mass+
2" ,efine the type of pathological process associated ith an increase in body
mass in this patient+
3" Explain the mechanisms of development of this pathological process"
'nsers:
1" -n general there are 2 variants of increase in body mass:
a" .besity /can be excluded0
b" 'ccumulation of ater /because of signs of generali1ed edema0
2" .verhydration /ater accumulation0" %ype: -so osmolar"
3" 2ause:
3igns of cardiac insufficiency li$e:
- increase in cardiac dullness /due to hypertrophy of ventricles
or dilation0
- decrease systemic 45
- -n this case is chronic cardiac insufficiency, since chronic is
characteri1ed by generali1ed edema /-n acute cases, it is
not0"
- -t is also uncompensated at this moment because it is
characteri1ed by generali1ed edema and decrease in 45"
6echanisms:
- 7irst this mechanism is associate ith compensative
reactions or adaptive reactions
- %o increase cardiac function, the body activates
antinatriuretic mechanisms to increase circulatory plasma
volume
- 4ecause, decrease in cardiac output, leads to insufficiency of
$idneys as a result of the general decrease in effective
arterial volume /volume of blood that is necessary to perfuse
all tissues and organs0
- 'nd so, decrease effective arterial volume compensation
/increase in diastolic volume0" %his may be achieved by
sodium retention and accumulation of ater"
- 6echanisms of sodium retention are activated through
increase in 8enin-'ngiotensin-'ldosterone 3ystem"
- 'lso, proximal sodium reabsorption may be also increase in
more severe cases of cardiac insufficiency"
3o, chronic cardiac insufficiency first starts ith osmotic edema"
4ut ith its progression and loss of contractile function, the start
may be insufficient to remove blood from the loer parts of the
body especially during the night by evening hours ith
accumulation of fatigue" 'nd so, one more mechanism is
hemodynamic edema /first as osmotic, no is hemodynamic0"
-t is uncompensated cardiac insufficiency, so it has 2
mechanisms at the same time: osmotic and hemodynamic"
)ith further progression of cardiac insufficiency after several
years, persistent congestion of venous vessels dystrophy
of organs especially liver /because it is a metabolically active
organ hich re9uires a large amount of oxygen0 cirrhosis
development of ascites loss of liver function ith poor
synthesis of albumin :-n this case more mechanism of edema
hich is oncotic;
Case 2
' !<-year-old patient =" as admitted to the therapeutic department of
hospital" .n examination: his face is pale and puffy, eyelids are sollen,
applying pressure to a rear aspect of the sole results in indentations that
persist for some time" .ver the last to ee$s the patient>s body eight
increased by 6 $g" =">s blood pressure is decreased, areas of the heart
dullness are increased" %he patient>s daily urine volume is close to the loer
boundary of the normal values" ?rine test: massive proteinuria /@! g protein
per day0, large amount of hyaline and axy casts, increased level of
aldosterone in the daily urine" 4lood test: hypoproteinemia, albuminAglobulin
ratio is decreased, moderate hypernatremia" 5athological changes in the
gastrointestinal tract or liver are not found"
(uestions:
1" )hat type of dyshydria developed in the patient and hat variety of it:
hyper-, hypo- or isoosmolar+
2" Explain the cause and pathogenesis of dyshydria in this patient"
3" )hat syndrome does the patient suffer from+
'nsers:
1" .verhydration /due to generali1ed edema in the body0" 7rom blood
test: there is hypernatremia, and since sodium is main osmolarity
substance that contributes largely to the total osmolarity, hypenatremia
leads to hyperosmolarity" 6aybe if later drin$ more ater, it may
become isoosmolar, but for no is hyperosmolar"
2" 2an see changes in content of urine /large amount of protein and
casts0 pathology of $idneys" 7urthermore changes in blood:
decrease albumin concentration and albuminAglobulin ratio" 3o,
diagnosis is nephrotic syndrome /-t>s not Bust renal insufficiency0
because protein losses are more than !g daily, it>s a very high loss, that
liver is unable to compensate by increase in protein synthesis and
there is hypoproteinemia" 3o in this case, it is renal nephrotic edema"
%he main mechanism of renal nephrotic edema is oncotic mechanism"
4ut at the same time there is hypernatremia, because it may be ith
some osmotic component" )ater is retained in the tissues less in
the lumens of the vessel decrease in the circulatory plasma volume
activates 8enin 'ngiotensin 'ldosterone 3ystem starts to retain
sodium hypernatremia" /.smotic mechanisms may also occur but
may be at some delay"0
.ther factors of edema:
5ericardiac factors /same symptoms as 2ase 10" %here are
signs of chronic cardiac insufficiency"
C3o, it may be a combination of 2 types of edema: cardiac and
nephrotic"
3" Dephrotic syndrome"
Case 3 (N 59)
' 22-year-old patient ho recovered from severe scarlet fever 2 ee$s
ago complains of headache, pain in the bac$, dyspnea, and palpitations"
,uring the last ee$ she has increased her body eight by 11"# $g" .n
examination: her face is pale& she has periorbital puffiness, and edema of
the shins and feet& the boundaries of the heart dullness are increased&
blood pressure is 18<A1<< mm Eg& daily urine volume is reduced" ?rine
tests sho the presence of erythrocytes, leu$ocytes, protein and granular
casts" 'n increased titer of the antistreptococcal antibodies /antistreptolysin
.0 is found in the blood"
(uestions:
1" -s there evidence of the $idney pathology in this patient+ )hat is the
possible cause of this pathology+
2" )hat is the cause of hyperhydration in this case: a decrease in ater
excretion by the $idneys or an activation of the ater-retention
mechanisms+
3" Explain the mechanisms of edema in this patient"
'nsers:
1" Fes" 3igns: 2hange in the volume of urine, change in components of
urine" -t is acute inflammatory pathology of the $idneys" -t develops
acutely and the urine contains blood, erythrocytes and lymphocytes
/sign of acute inflammation0" 3o e call this pathology nephritis, in this
case, glomerular nephritis because glomeruli are definitely affected"
3o, this pathology is associated ith infection" ,isorder
developed after the infection" 3o it>s not the direct effect of
streptococcus on $idney parenchyma" -t is the aftermath of the
infection"
6echanism of disorder is associate ith immunity against the
infection, called acute post-streptococcal glomerular nephritis"
4ecause streptococci do not cause diffuse inBury to parenchyma"
%hey may cause abscesses during septicemia /but there are no
signs of septicemia0" 3o, the mechanism of pathology in this
case is production of antibodies against the streptococcus and
not any streptococcus can cause the disorder, only some
specific strains i"e beta hemolytic of 6 group, because the
superficial antigens of this strain of streptococcus resemble
antigens of glomerular basement membrane in some individuals
and so antibodies produced against antigens of the
streptococcus may cross react ith the basement membrane"
)hen they react, they bind complement and activate it and
starts the inflammation of the glomeruli"
%ype of edema: Dephritic edema"
2" 4oth of these mechanisms can operate"
,ecrease excretion is the result of decrease in glomerular
filtration rate /poor filtration of blood0" %his is due to the
disturbance of blood flo through the glomeruli, probably
because of some obstruction" -nflammation had caused
activation of the clotting system and thus clots may obstruct the
capillaries of the glomeruli" 3o, sitching off some nephrons
from filtration process" 't the same time, the inflammation may
activate 8enin 'ngiotensin 'ldosterone 3ystem and initiate
retention of sodium and then ater"
%ype of edema: .smotic /by its mechanism0
3" 3ee both (1 G (2"
Case 4 (N 60)
' H-year-old boy developed a progressive selling of the soft palate ith
a salloing difficulty, and then asphyxia after he had drun$ mango Buice"
%he mucosal membrane in the selled area is hyperemic ithout
tenderness& a moderate increase in eosinophils is seen in the blood" %he
patient*s body temperature is normal" Eis senior sister suffers from attac$s of
bronchial asthma"
(uestions:
1" -s edema in this case the result of ordinary inflammation+
2" )hat is the cause of edema in this patient+
3" Explain the pathogenesis of the given pathology"
!" ,oes this type of edema lead to life-threatening condition+
'nsers:
1" 'llergic reaction" Dot Bust ordinary inflammation but also allergic
reaction" ,ifference beteen allergic inflammation and non-allergic
inflammation /for example caused by infection0:
.rdinary inflammation has the first stage that is alteration
/destruction of tissue0" 'llergic inflammation especially allergic of
the 1
st
type has no destruction of tissue" -t is not inBury that
initiates inflammatory process" -t starts ith the release of
mediators" -n ordinary inflammation, it starts ith inBury then
release of mediators"
2" 2auses of edema:
6ediators that increase permeability"
3" 3o by mechanism, this edema is membranogenic edema" -t leads to
exit of plasma proteins in the surrounding tissue and accumulation of
ater"
!" Fes" Emergency state especially in children" 4ecause selling of the
soft tissues of throat and trachea leads to complete obstruction of the
upper airays" 3o sometimes there is a necessity to cut trachea and
insert a tube for breathing"
Case 5
' #<-year-old male patient visited his physician ith complaints about
rapid gaining of body eight and edema of the feet" Eis usual body eight of
about H<$g recently increased to 11<$g" %he medical history of the patient
includes a long period of alcohol abuse" .n examination: blood pressure is
11<AH< mmEg& the s$in has signs of the dilated capillaries on the torso /spider
angiomata0 and hands /palmar erythema0" Evaluation of the respiratory and
cardiovascular systems reveals no pathological changes" %he abdomen of the
patient is significantly distended& on percussion, the region of dullness is
shifting hen the patient is turned from supine position to side-lying /shifting
dullness0" =oer extremities are sollen" %here are signs of testicular atrophy"
4lood test results: glucose I !"!! mmolA=, total plasma protein I #3 gA= /D:
68-81 gA=0, albumin I 2< gA= /D:3#-#3 gA=0"
(uestions:
1" )hat forms of pathology can be diagnosed in this patient+
2" )hat is the etiology and pathogenesis of these forms of pathology in
the patient+
3" ,efine the pattern of ater-mineral dysbalance in this patient" )hat is
the cause of this dysbalance+
'nsers:
1" Eepatic insufficiency due to cirrhosis" 5atient has signs of cirrhosis:
portal hypertension ascites /significant sign of portal hypertension is
ascites0" 'scites in this case is manifested as excessive distention of
the abdomen and shifting dullness, because of free ater that may
move inside the abdominal cavity"
2ause of cirrhosis: alcoholic"
2" Etiology G pathogenesis:
7irst, starts as hemodynamic, because of high pressure in portal
vein"
%hen ith liver insufficiency, it becomes oncotic"
3" -n general the pattern of ater-mineral dysbalance in this patient is
overhydration"
Case 6
' 2#-year-old patient ho suffered from diabetes mellitus as admitted
to hospital ith complaints of episodes of syncope" Ee used propranolol
/beta-adrenobloc$er0 to treat his arterial hypertension" %he physician of the
admission ard too$ a sample of the patient>s blood to ma$e an electrolyte
analysis" Eaving assumed that the patient had lo blood glucose levels the
physician inBected him 2<ml of the #<J glucose solution" 3oon after the
inBection of glucose the patient developed collapse and cardiac arrest"
8epeated administration of the blood electrolyte concentration shoed:
.n admission 'fter inBection of glucose Dormal values
DaK 13< mmolA= 12L mmolA= 13#-1#6 mmolA=
2l- L< mmolA= L1 mmolA= L#-1<# mmolA=
MK 6"# mmolA= 8"# mmolA= 3"#-#"3 mmolA=
E2.3- 1< mmolA= 11 mmolA= 2!-32 mmolA=
Nlucose !<< mgAdl 6<< mgAdl 6#-11< mgAdl
(uestions:
1" )hat disorders of electrolyte balance are found in the patient on
admission+ Explain their causes"
2" )hat disorders of electrolyte balance are found in the patient after
inBection of glucose+ Explain their causes"
3" Explain the development of cardiac arrest in this patient"
'nsers:
1" Eigh concentration /increase0 of potassium on admission" 2ause:
=ac$ of insulin because the normal effect of insulin is increase in
transport of potassium inside the cell" -f insulin is deficient, more
potassium remains in external environment" 6oreover, use of
propranolol may exacerbate this hyper$alaemia because beta-
adrenobloc$ers prevent active transport of potassium inside the
cell"
2" %here is more hyper$alaemia after inBection of glucose /more severe0"
2ause:
-ncrease in glucose concentration leads to increase osmolarity"
4ecause in diabetes mellitus patient, glucose is osmolatically
active agent" -t is not the case in normal individuals" -f in normal
individuals, glucose ill be consumed by the cells and ill not
increase the osmolarity of blood"
)hen osmolarity of plasma is increased, ater ith dissolved
solutions /potassium in this case0 exit from the cell into the
interstitial media and plasma hyper$alaemia"
4ecause osmolarity dras ater from inside the cell" -f
osmolarity of media outside is higher than inside, ater is dran
out"
3" 2ause of cardiac arrest:
5otassium" 2oncentration of 8"# mmolA= is already fatal"
Dot because of calcium"
,ue to depolari1ation of cardiomyocytes, especially cells of the
conducting system"
4ecause resting potential is formed by exit of potassium from
inside the cell /outflo of potassium0" 'ctually, there is balance
beteen inflo of sodium and outflo of potassium" 3o the
internal surface potential is negative" %hat>s hy resting potential
inside the cell is negative" -f current of potassium is disturbed
/decreased0, there is accumulation of positive charge and
depolari1ation"
4ut ith high concentration of potassium, the gradient is
decreased and so sloing of outflo potassium current and this
causes relative accumulation of positive charge inside the cell
and depolari1ation" 5artially depolari1ed cells are unable to
conduct impulses, can>t develop action potential heart stop
because of bloc$ade of conduction"
4loc$ade: stop of propagation of impulses in the heart& due to
partial depolari1ation of the cells"
'ction potential is produced due to opening of fast sodium
channels" )ith partial depolari1ation, fast sodium channels are
closed"
Case 7
' H#-year-old female patient as transported to hospital by ambulance that
as called by a health visitor ho as used to regularly visit the patient" %he
nurse reported to the physician that the patient lived alone and during the last
ee$ suffered from fever and cough" .n examination: the patient is confused,
responds sloly to 9uestions& her s$in and visible mucous membranes are
dry, turgor of the s$in and eyeball is notably decreased" 4ody temperature is
3H"# degrees, blood pressure I 1<<A6< mmEg /according to the nurse her
usual 45 is 1#<AL# mmEg0, heart rate I 12< beatsAmin, breathing rate I
2<Amin" electrolytes of the blood plasema: DaK O 16< mmolA= /D: 13#-1#6
mmolA=0, MK -#"L mmolA= /D:3"#-#"3 mmolA=0, 2l- 82 mmolA= /D:L#-1<#
mmolA=0, E2.3- 2# mmolA= /D:2!-32 mmolA=0
(uestions:
1" )hat forms of dyshydria developed in the patient+ )hat is its li$ely
cause+
2" )hat changes in the volume and osmolarity of the intracellular
compartment, interstitial fluid, and extracellular compartment are typical
in this type of dyshydria+
3" )hat other pathological conditions are accompanied by this type of
dyshydria+
!" )hat solution of Da2l /hypo-, hyper-, or isoosmolar0 is recommended
for infusion to this patient to normali1e her ater-electrolyte balance+
'nsers:
1" ,ehydration" 2linical signs: dryness, loss of turgor, decrease 45,
tachycardia"
2" -ntracellular compartment becomes less, it losses ater" -nterstitial
fluid: osmolarity is increased hile volume is decreased" Extracellular
compartment is decreased"
3" )ater starvation" Eyperosmolar dehydration" 5atient lived alone and
probably develops an infectious disease and so as lying on the bed
most of the day drin$ less ater than re9uired /accompanied by
more ater loss due to fever0" 'fter several days, develop dehydration"
!" -soosmolar" 4ut infused sloly, because of great ris$ of brain edema"
Even if you start to infuse hyperosmolar solution to decrease
concentration of sodium, osmolarity of the intercellular
compartment in the brain may occur higher than osmolarity of
plasma because brain during slo development of
hyperosmolarity develops their on adaptive mechanisms to
prevent ater loss" -t tries to increase osmolarity by
accumulation of substances li$e amino acids, myoinositol and
other substances to increase osmolarity"
)hen start infusion of isoosmolar /or especially hyperosmolar0,
the osmolarity of intercellular compartment may occur higher
than extracellular and ater may start to enter the cells in
excess and increase the volume of the brain"
3o normally there should be infusion of isoosmolar solutions for
one period of time /eg 2 days0 but not Bust several litres at once"