Samenvatting
Summary Lectures PAC
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- Universiteit Leiden (UL)
Summary of all lectures and workgroups PAC
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Voorbeeld 2 van de 12 pagina's
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SepsisLecture 1
Sepsis is a disease that is pretty prevalent. These patients may have a severe infection. The response
of the body will be heavy and may lead to pathology. This can be seen with low blood pressure,
tachycardia and neurological symptoms.
Severe sepsis --> organ failure
Septic shock --> need a lot of medication to keep pressure normal
Toll like receptors were discovered in the fruit fly. What happens is that if a pathogens enters the
human body then parts of the pathogens stimulate an innate immune response. TLR4 will be
triggered by LPS which can be found on gram negative bacteria outer wall. This leads to the
activation of pro-inflammatory cytokines which will activate the immune system. The inflammatory
response is propagated in order to fight the infection at other sites.
But there is a threshold. If the activation of the immune is too much you can get sepsis. This is
uncontrolled amplification of the immune response throighout the whole body.
Sepsis is thsu caused by infection but it's not a disease, it's a syndrome. It is due to amplified
immune response to the infection. It is made up of organ dysfunction caused by dysregulated host
response to infection.
If a septic patient is admitted, we evaluate the severity with the SOFA score to know hot to treat
him. We ask ourselves if there is hypotension, an altered mental status, a tachypnea? More than 2 is
a greater risk of a poor outcome so the patient is taken to ICU.
A septic shock is due to decreased O2 perfusion which can lead to hypotension and organ
dysfunction. It needs a vasopressor in order to raise blood pressure. We can see a lactate > 2.
The blood pressure decreases due to leakage of fluid into interstital compartment. For this, we give
extra fluid. Also, the vessels dilate. We give norepinephrine because it works on alpha-receptors of
blood vessels in order to constrict them. It also works on beta receptors on the heart so the heart
pumps better so the heart rate is raised. If the effect is not enough, we add ADH which stimulates
vasoconstriction and H2O reabsorption. But we also may have side effects because if you constric
too much you can have ischemic toes and fingers.
Butinine and milrinone can also be used. The heart is affected during sepsis with a decreased
function. Dobutamine will work on beta receptors and will increase the heart rate and contractility.
However it might lead to vasodilation which you don't want to have. Milrinone also leads to
increased function of the heart by working on PDE3 (more cAMP --> more Ca2+ influx --> increased
contractility). But you also have vasodilation so you might want to add epinephrine.
Finally, phenylephrine works on alpha receptors to lead to vasoconstriction.
Steroids can also be given. If you want to dampen sepsis you can give them because they negatively
impact on the effect of the immune system.
Lecture 2
A shock is a decrease in the ECV leading to organ dysfuntcion. We have BP = CO x PVR. In sepsis, we
have both low CO and PVR. The kidney will try to retain fluid using Na. So a patient with septic shock
would have low urine output and low Na in the urine.
Microbes invade the bloodstream. This leads to poor perfusion of microcirculation and tissue
damage. We need to constrict the vessels to make the BP higher.
, We have kidney damage due to the sepsis. Kideny disease can occur when components of the
filtration barrier is damaged. When BP decreases, the flow in the glomerulus decreases. You thus
have the myogenic reflex which leads to lower transmural pressure on the afferent aretriole, which
reduces activation of strectch activated receptors, which causes the afferent to dilate. The
tubuloglomerular feedback will sense low GFR and low NaCl at macula densa due to low flow. The
afferent will dilate and make ANG II so efferent will constric which will lead to a combined effect of
increased flow and increased GFR so thr Gfpressure is kep constant. But you cant keep it completely
constant so you still have lower RPF and GFR. You thus have a higher FF which will lead to higher
oncotic in peritubular so more reabsorption. Damage to the kidneys can be seen with a higher Na in
such a scenario. This woud be a renal injury.
In such an ischemic renal injury, the tubular cells don't get enough energy so they get damaged.
They will fall of and you will get casts. The nephrons won't be able to function anymore. You have
acute tubular necrosis, which is not reversible. Mitochondria get damaged, so no energy production.
Also, the proximal tubular cells cant swutch to anaerobic glycolysis, which contributes to all of this.
Thrombotic microangiopathy may occur in sever inflammatory conditions and can lead to kidney
injury.
Case 1 --> has a high BP. You want to see if he has an injury in his microcirculation and you find he
has retinopathy. The danger is that he may have microvascular damage which can lead to the
thrombosis of small blood vessels in major organs. This can lead to organ dysfunction and death.
To know if this organ damage is occuring you look at the erythrocytes because if you have the
syndrome those would break and thus lead to low Hb and you would have fragments of RBC called
schistocytes. Also you would find increased LDH in blood because those normally are in the RBC but
leakage. You would also find haptoglobin because those carry broken erythrocytes to the spleen.
Becauese we have a higher BP we would have a higehr RPF. If it crosses a threshold it breaks through
the autoregulation and you wont have laminar flow which will activate endothelial cells. This can
lead to thrombosis on the blood vessel wall due to coagualation due to shear stress leading to
damage. This can lead to kidney vailure.
Case 2 --> confused female with low thrombocytes, schistocytes, increased LDH, decreased
haptoglobin and ADAMTS13 activity being low. ADAMTS13 is a proteins which is very large that
cleaves the van Willerbrand factor which is important in coagulation. Shear stress causes there
enrolling so monocytes stick to them. By cleaving them, it prevents thrombosis. Low ADAMTS13 will
lead to more thromobosis. This means she has a TMA cause by ADAMTS13 abnormalities --> TTP.
The neurological symptoms are very prominent in this case.
Case 3 --> ESRD and treated by hemodialysis. He wanted a new kidney. He was transplanted on the
7th and he had K of 6.3 and increased creatinine which is not normal. This means that the patient
may have renal failure, with intrinsic issues related to vascular, glomerular, tubular damage. When
you look at details, for this patients you find that the has TMA due to problems in complement
regulation (atypical HUS) which is genetic. After 2 days he also had high LDH so he has TMA. You see
that you have over acivation of alternative pathway (low activation tho). You get microtrombi in
arterioles and glomeruli. The alternative pathway of complement know not to activate on
endothelial cells which is done using factor H and factor I and MCP. In this patient you have
overactivation on endothelial cells which means you probably have a problem in a regulatory
protein. Most commonly, it is a mutation in factor H. So you have low C3 due to overactivation. You
have less readout of the alternative pathway because you have depletion of parts of the pathway
because they have less of these factor because they have been used in the patient. This patient has a
mutation of Factor H so it doesnt work properly so it is activated by endothelial cells of the given
kidnet due to some ischemia due to transplantation.
Lecture 3
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