Xalatan

:,)

Yeah blood in the stool from the upper GI tract is typically mixed in, called malaena. Blood from lower Gi is typically described as streaky and coating the stool, splashing the pan. OP is talking about diarrhoea though, it is usually regarded as a separate clinical problem then blood in the stool. The point I was trying to make was, watery vs. bloody diarrhoea may be a function of the pathogenic agent rather than the location of bowel. Vibrio diarrhoea will probably look different to Shigella vs campylobacter.

It may be better to ask about forms of stool because diarrhoea typical refers to some form of infective gastroenteritis. Ps I was referring to the distinction made by the op in the original post. i understand your explanation, he/she seems to be talking about diarrhoea from different bowel locations being mucous or bloody, which doesn't ring a bell.

Strangulation will lead to ischaemia and coagulative necrosis. Inflammation and necrotic perforation may both occur secondarily and they are not mutually exclusive, end result being peritonitis. Bowel perf will cause faecal peritonitis. So with both conditions you are looking at acute peritonitides giving clinical toxicity, both surgical emergencies. Not sure what the equivalent in thorax called - pyothorax? Or empyema. It's proabably possible to get purulent mediastinitis.

there can be other causes of acute cholangitis outside of gall stones, as long as the pathology leads to biliary duct obstruction - benign strictures, cholangiocarcinomas, CA pancreas etc. so I think charcots triad describes the typical symptoms of all cholangitides, not just from gall stone aetiologically.

I've not read of this distinction in the past... Form of the diarrhoea probably relates more to the type of exotoxin being secreted. Eg. Cholera toxin will induce cAmp production and chloride secretion leading rice water stool. Enterohaemorrhagic E. coli releases verotoxin to inhibit protein synthesis to cause bloody diarrhoea and HUS.

Kinda odd that oxytocin is released in social interaction as well as labour and lactation.

So... moldy beards protects against MRSA? The micro-abrasion hypothesis seems more attractive - this is why shaving at surgical sites may not be recommended pre-operatively.

Fatty acids are broken down into acetyl CoAs in the mitochondria via beta oxidation and fed into the Kreb's cycle. Citrate synthase metabolises OAA and Acetyl-CoA into Citrate. In reverse, citrate can exit the Kreb's cycle via fatty acid synthesis.

The question seems to be framed around nasal decongestants and phenylephrine, so it'd be prudent to choose sympathomimetics.

Yep I think you are right. Vascular smooth muscles are controlled by SNS but not PSNS. That's why nasal decongestants are mostly sympathomimetics like ephidrine and pseudoephidrine. Also you see epinephrine combined with local anaesthesia to prolong the anaesthetic effects, but not parasympatholytics. To me this may be the major differentiating factor, since muscarinic antagonists can give mydriasis. PSNS has more of an effect on HR, but not necessary BP.

Difficult to say what exactly is the cause of the tall tented T waves in hyperkalaemia, chances are it's not due to hyperepolarisation from K efflux since extracellular K is higher. Also not sure if it is related to VGNaC changes since action potentials are all or none responses by nature. If Phase 0 Na influx is inactivated then there may be no subsequent phases I, II, and III. It may have something to do with the calcium influx during ventricular repolarisation from VGCC. This study observes serum calcium levels are inversely proportional to T wave height. http://ndt.oxfordjournals.org/content/17/9/1639.abstract?ijkey=c72f861993db16339c41fd8c7b6ff6b9167e12cd&keytype2=tf_ipsecsha. Makes sense to me because calcium antagonises K efflux to give the plateau phase. So, hypocalcaemia with less calcium entry should give a relatively larger repolarisation effort from K efflux, which may cause an exaggerated T wave. Yeah Renal physiology is a grind. Ganong is a really good resource book, many thanks for recommending it to me! Will take a look at Kandel, iirc it's quite a tome!

I am not qualified to give an answer because I am not a psychiatrist, but according to DSM V, a diagnosis of delusional disorder does not need to be based on harm to self or others. In fact, if the clinician judges there is a risk for the delusions to leading to self-harm or harm to others, then it may be possible for the diagnosis to be upgraded to schizophrenia. Delusional disorder may be the diagnosis of exclusion when the delusions are not bizarre enough or not severe enough to lead to social dysfunction. Also, the diagnostic manual DSM is called the "Diagnostic and Statistical Manual" because these diagnostic criteria evolved precisely from census and psychiatric hospital statistics. So it's perhaps not surprising that the wording of these criteria uses terms like "Unlikely". In reality it is often difficult to disprove something to be absolutely untrue. Eg. If someone says that he thinks he believes the Martians will come and get him on the 3rd of March, how would you go out and disprove such a notion? But statistically it may be so unlikely that a fixed belief falls outside the 95% confidence interval that it may be considered diagnostic. Of course, if the person could prove that in fact the Aliens will come and abduct him on the 3rd of March, and he in fact is abducted, then he would not be delusional, but statistically speaking the chances of this happening is so low that the clinician may be inclined to diagnose him. It may not be a perfect system but it's the working one. Diagnostic criteria (DSM-5)The specific DSM-5 criteria for delusional disorder are as follows:[1] Presence of one or more delusions with a duration of one month or longer. The criteria for schizophrenia has never been met. Note: Hallucinations, if present are not prominent and are related to the delusional theme (e.g., the sensation of being infected with insects is associated with the delusions of infestation). Apart from the impact of the delusion(s) or its ramifications, functioning is not markedly impaired, and behavior is not obviously bizarre or odd. If manic or major depressive episodes have occurred, these have been brief relative to the duration of the delusional periods. The disturbance is not better explained by another mental disorder such as obsessive-compulsive disorder, and is not attributable to the physiological effects of a substance or medication or another medical condition.

Hey that's very well explained. So the VGNaCs have two gates, M activates with depolarisation and H inactivates with depolarisation in a delayed manner. That's very tight control for Na influx. Thank you very much hyperkalaemic arrhythmia is well described. Good stuff! Yeah interesting point about the distinction between 5.5mmol/L and 8mmol/L. I suppose that's how a lethal injection of KCl works - it raises serum K so high that it just shuts down all the H-gated Na channels leading to lethal asystole. Thing about cardiorespiratory systems is, in many ways the principles of autonomic nervous system apply to both those organs, so being well versed in the CNS helps out a lot. Renal to a lesser degree since the RAA system may be the major focus.

Found this: https://microbewiki.kenyon.edu/index.php/Silver_as_an_Antimicrobial_Agent

Nice one! i wonder how this concept applies to the pathology of hyperkalaemia and cardiac arrhythmia? Supposedly myocytes or the SA node may be more prone to depolarise, setting off the voltage gated na channels leading to increased cardiac irritability? But I'm reading wiki and it says above a k concentration na channels paradoxically inactivates, setting off ventricular pacing and v arrhythmias... I wonder how the VG na channels works exactly... Good luck for your exam! I'm sure you would fly through. Did the testing taste question come up?

The RMP for a neuron sits around -70mV, and the major contribution to the RMP is K channels. This means At rest the inside of the cell is more negative than the outside by 70mV. Intracellular K sits at around 145mmol/L where as extraxellular k is around 4mmol/L. So naturally there is a constant flux of k out of the cell, the RMP being maintained by na/k atpase pump. If it weren't for the na/k atpase the RMP would tend towards k's equilibrium potential of around -90mV. Let's say you increase extracellular k. This will decrease the electrochemical gradient for the potassium to efflux out of the cell. Less K going out of the cell means intracellular k will increase. Since k determines the RMP, having more cations in the cytoplasm will increase the net charge in the cell relative to the outside, by definition increasing the resting membrane potential and depolarising the cell.

Leading and lagging strands in general refer to the process of DNA replication. Both strands Are synthesised 5'-->3', but since the replication proceeds in a direction one strand has to be fragmented in Its synthesis, later patched up by DNA ligase. Hence the terms leading and lagging strands. Coding and non-coding strands generally refer to the process of transcription. The coding strand is the non-transcribed strand running 5'-->3', while the non-coding strand is the transcribed strand running 3'-->5'. The coding strand is named because it should be exactly the same as the mrna except thymidine is substituted for uracil.

Km is a measure of enzyme affinity for the substrate, the definition being the substrate concentration when reaction velocity is 1/2 Vmax. So, having a Km of 0 does not make physical sense because enzymatic affinity cannot be infinite; the substrate concentration at 1/2 Vmax cannot be zero because at least some substrate is needed for the reaction to proceed.

Suffocation is not strictly speaking inaccurate, the pathophysiological term being histotoxic hypoxia or histotoxic shock. Cyanide shuts down cytochrome c oxidase. "Tissue cannot use oxygen anymore" because the functioning of the mitochondrial electron transport chain is dependent on cytochrome c oxidase (or complex 4) passing the electrons to molecular oxygen. Inhibiting complex 4 will stop the ETC "Using" oxygen to produce the proton gradient required for ATP synthase to generate ATP, and without ATP the cell will go into histotoxic shock.

Cancer metabolism is one of those interesting emerging fields to keep an eye on. Is a cancer dependent on glucose? What would happen if you fast and starve the tumour of glucose? Will it switch to glutamine? How would glutamine be used in a cancer cell? Would it enter the Kreb's cycle as alpha ketoglutarate? Is the Kreb's cycle turning over in cancer cells? Some cancers have a block in the TCA, for example mutation in isocitrate dehydrogenase, succinate dehydrogenase, and fumarate hydratase. What does this mean? Does the TCA run in reverse? What's the role of HIF in all this? These questions are definitely interesting and require scientific investigation.

L-arginine is the substrate for nitric oxide synthase (NOS) to produce NO. So while arginine itself is not a gas (it is an amino acid), its enzymatic product is a gas, (plus citrulline). Not sure if there is a linear correlation between ingesting L-arginine and NO production in the muscle though - you may need to read up on whether exercise stress will stimulate iNOS or eNOS to use the dietary L-arginine available. Also, what goes through my mind when I read this is, you could try something like viagra with your workout?? Viagra boosts the NO effects and may give you robust vasodilation for your workout (if you don't mind the erection down low). Second, Caffeine is not a straight forward vasoconstrictor - it's a methylxanthine, and while it will induce tachycardia and increase cardiac contractility, it also relaxes bronchial smooth muscles to cause bronchodilation, as well as diuresis and psychostimulation. The pharmacological basis of caffeine is that it is a phosphodiesterase inhibitor, so it will raise cAMP levels systemically. In beta-1 areas it will cause cardiac contraction, but in beta-2 regions it will induce smooth muscle relaxation. You may need to find a purer vasoconstrictor to test it out with L-arginine. Maybe a serotonin agonist... In terms of speeding up recovery, in theory nitric oxide may vasodilate the muscles, which may help to clear out the lactate buildup post work out. However, again, the NOS enzymes would have to increase their NO output to make use of the extra arginine in the body.

Endotoxin is just another name for LPS. It is so named to provide contrast to exotoxins, which are heat labile proteins secreted that are toxic to the host. Endotoxins are "endogenous" to the bacterial cell wall, the lipid A component in situ is toxic to the host in the sense that it is pro-inflammatory and can induce septic shock.

Rice is just carbs, so there may not be a direct link with being a central depressant that causes hypersomnolence. Maybe it's the spices in the curry? Oversleeping from a neurochemical standpoint may be to do with stimulating GABAergic or glycine channels, or inhibiting histamine, cholinergic, and adrenergic receptors. So if you do think it's the food, it may be worthwhile analysing the ingredients and seeing if there isn't any substances that could be psychotropic.

It probably won't affect endurance too much - creatine is metabolised in the first few seconds of muscular activity to provide a burst of ATP before glycolysis kicks in. You need a different kind of energy metabolism for muscle endurance. It should make the person stronger though. After all this is how body builders supplement their diets. These trainers are essentially loading their myocytes with creatine phosphate, albeit not via biotechnology.