Xalatan

I think the answer you are looking for is, in starvation, gluconeogenesis is in full steam and there is a relative lack in oxaloacetate. This may be the catabolic block you are referring to, since the tca cannot turnover. In this case the acetylcoa from beta oxidation cannot enter the krebs cycle, so it is converted to hmg coa for ketogenesis. Since keto acids are organic acids insulin deficiency will lead to organic acidaemia and will show up on your anion gap.

Tryptophan to niacin is good and I would write about pellagra. The pathology is interesting. The biochemistry is also interesting if you write about NADH and associated pathways like oxidative phosphorylation and malate shuttling. Vit b12 is pretty standard if you write about pyrimidine biosynthesis, the role of folate and b12 for transmethylation, and the role in methionine biosynthesis. Pernicious anaemia and intrinsic factor would be the pathological angle to pursue.

Itch is caused by vasoactive amine release like histamine, this causes nerve stimulation and give rise to the itchy sensation as well as whealing and other allergic changes. This process can be regulated at the genetic, epigenetic, and the chromosomal level (and pharmacoligically actually) by coding for both histamine release and the receptor and signal transduction efficacy. Eosinophilic histaminase is designed to stop this reaction.

As far as I am aware people who undergo sex change may take hormone replacement to modify their biochemical makeup. Oestrogen and progesterone supplement will make a male become more feminine, while androgen supplement will make a female more hirsute and masculine. Gonadal hormones are the biochemical basis for gender and secondary sexual characteristics so it may be possible for people to manipulate this.

Yeah you are probably being asked to describe the relationship between glycolysis, private dehydrogenase, tca, gluconeogenesis, beta oxidation and lipid synthesis. Most metabolites feed into pyruvate, acetyl coa and various intermediates of the tca so as long as you know your way around you should be able to describe anabolic and catabolic pathways. Don't forget cholesterol and ketone bodies come from acetyl coa too. Also glycogen metabolism and the pentose phosphate pathway branch off g6p, and you should describe oxidatve phoshorylation. there's enough for 20 points if you break down the different pathways systematically. You can probably even go into purine synthesis, breakdown and salvage from ppp, as well as the urea cycle and haem synthesis from the tca for extra marks.

Good question - if you combined monoamine oxidase inhibitor with a specific serotonin agonist that was selectively vasoactive you could probably still induce ss. The threshold would need to look at vitals and the clinical picture - there are probably clinical criteria that define serotonin syndrome but if someone is decompromised from serotonin overdose then this may be ss.

You are on the right track. Taste is vii ix and x so as long as you mention the muscles supplied by these cn related to articulation you should be fine - buccinator, stylopharyngeus, palatopharyngeus, pharyngeal constrictors, intrinsic laryngeal muscles etc. Not sure about diplopia - iii iv vi don't seem related to taste, unless there is some more generalised brain stem lesion (but patient would probably be decerebrate and comatose), or maybe disease like ms or tuberous sclerosis. Loss of hearing you will probably mention the internal acoustic meatus and facial canal shared by vii and viii. Lesions obstructing the path of chorda tympani will affect taste to anterior 2/3. Like acoustic neuroma you mentioned. Hemifacial pearlysis is ipsilaterial vii so this directly related to taste sensation by vii.

The physiological basis for hallucinations may be firing up the dopaminergic neurons in the mesolimbic and mesocortical pathways. There may be ways to achieve this non-pharmacologically. Schizophrenia is the disease that does it, there may be physical or phototic ways of doing so, maybe deep brain stimulation or something like this.

First rib: anterior connection to the manubrium, posterior connection to the body of t1. Second rib: anterior connection to the sternal angle, posterior connection or facets between t1 and t2 3rd to 7th: anterior connection to the sternal body, posterior connection to the top of respective vertebrae (and bottom Demi facet of one vertebra above) 8-9th: anterior connection to t7 and posterior connection to top of respective vertebrae (plus Demi facet of one vertebra above). 10th rib: anterior connection to t7 and posterior to full facet on body of t10. 11-12th: floating ribs, posterior connection to full facets of respective vertebrae.

That area of skin is between the medial canthus and the bridge of nose. Not sure if there is a specific name for it - some facies are described as having a wide nasal bridge, or a wide intercanthic distance. If you want to give it a name... maybe call it the nasocanthic interval or something to that effect.

Agree - I'm not qualified as a surgeon to give an opinion, and this is not medical advice, but peritonitis from bowel perf will not be controlled by IV antibiotics alone. Surgical intervention may needed to clear up the situation. The person may be damn sick, that's a problem for the anaesthetist and a discussion about the pink form may be warranted, but emergency surgery may be the optimal treatment.

Urinary retention is multiaetiological, but coming back to physiological principle, detrusor and internal urinary sphincter are sympathetically innervated. If there is fight or flight response to the MI, then likely there may be a degree of urinary retention. Especially if you end up infusing inotropes. Diuretics reduce renal resorption of the urine, bladder control is a separate matter. It may be possible to diurese someone but run into retention at the level of the bladder - think prostatic hypertrophy for example.

Scopolamine is a Muscarinic antagonist, it's used for car sickness, maybe because the chemorecepror trigger zone signals in part using acetylcholine. You can be prescribed patches of it called scopoderm. Since it acts centrally, depending on dose it may be possible to get cns side effects but it may not be what it's indicated for.

I'm not qualified to answer as I am not a psychiatrist, but the symptoms you are describing may be consistent with delusions. Delusions are defined as beliefs held with strong conviction despite superior evidence to the contrary. Delusional beliefs may fall into a spectrum of psychotic disorders including schizophrenia, mania, or psychotic depression. Delusional disorder and schizotypal personal disorder also come to mind.

You may be confusing the function of APC vs. that of CD8+ Tc cells. If a CD8+ lymphocytes binds to and is activated by the MHCI molecule on a virally infected cell, it receives a second signal via T Helper cells, eg. IL-2. Co-stimluation by MHC-1 and Th will activate the cytotoxic T cells on site, to release perforin, granzyme, and CD95L to apoptose the virally infected cell in situ. This is why Tc cells are called cytotoxic. APCs in the skin will process external antigens, present them on MHC II, and travel to the regional lymph nodes for paracortical activation. If the antigen happens to be in the blood, then it will be circulated to the spleen instead of lymph nodes for white pulp activation. So the site of antigen presentation isn't always in Lymph nodes, it depends on whether the antigen has access to haematogenous or lymphatic circulation - much like different routes of cancer spread coincidentally.

You can understand cellular organelles in terms of membranous organelles, non-membranous organelles, and inclusions. Organelles like endoplasmic reticulum, golgi apparatus, mitochondrion, and nucleus, they are basically membranous compartments, the membrane composed of phospholipids. Each membranous compartment has its own set of proteins/contents, and this defines its function. Eg. Cytochrome C and ATPase on the inner mitochondrial membrane; ribosomes on the ER. Lysozyme and protons in lysosomes, catalase in peroxisomes. Then there are non-membranous organelles like centrioles, cytoskeleton, they provide structural support for the cell, and they are made from microtubules (tubulin protein is the quantal unit), intemediate filaments and microfilaments (actin is protein also). They make up things like mitotic spindles, basal bodies, flagella, cilia, belt desmosomes etc. Inclusions are substances like glycogen and lipid droplets stored in cells.

When you refer to a specialist, you mean a clinical specialist? Pathologists are the clinical specialists who look at cells for pathological diagnoses. Outside of clinical practice, you can speak to a cell biologist, molecular biologist etc. but it would be for research purposes rather than trying to achieve a diagnosis per se.

Intrinsic laryngeal muscles: Cricothyroid - tenses the vocal cord. Thyroarytenoid - relaxes the vocal cord. Posterior cricoarytenoid - abducts the vocal cords to open the rima glottidis. Lateral cricoarytenoid - adducts the vocal cords to close the rima glottidis. Oblique and transverse arytenoid muscles - helps to close the rima glottidis.

Not an expert on sleep, but my understanding of the dreaming process is that it occurs primarily during REM sleep, when muscles go into a state of atony except for the eyes. The rapid eye movements may be indicative of the dreaming process. NREM is part of the sleep cycle where brain wave frequency gradually slows from alpha to theta to delta. This cycle is then repeated until the person wakes up.

You're describing being winded from being punched in the stomach. Don't know the exact cause, but working off first principles, the stomach is innervated by the vagus nerve and the greater splanchnic nerve. So reflex visceromotor symptoms may include vasovagal reflex, and perhaps there may be an adrenergic component. Referred pain to T5-9 may factor in also. Plus there is a concentration of viscera in the epigastrium - pancreas, liver and gall bladder to the right, spleen to the left.it may be more sensitive vs. the umbilical region. The hypogastrium is protected by the pubic symphysis to a point.

The abstract states, "Production of inflammatory cytokines (IL-1 beta, TNF-alpha, IL-6, IL-8) was significantly increased, mostly by the Sambucol Black Elderberry Extract (2-45 fold), as compared to LPS, a known monocyte activator (3.6-10.7 fold). The most striking increase was noted in TNF-alpha production (44.9 fold)". Based on this result, it may be hard to argue there is an anti-inflammatory effect for Elderberry. IL1, IL6 and TNFa are the classic inflammatory cytokines, and IL-8 is a chemokine. TNFa levels stimulated by Elderberry were folds higher than that induced by LPS positive control. To show an anti-inflammatory response, I would expect the levels of IL-10, TGF-b to increase, rather than this way around. ​Perhaps more studies need to be done.

Ah that explains it. All the best for your upcoming exam! Merry Christmas and Happy New Year :,)

I'm not qualified to give an answer since I'm not a radiologist, but you can see the entire thalamus next to the third ventricle. So why not the LGN? Unless it's a super small nucleus - I can't quote the exact dimensions of the LGN, but I can't imagine it would be microscopic given all the fibres that need to relay from the retina. It's like, optic nerve, optic chiasm, optic tract, then poof, gone. Maybe what your professor meant was it's hard to distinguish the LGN from the rest of the thalamus? If you have found the tectum and there seems to be a lump of grey matter... Maybe. You need a second opinion.

Some infections can be latent. Some pathogens also have the ability to change surface antigens so to be undetected. Testing for wbc, igg etc only look at the immune side of the equation, it doesn't account for what the pathogen is doing to evade the immune system, nor if the person is immunocompromised. This is why you do tests like viral load, and HB surface core envelope antigens as well.

Hpv is a sexually transmitted disease.