#liddle's syndrome

[ioletia]

So. I'm super fucking rare, ya'll!

Above is a picture of the literal genetic mutation that I have. It's so rare that it's only been reported in ONE medical article as a bynote of a patient within a study- and a link to said study. It's so rare that genetic databases don't even have a frequency for it... Because it's so fucking rare (and genetic testing is still expensive and prohibitive to a lot of people).

Basically, it's a mutation that causes my kidney to not regulate my blood pressure correctly. Yeah, did you know that your kidneys regulate your blood pressure?! I mean, I did, but I'm wondering if you did.

This mutation causes Liddle's Syndrome, but my mutation is so rare that my symptoms don't entirely match up with the disease. Which is why it has taken doctor's 36 years to diagnose me- but, not really diagnose me, because I don't see my actual doctor until Friday... But, it's pretty clear that the mutation causes issues. So. Yeah.

It's incurable. There are only two drugs approved for its treatment- and they are rather cheap, so that's nice.

I feel like Dorthy Zbornak (Golden Girls) after she got her diagnosis of chronic fatigue syndrome. I had been blown off by doctors for YEARS because I was young and, somewhat, average in weight. I had insane blood pressure and they just... Ignored it? When I pointed out to a doctor that I still had high blood pressure after they increased the dosage of meds (that didn't work), she literally told me in the most condescending voice- "What do you want, more pills?" She also told me that I couldn't be having migraines because they lasted more than four hours and- "Migraines don't last more than four hours, you have something else." A cardiologist told me over a ten minute zoom call that I was fat and stupid, and that was why I had high blood pressure before changing a med that I took for ANXIETY to a different drug that turns out has been upsetting my gastrointestinal track for the last year (and also didn't work). It was the first time I met her. And, she told me to follow up in a week, which I couldn't and never did because she literally never had an open appointment slot over the following YEAR!

And if it needs to be said, this was in America.

But, I probably have a diagnosis now.... So, I can be a case study? Fun.

[clatterbane]

I am feeling greatly vindicated about now, in a way that I am very aware is probably verging on bitchiness on this end too. But, some people just affect me that way.

What do we have here, through the portal? Starting cortisol levels toward the lower end of normal for that time of day. And also well within the normal range? The cortisol-stimulating hormone which is what goes screwy and gets overproduced to make your adrenal glands pump out too much cortisol, if the problem is on the pituitary end.

The point of this overzealous testing?

The dexamethasone suppression test is used to diagnose endogenous Cushing syndrome by assessing the lack of suppression of the hypothalamic-pituitary-adrenal axis in response to exogenous corticosteroids.[1] The first use of dexamethasone for diagnosing Cushing syndrome was in 1960 by Liddle; he developed a test based on the non-suppressibility of endogenous cortisol production in Cushing syndrome versus the physiological suppression in nonaffected individuals achieved by dexamethasone.[2]

So yeah, if you give someone even a single dose of dexamethasone (never mind the sledgehammer 8-dose multiday protocol they hit my endocrine system with!), their body should cut way back on its own cortisol production to compensate. If the regulating mechanism is borked, it will just keep pumping out the ACTH and then a bunch of cortisol anyway.

What happened in this case?

Whoosh!

Straight down within the expected time frame, from totally fine levels starting out. The usual low single-dose test would have more than done it, without fucking my blood sugar up or giving me its own version of the Prednisone Crazies to anywhere near the same extent. They are apparently looking for at least a 50% reduction in levels, and we have more than met that goal!

(Yeah, they are close enough drugs to have similar effects. I've unfortunately had to take courses of prednisone multiple times, mostly for particularly nasty allergic skin reactions. But dexamethasone is stronger stuff and the effects apparently last longer. 👿 I am very relieved to be done taking the shit as of like 6:30 this morning. Probably a few more days of lingering fun to look forward to.)

It was a dramatic enough drop during that first day, that the nurse actually went ahead and reassured us this morning that things were obviously perfectly fine there when I went in for the second steroided-up blood draw.

Gotta say the lab was quick! They drew the samples just before 8:30 again today, and the results were up on the portal when I logged in somewhere around noon. That clinic is right in the university medical center complex, but still.

They took so much blood the first time because the endo also decided to throw in All The Tests while she was at it. Including a bunch of the diabetes-standard ones that she already ordered before the recent routine check-in appointment where she sprung this xenophobic concern-trolling bullshit on me in the first place. Also got expanded kidney and liver panels, what seemed like every other major hormone in my body checked, and a whole new battery of tests prompted by the chronic anemia. A lot of those repeats of what primary care just recently ordered (and she could see the results of) after she kicked that over to their side. At least it was just two tubes for the cortisol and ACTH today.

But yeah, at least nothing out of that huge battery of tests came back looking weird in unexpected ways! I am still slightly anemic, my sodium and potassium levels are still running just barely under range, and a couple of kidney indicators are still looking borderline wonky in a very diabetic way.

(Which seems to be staying pretty stable for years now, not even far off enough that anyone has seemed to feel like it's needed treatment--and it's frankly a miracle that my renal function isn't way more thrashed than that, after the number of years of earlier negligence and uncontrolled blood sugar. Ruined kidneys was honestly one of my big nagging worries while all of that was still going on.)

Anyway, one thing I WAS actually glad and somewhat relieved to see while scrolling through that huge mess of reports:

Because it was primarily a pituitary prolactinoma that I got removed back in high school. And especially with the healthcare mess back in the US? I am not aware of that ever having been checked again within the past 30 years. My family ended up uninsured within a year or two of the surgery, and the last follow-up probably happened in 1992-93. The symptoms thankfully did go away over time--along with the freaking cortisol side bonus staying distant history!

(None of which was the endo aware of when she decided I looked weird enough to constitute a medical problem, I just can't restrain myself from emphasizing again.)

The little fuckers do have a distressing tendency to come back sometimes. But yeah, BTDT and I am pretty confident that I would have noticed if that were causing problems. But, I am still glad for the confirmation that my prolactin levels are fine now.

This whole thing was, indeed, uncalled for. And I am still perversely gratified to be proven right about this, when it's been taking up so much rent-free space in my head. (Thanks, PTSD!) And also to see that I am honestly looking healthier across a whole slew of bloodwork measures than I was half-afraid I might.

[expertacademicassignmenthelp]

The pathophysiology of hypertension

Introduction

Hypertension, or high blood pressure, is a complex medical condition affecting a significant proportion of the global population. Despite its prevalence, there remains uncertainty regarding its pathophysiology, with essential hypertension constituting a substantial portion where no single identifiable cause is found. This comprehensive discussion aims to delve into the physiological mechanisms involved in the development of hypertension, exploring factors such as cardiac output, peripheral resistance, the renin-angiotensin-aldosterone system, the autonomic nervous system, endothelial dysfunction, genetic factors, and intrauterine influences.

Cardiac Output and Peripheral Resistance

Maintaining normal blood pressure relies on the delicate balance between cardiac output and peripheral vascular resistance. Essential hypertension often involves a normal cardiac output but elevated peripheral resistance, primarily determined by small arterioles. The role of smooth muscle cells, calcium concentration, and structural changes in arteriolar vessel walls contribute to the irreversible rise in peripheral resistance.

Renin-Angiotensin System

The renin-angiotensin system plays a crucial role in blood pressure regulation. Renin, released in response to various stimuli, initiates the conversion of angiotensinogen to angiotensin I, which is then converted to the vasoconstrictor angiotensin II. This system also stimulates aldosterone release, promoting sodium and water retention. While the circulating system may not be directly responsible for essential hypertension, local renin-angiotensin systems in organs like the kidney, heart, and arterial tree gain significance in regulating regional blood flow.

Autonomic Nervous System

Sympathetic nervous system stimulation affects arteriolar constriction and dilation, playing a pivotal role in maintaining normal blood pressure. Although the exact role of epinephrine and norepinephrine in hypertension etiology remains unclear, drugs blocking the sympathetic nervous system demonstrate therapeutic efficacy.

Endothelial Dysfunction

Vascular endothelial cells, producing vasoactive agents like nitric oxide and endothelin, play a key role in cardiovascular regulation. Endothelial dysfunction, implicated in essential hypertension, involves impaired production of nitric oxide. This dysfunction, once established, becomes irreversible, highlighting its primary nature in hypertension.

Vasoactive Substances

Various vasoactive substances, such as bradykinin, endothelin, atrial natriuretic peptide, and ouabain, influence sodium transport and vascular tone. These substances contribute to the delicate balance in maintaining normal blood pressure.

Genetic Factors

Genetic predisposition significantly contributes to hypertension, with specific mutations linked to disorders like Liddle’s syndrome, glucocorticoid-remediable aldosteronism, and others. The intricate interplay of multiple genes makes it challenging to pinpoint individual contributions.

Intrauterine Influences

Fetal influences, particularly birth weight, emerge as determinants of adult blood pressure. The Barker hypothesis suggests a link between low birth weight, metabolic abnormalities, and hypertension in later life. However, the role of genetic factors in this relationship requires further exploration.

Diastolic Dysfunction

Hypertensive left ventricular hypertrophy leads to impaired diastolic relaxation, affecting ventricular input during exercise. This dysfunction contributes to increased atrial pressure, pulmonary congestion, atrial fibrillation, and potential complications like pulmonary edema.

Conclusion

In conclusion, understanding the pathophysiology of hypertension involves a multifaceted exploration of various physiological mechanisms. While essential hypertension remains a complex and often multifactorial condition, advancements in research shed light on factors such as cardiac output, peripheral resistance, the renin-angiotensin system, the autonomic nervous system, endothelial dysfunction, genetic influences, and intrauterine factors. A comprehensive understanding of these elements is crucial for developing effective therapeutic strategies and preventive measures against the global burden of hypertension.

We hope this helps in improving our comprehension of the Hypertension condition. All the best in your journey in the medical field.

Incase of any challenges' and in need of professional guidance, contact;

Expert Academic Assignment Help at;

williamsassignmenthelpfredrick@gmail.com

[god-mouths]

Does my art have same face/same body syndrome ?

[phillipgallagher]

WHY DID THEY HAVE TO STAND SO CLOSE SJSKJSS WHAT WAS THAT ?!!?????

we know why 😏😏

[mcatmemoranda]

[knifeprtys]

what job do you do? 💸💰👠

unfortunately i’m unable to work due to illness! i’d just saved up a lot of money from christmas and my birthday! (which is on friday🎉 this trip was to celebrate!) i’m usually broke sfklsj

[creampill]

Thinking about the human hybrid versions of the animatronics for the high school au so here’s some shit about that

HUMAN-HYBRID GLAMROCKS HEADCANNONS

FREDDY

- he’s got freckles, no doubt about it. They’re sprinkled all over his face and body :)

- got fluffy, curly brown hair that looks perfect for ruffling

- his eyes are blue, and he’s got that kinda warm beige colour skin that looks like it’d taste like honey

- he’s always a little bit flushed in the face, he’s got that cute boy red cheeks syndrome

- for his hybrid parts, he’s a lot taller and broader than a regular human kid, build like… well, a bear. He has sharper canines than usual and, on his chest, a birthmark that looks vaguely like a lighting bolt

- He has lil ears that, like in the game, wiggle when he does certain things. They’re sensitive to touch and also get warm when he blushes

- he also has a liddle tail :)) Monty puts bows on it as a prank sometimes

MONTY

- this man is a poc of colour, that’s fact.

- he’s got red hair that he probably dyes ofc, and he probably buzzed his mohawk himself for the first time as a dare and now likes it

- he hides his red eyes behind his sunglasses because he’s self conscious :((

- this man is BUILT, but unlike Freddy who’s solid kinda strong this man is more the lean kinda strong. He’s still size comparable to Freddy but he’s got more noticeable muscles and a swimmer’s physique

- veery slightly shorter than Freddy but he wears shoes that give him an inch lol

- he has a tail :) it wags when he gets happy

- TEETH TEETH TEETH TEETH BIG POINTY TEETH

- his tongue is slit hwhehehe

- unlike Freddy who finds it embarrassing and won’t, Monty will openly snarl and growl to intimidate/seduce people because he’s a feral mf

- the spots on his body in his normal design are little scales on his human skin

ROXY

- wolf girl wolf girl wolf girl wolf girl

- she’s mixed, she’s got darker skin and her hair is the puffy kinda curly

- like Monty, she dyes some of her hair, specifically her one green streak

- WOLF GIRL EARSSSSS YUHHHH she pierced them herself :), she’s got a tail that also wags like monty’s, and she growls n shit as well aha

- she doesn’t shave, deal with it. body hair is not something she cares about

- she pants when she gets tired :) puppy

- her nails are always pointy and they grow fast, she’s scratched many things due to this

- she’s got them muscles…. Oh… strong woman strong arms, buff n shit, she works out ;)

- again she has big teeth, chompers

CHICA

- she’s a white girl, we love her

- her hybrid-ness is a lot less visible than everybody else’s

- there are little feathers growing through her hair and they shed sometimes, she collects them

- she LOVES fashion and makeup and does her own a bunch

- she’s vegetarian :)

- sometimes she makes little squawking noises when surprised and cooes like a dove when happy :)

- TOOTH GAP

- she’s blonde, but so light it looks almost white. It’s wavy and she has it short on the bottom

- here eyes are also blue but hers are more ice blue than saturated blue compared to freddy’s

- roxy helped her dye her hair pink :)

[doctorfoxtor]

i wanna cry cry cry but i like to party

100 days of productivity

day 36 + 37

CVS/RS

PDAs beyond 3-4 days are actually unlikely to spontaneously close and require indomethacin

both hyper- AND hypokalaemia cause PR prolongation

CHF: consider biventricular pacemaker if pt w/ LBBB or QT prolongation or persistent NYHA 3/4 despite treatment

aortic root dilation z-score >2 (by extension, active AR) is a major criterion for Marfan's diagnosis

posteromedial papillary muscle ruptures more frequently than anterolateral as PM is only supplied by RCA vs AL is supplied by both LAD and LCx

pleural fluid eosinophils actually signifies air in the pleural cavity and unlikeliness of TB/malignancy

CNS/Ophthal/Psych

cerebellar stroke vs BPPV or vestibular neuritis: vertical nystagmus + dizziness >1 min + difficulty standing up w/o support even w/ eyes open in stroke

brachial plexitis/neuralgic amyotrophy: severe pain followed by patchy LMN-type weakness and wasting of a limb with (characteristically) winging of ipsilateral scapula and mild sensory disturbance after vaccination, childbirth, surgery/trauma or infection; CSF: mild ↑albumin/lymphocytes, EMG: axonal neuropathy; spontaneous recovery over months

HIVANDs: diffuse, hazy white matter signal change & NFNDs vs PMLE: localised, posterior brain changes w/ focal signs

oscillopsia (jerky nystagmus with alternating direction) localises to the flocculonodular lobe of the cerebellum

convergence-retraction nystagmus localises to the midbrain

Derm/Immuno

erythema gyratum repens = concentric erythematous annular plaques that evolve into polycyclic lesions with raised edges and a 'wood-grain' appearance (IRL, it has a serpiginous look, sort of like cutaneous larva migrans) (!internal malignancies)

erythema annulare centrifugum = expanding annular lesions with bumpy raised edges; extremely similar to tinea, differentiate by the trailing scale (WITHIN the edge in EAC, ON or WITHOUT the edge in tinea)

bullous pemphigoid: biopsy can show a neutrophilic infiltrate w/ eosinophilic predominance

DLE: sun-exposed well-demarcated eryth plaques, patchy alopecia that heals w/ scarring, PIH; tx w/ high-potency topical steroids, even if on the face (usually we do not use HPTSs on the face but this is a rare indication)

in GPA, frequency of organs involved is LRT+URT (90%) > kidneys (80%) > muscles > GIT > skin

hyposplenism in coeliac/IBD thought to be d/t enteric loss of lymphocytes and macrophages through inflamed mucosa leading to atrophy of reticuloendothelial system, and/or d/t intereference by circulating AgAb complexes

maternal anti-Ro more common than anti-La in congenital heart block

Onc/Haem

VTE in DCLD: although hepatic clotting factor synthesis is lost, hepatic synthesis of antithrombin/protein C/protein S is also lost, and hepatic clearance of factor 8 (which is synthesised purely in endothelium) is also lost

platelet transfusions → ↑risk of bacterial contamination vs other types of blood products

Renal/GIT

Liddle syndrome: epithelial Na-channel hyperactivation characterised by resistant HTN, ↓K, ↑pH, ↓renin, ↓aldosterone; exquisitely sensitive to triamterene/amiloride

medullary sponge kidney: dilation of collecting ducts in papillae, cystic changes w/ small calculi inside, hypercalciuria, ±RTA, ±hemihypertrophy

acute severe ulcerative colitis → Truelove and Witts criteria: core temp >38, bloody stools >6x/day, ESR >30, PR >90

Pharm/Toxo

amitriptyline has anti-dopaminergic effects → hyperprolactinaemia

lead neuropathy is motor (nerve palsies), very rarely sensory, and not commonly assoc w/ tremors

lead also only causes anterior uveitis, not mid-/pan-/posterior uveitis; and proximal tubule or interstitial kidney disease, not glomerular disease

[biglittlecrane]

@realDonaldTrump

This is why DJT wins. With all of the weeds of “beaten housewife honeymoon syndrome” going around, it was SUCH a relief to read this by @realdonaldtrump on GAB.

Statement by Donald J. Trump, 45th President of the United States of America Karl Rove has been losing for years, except for himself. He’s a RINO of the highest order, who came to the Oval Office lobbying for 5G for him and a group. After a lengthy discussion with Rove and Chief of Staff Mark Meadows, I said no, they’re not qualified. Our Nation can do much better! On Election Evening, Nov. 3rd, at 10:30pm, Rove called to congratulate me on “a great win.” I said thank you Karl, only to watch the rigged election take its final form. Karl Rove’s voice on Fox is always negative for those who know how to win. He certainly hasn’t helped Fox in the ratings department, has he? Never had much of a feeling for Karl, in that I disagreed with so many of the things he says. He’s a pompous fool with bad advice and always has an agenda. He ran the campaign for two Senators in Georgia, and did a rotten job with bad ads and concepts. Should have been an easy win, but he and his friend Mitch blew it with their $600 vs. $2,000 proposal. Karl would be much more at home at the disastrous Lincoln Project. I heard they have numerous openings! If the Republican Party is going to be successful, they’re going to have to stop dealing with the likes of Karl Rove and just let him float away, or retire, like Liddle’ Bob Corker, Jeff “Flakey” Flake, and others like Toomey of Pennsylvania, who will soon follow. Let’s see what happens to Liz Cheney of Wyoming. If it weren’t for me, the House would have lost 25 seats instead of gaining 15—it was a shock to everyone, and almost cost Pelosi her Speaker position. Likewise, 8-10 Senators would have lost their position, including Karl’s friend Mitch, our wonderful leader who would rather spend his time fighting me than Pelosi, Schumer, and Sleepy Joe. In last year’s Congressional primaries, 120 of the 122 candidates I endorsed won - and the two that lost were beaten by people claiming to be more Trump than their opponent. In the Senate, I was undefeated in primary endorsements with a record of 21 and 0, and close to that in the general election. 31 million people listened to my CPAC speech online, and it had among the largest television audience of the week, even though it was on cable at 4pm on Sunday afternoon. Karl Rove is all talk and no action! Next time Karl, save your Election night phone call and keep doing a great job for the Democrats. Fox should get rid of Karl Rove and his ridiculous “whiteboard” as soon as possible!

https://gab.com/realDonaldTrump

Well, I’ll steer clear, I’ll tell you that.

[ioletia]

This is today's mood. I've been sick all week, which means I haven't been able to do my job of merchandising things at stores. So, tomorrow I have to do all the work... And I really don't even want to leave the house.

But, I have lost twenty pounds over the course of the last month and a half by literally doing nothing out my ordinary. Cancer? Oh, no, I wish. It's just that my chronic genetic condition, liddle syndrome, is actually being treated effectively for the first time in my entire life.

Fun. Yet, I feel incredibly depressed lately. And I weep at the drop of a hat. I feel like someone has spiked me with estradiol.

[d2kvirus]

Dickheads of the Month: January 2019

As it seems that there are people who say or do things that are remarkably dickheaded yet somehow people try to make excuses for them or pretend it never happened, here is a collection of some of the dickheaded actions we saw in the month of January 2019 to make sure that they are never forgotten.

It seems that Rachel Riley is quite smart at maths but a complete moron at anything else, what with her accusing Noam Chomsky of antisemitism in spite of the fact that Chomsky is a little bit Jewish, before following it up by encouraging her far-right Twitter followers to dogpile onto anyone voicing different opinions to her - which mainly involved a 16-year old girl bearing the brunt of it.  However she wasn’t finished there, as when she was rightly being criticised for encouraging her followers to dogpile onto people she then went whinging to the press about being bullied by left-wing trolls before announcing she needed personal security for when she was attending Countdown tapings, which sounds uncannily similar to the same stunt Laura Kuenssberg pulled a couple of years ago

Starting the year with a bang we had Chris Grayling first try and defend the Seaborne Freight farce by saying he was supporting up-and-coming British business (while omitting the parts about them being owned by the brother of a significant Tory donor, or not having any ships or trading history, let alone the fact the contract wasn’t even put out to tender) and followed that up by claiming the rail fare hikes are entirely the fault of the unions and definitely nothing to do with shareholder dividends or years of rail services taking the piss with fare hikes on January 2nd every year.  Of course, Grayling being Grayling, he also helped out the Britait debate by saying that a second referendum shouldn’t take place because if the result came back in support of Remain it would go against The Will Of The People™ - which apparently said people willingly voting to remain wouldn’t be

It didn't help Grayling that those checking the Seaborne Freight website found that their Ts & Cs were from the template used when setting up a website for a takeaway food outlet, the timetable for services was blank (and, for some reason, in Latin), while their privacy page had forgotten that the fields marked [Business Name] are supposed to be filled with the name of the business using the website

Overly sensitive snowflake Piers Moron Morgan spent a hell of a lot of time and energy yelling from the rooftops how appalling it was that Greggs are selling vegan sausage rolls, which is apparently the downfall of humanity as we know it and definitely not the hourly cry for attention from an attention-seeking lunatic - and while some claimed it was a stunt because he and Greggs share a PR agency, that theory appears to have been ever so slightly undermined by him then spouting off about McDonalds selling vegan Happy Meals

It’s funny how James Goddard demonstrated just how much of a difference a day makes, with him threatening Anna Soubry and Owen Jones on January 7th and bellowing at police officers that if they so much as touched him he’d start a a war...yet on January 8th he was bawling his eyes out on Twitter because his Facebook and PayPal accounts had been terminated

Lying (through his teeth) in front of a tractor Boris Johnson claimed he never mentioned Turkey at any point during the EU Referendum campaign - and when confronted with his numerous comments about Turkish immigrants flocking into the UK if the country voted Remain by Channel 4 journalist Michael Crick, he ran away to hide like an utter coward

Proving that gaslighting is the in thing at the BBC, Director General Tony Hall stated in an interview with the Financial Times that there is no need to discipline Andrew Neil for referring to Carole Cadwalladr as a “mad cat woman” as he had apologised - except for the fact that, while it may be plausible that Neil apologised to the BBC, there has not been a public apology for his comments

Sticking with the BBC, it took just two editions of Question Time before Fiona Bruce showed her true colours as she spent ten minutes making jokes about Diane Abbott (including suggesting that she only became Shadow Home Secretary because she once slept with Jeremy Corbyn) prior to one edition which Abbott was a guest on, and for the remainder of the episode constantly talked over Abbott while letting the other guests speak uninterrupted, including allowing Isabel Oakeshott to not just make a patently false statement but use said patently false statement to attack Abbott.  It wasn’t helped that when the BBC finally got around to admitting fault almost two weeks later, their statement actually said it was a joke - you know, like the school bully tries to claim when they get caught

Oh boy, there were so many triggered manbabies were up in arms about a Gillette advert for suggesting that maybe, just maybe, being a toxic dickhead isn’t any way to behave - to which they responded by acting like a bunch of toxic dickheads throwing a temper tantrum all over social media not seen since Nike featured Colin Kaepernick in an ad campaign

I’m going to assume AnonymousQ1776 thought they were being really, really clever when posting that video clip of Alexandria Ocasio-Cortez coupled with their sneering comment that made them sound uncannily like a teenage edgelord who doesn't know what communism is but throws the word around a lot.  I’m also going to assume they weren’t happy when the stunt backfired on them by not only making Ocasio-Cortez look like a normal human being who does normal things, but doing so also reopened the can of worms about what Brett Kavanaugh was up to when he was younger...

Middle England’s favourite edgelord Rod Liddle obviously needed to be extra quote-unquote provocative this month after using his column in The Sun to suggest that what Britain needs is a new political party that represents traditional values - which means neither Muslims nor the entire LGBT spectrum are not allowed

Just when you thought John Humphreys couldn’t sound any more like a pompous windbag with the credibility of a arthritic toad, he only goes to suggest that the Republic of Ireland should rejoin the UK - because who gives a toss about centuries of history or the minor inconvenience of 92% of irish people preferring to remain in the EU when Radio 4′s most jumped-up presenter suggests they swallow their pride and return to the warm chokehold of the British Empire? 

It appeared The Daily Star had a real scoop when they printed an interview with Dwayne “The Rock” Johnson in which he made scathing comments about the “snowflake generation” and how they were “looking for reasons to be offended” - that is until Dwayne “The Rock” Johnson issued a statement saying that not only did he not say those things, but he also never gave that interview

It seems The Board of Deputies of British Jews never got around to reading The Crucible judging by their going Full Baddiel and accusing Tottenham fans of antisemitism and, in the same statement, said they should follow the model of Chelsea fans - yes, the same Chelsea fans who have subjected Spurs fans to songs about Hitler and gas chambers for decades, who just so happen to be under investigation by UEFA for their anti semitic chanting during a Europa League match against Vidi in December

This month’s worst case of Trump Derangement Syndrome comes from Sarah Huckabee Sanders after she said that God wanted Donald Trump to become President in an interview with the Christian Broadcasting Network

Lucky for Lara Kollab there��s nothing in the hippocratic oath forbidding being an anti semitic bigot on Twitter.  On the other hand, there certainly was in the employment contract at the hospital she worked at, which is why they fired her

Somehow the British Army paid £1.5m on an recruitment ad campaign that was so successful that it led to members of the army quitting when finding out their photos were used to recruit “Snow flakes" (sic) and “Me me me millennials” - but that didn’t stop Gavin Williamson claiming it was “a powerful call to action” (rather than “bloody patronising”) while James Cleverly mouthed off like an idiot on Twitter in support because mouthing off like an idiot on Twitter is all that somebody who makes their surname fair game on a regular basis like James Cleverley knows how to do

It took a while but Jake Paul finally found a way to reclaim his crown of Most Odious Paul Brother by hitting upon a loot box scheme to encourage his viewers to, in effect, gamble - because apparently he (and Ricegum) only paid attention to the part where the likes of Electronic Arts were making money hand over fist when they were shoving loot boxes in all their games, but didn’t bother listening when various gambling commissions began looking into the practise

To prove my point James Cleverly took it upon himself to take to Twitter and sneer “You do realise that it’s not a documentary” when I, Daniel Blake was airing on TV - because it's better to score points on Twitter than admit that a UN report late last year was damning of the Tory government’s treatment of their less well-off citizens, isn’t it?

Trying to explain away his dickheadishness saw Wayne Hennessey claim he wasn’t doing a Nazi salute in a photo that happened to be taken by German teammate Max Meyer, he was actually waving at somebody - and the reason he had his finger on his top lip wasn’t the well-known mimicry of Hitler’s ‘tache but he was putting his hand to his mouth so somebody on the other side of the room could hear him.  For some strange reason nobody was convinced...

Attention-seeking loon Laura Loomer didn’t learn from the humiliation conga line that was her so-called protest at Twitter HQ judging by her protest against illegal immigration that involved her climbing over the fence around Nancy Pelosi’s property and setting up a stall on Pelosi’s lawn - at which point she appears to have forgotten what she was protesting about and instead kept yelling for Pelosi to respond to her, even though anyone with C-SPAN would’ve told her Pelosi was currently in the Senate

In order to promote her UK tour Azealia Banks thought the best idea was to vomit a long string of invective about the Irish on her social media all because she got irked by one Aer Lingus flight attendant

Can somebody tell Bill Maher that he doesn’t make himself sound more correct every time he regurgitates the “adults shouldn’t read comics” rant he first brought it up in the wake of Stan Lee’s death?  Because it appears nobody has

Out of curiosity, is Gregory Prytyka Jr. still popping over here in an attempt to find material to try and attack me with because they can’t handle the fact I called them out for their tedious shitposting, or have they crawled back under the rock they usually live under?

And finally, harrumphing to himself in a way that everyone can hear (although they wish they couldn’t) is Donald Trump and his banquets that look suspiciously like those given by the megalomaniacal villain of Kingsmen, continuing to throw a diplomatic temper tantrum over a wall he said Mexico would pay for

[expertacademicassignmenthelp]

The pathophysiology of hypertension

Introduction

Hypertension, or high blood pressure, is a complex medical condition affecting a significant proportion of the global population. Despite its prevalence, there remains uncertainty regarding its pathophysiology, with essential hypertension constituting a substantial portion where no single identifiable cause is found. This comprehensive discussion aims to delve into the physiological mechanisms involved in the development of hypertension, exploring factors such as cardiac output, peripheral resistance, the renin-angiotensin-aldosterone system, the autonomic nervous system, endothelial dysfunction, genetic factors, and intrauterine influences.

Cardiac Output and Peripheral Resistance

Maintaining normal blood pressure relies on the delicate balance between cardiac output and peripheral vascular resistance. Essential hypertension often involves a normal cardiac output but elevated peripheral resistance, primarily determined by small arterioles. The role of smooth muscle cells, calcium concentration, and structural changes in arteriolar vessel walls contribute to the irreversible rise in peripheral resistance.

Renin-Angiotensin System

The renin-angiotensin system plays a crucial role in blood pressure regulation. Renin, released in response to various stimuli, initiates the conversion of angiotensinogen to angiotensin I, which is then converted to the vasoconstrictor angiotensin II. This system also stimulates aldosterone release, promoting sodium and water retention. While the circulating system may not be directly responsible for essential hypertension, local renin-angiotensin systems in organs like the kidney, heart, and arterial tree gain significance in regulating regional blood flow.

Autonomic Nervous System

Sympathetic nervous system stimulation affects arteriolar constriction and dilation, playing a pivotal role in maintaining normal blood pressure. Although the exact role of epinephrine and norepinephrine in hypertension etiology remains unclear, drugs blocking the sympathetic nervous system demonstrate therapeutic efficacy.

Endothelial Dysfunction

Vascular endothelial cells, producing vasoactive agents like nitric oxide and endothelin, play a key role in cardiovascular regulation. Endothelial dysfunction, implicated in essential hypertension, involves impaired production of nitric oxide. This dysfunction, once established, becomes irreversible, highlighting its primary nature in hypertension.

Vasoactive Substances

Various vasoactive substances, such as bradykinin, endothelin, atrial natriuretic peptide, and ouabain, influence sodium transport and vascular tone. These substances contribute to the delicate balance in maintaining normal blood pressure.

Genetic Factors

Genetic predisposition significantly contributes to hypertension, with specific mutations linked to disorders like Liddle’s syndrome, glucocorticoid-remediable aldosteronism, and others. The intricate interplay of multiple genes makes it challenging to pinpoint individual contributions.

Intrauterine Influences

Fetal influences, particularly birth weight, emerge as determinants of adult blood pressure. The Barker hypothesis suggests a link between low birth weight, metabolic abnormalities, and hypertension in later life. However, the role of genetic factors in this relationship requires further exploration.

Diastolic Dysfunction

Hypertensive left ventricular hypertrophy leads to impaired diastolic relaxation, affecting ventricular input during exercise. This dysfunction contributes to increased atrial pressure, pulmonary congestion, atrial fibrillation, and potential complications like pulmonary edema.

Conclusion

In conclusion, understanding the pathophysiology of hypertension involves exploration of various physiological mechanisms. While essential hypertension remains a complex and often multifactorial condition, advancements in research shed light on factors such as cardiac output, peripheral resistance, the renin-angiotensin system, the autonomic nervous system, endothelial dysfunction, genetic influences, and intrauterine factors. A comprehensive understanding of these elements is crucial for developing effective therapeutic strategies and preventive measures against the global burden of hypertension.

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[cotestuck]

mental health headcanons- odd numbers for ray

1. Has Nurray been diagnosed with any mental health conditions? If so, what and when was she diagnosed?

"Babe, this heah's Altuhneah. Ain't nunuv us widdout PTSD an' anxieteh."

"Ah lit'ralleh c'ain't teyya just how much physical, mental, and emoshunal trauma we all gotta slog thru t'not die immediately."

"Depreshun's pretteh common too."

"Ah hav all three'a those, Serahtonin Defishunsy Syndrom, an' Ah'm on the autism spectrum."

3. Has Nurray experienced any trauma in her life?

"Did... didja not heah wheyya standin?"

"Ain't a troll hatched onwurld 'at ain't!"

"Ah bin branded w'mah own microphone. Mah ahms ah covahd in mahks frun bein' grabbed an' struck."

"Theyahs a whole prosejur f'hostil big fuckahs Ah get sent to as a prank."

"Ah y'shittin' me?

5. Talk about Nurray's sleep patterns and quality of sleep.

"Ah'm up widda moons an' get pretteh gud sleep. Easiah an' deepah 'f Kahni'r Kai ah stayin' tha lite, but 'tain't... too bad... alone."

7. Talk about Nurray's appetite and how it changes with mental heath.

"Tain't bad. Mah diet's widely varied."

"It gets a liddle hahd t'wanna cuk when Ah'm stressed, but Ah switch mostleh t'raw forage when cukin' ain't a thing."

9. Does Nurray tend to worry more about past regrets or future fears?

"Past's passed, hun. C'ain't un-do et."

"You'n take wutcha luhned witcha inta tha fuchah, but ain't no way t'count f'evreh evenchu-aliteh."

11. Has Nurray ever experienced mania or Hypomania (abnormally elevated arousal, affect, and energy levey)

"Hmm...naaaah.'

13. Has nurray ever expertienced dissociation from her surroundings.

"Few times."

She refuses to extrapolate furrther.

15. What does Nurray feel most guilty about:

"Wantin' t'take Kai on as mah own... acshul pale luv."

"Ah want such gud things f'em.. but tha fact is Ah just ain't ginns liv too long.

17. Has Mental illness ever interfered with Ray's abilities to work or attend school?

"Notchet. Vis'ralleh knowin' what theyah goin' thru helps me find folks theyah wurk arounds."

19. Has Nurray experienced stigma relating to mental illness?

"Ah liv alone an' mask in public realleh well, but about a thuhd'a mah visits ah to folks Ah bin sent to as a prank 'caus'a that stigma."

"Chances ain't great f'me makin' et outta those alive."

21. Has Nurray begun recovery? What are her goals?

"How d'y'all think 'is wurks? Mental illness is manageable with wurk rounds, a gud support system, an' meds f'chemical imbalance. Et dun go 'way."

"Ah manage pretteh well. Th'jobs help."

"Ah just need t'be able t'funkshun in publik."

23. What are Nurray' coping mechanisms? Are they healthy?

"Mah jobs. Wurkin' w'othah folks in tha same p'sishun helps me tweak mah own wurk arounds."

"Ah accept venue invitations an' choose mah sets based offa what Ah need t'express'r feel 'at night."

"Ah keep busy when Ah ain't singin'r expectin'a client. Miyyon liddle chores t'do t'be shur Ah'm prepayah'd f'folks."

25. Talk about you hopes and dreams for the future, Ray.

"Ah... Ah'm livin' most of 'em now."

"Especially as Buhgundehs go? Holeh fuck, Ah cuddn'a imagined gettin' this fah!"

"Hopefulleh, Ah'n keep goin' a gud while!"

"Like t'get more blocks cahved out, 'stead'a just havin' tha wun guest block w'like twenny dif'rent pile opshuns."

"Lukkin' real fahwahd t'gettin' t'know as much 'a Kahni as 'e feels like sharin'."

"Realleh hope Ah'n do anehthin' attall f'Kai bah tha time... Well, that mine runs out."

"Wuddat Ah was coldah... Mah lifespan's gonna be a blip t' theyahs..."

[mcatmemoranda]

Basically, Conn syndrome = too much aldosterone (due to adrenal adenoma)--> Na+/H2O retention, low K+ (because aldosterone causes K+ secretion), high pH (because H+ is secreted with K+). Conn syndrome = primary hyperaldosteronism.

Liddle syndrome (pseudo-hyperaldosteronism) = Autosomal Dominant ENaC mutation; aldosterone levels are normal or reduced (because the adrenal gland isn’t making too much aldosterone), but symptoms are the same as Conn syndrome; there are gain of function mutations of ENaC, which cause them to be constitutively active--> activation of Na+ reabsorption and K+ secretion even without aldosterone stimulating it--> HTN, low K+, high pH; but the renin-angiotensin-aldosterone axis is down-regulated, which is the differentiating factor between Conn syndrome and Liddle syndrome.

Basically, Conn syndrome is when there is too much aldosterone. Liddle syndrome is when there is a gain of function mutation of ENaC. These syndromes present the same way—increased Na+ and water reabsorption, low K+, high pH. But in Conn syndrome, the problem is too much aldosterone whereas in Liddle syndrome, the problem is just too much activity of ENaC.

Not enough aldosterone--> hypoaldosteronism; failure of adrenal cortex (Addison’s disease); congenital adrenal hyperplasia = not making the right component, so adrenal glands respond by trying to make more, so they hypertrophy, but they're not making what you need. You get reduced levels of aldosterone. ACE inhibitors inhibit the RAAS--> reduced aldosterone. No aldosterone stimulating collecting duct--> Na+ and water lost in the urine. You will end up with hypotension. K+ goes in the opposite direction (instead of being secreted, K+ is maintained in hypoaldosteronism). pH will be low because aldosterone is not stimulating H+ ATPase--> increased [H+]. Type 4 renal tubular acidosis (renal acidosis associated with low aldosterone levels).

[ayurvedickidneycare]

How is Hypokalemia Related To Kidney Disease?

Kidneys are not just fist-sized organs. Instead, they are of great importance to our bodies. Without kidneys, it would be impossible to remove excess amounts of water and other waste compounds from the body. Moreover, kidneys are also responsible for filtering our blood from toxins and other compounds that are no more required by the body. However, there are many factors or other diseases that lead to various kidney problems.

One such problem we will be discussing today is "Hypokalemia." We will be discussing every possible detail related to Hypokalemia and how does it affect our kidneys. It will be followed by the hypokalemia Ayurvedic treatment that treats this ailment from the root level using natural ways.

All About Hypokalemia!

If a person has Hypokalemia, it means that the potassium levels in his blood are very low. This is why Hypokalemia is also known as "Low Potassium." Potassium is among those essential minerals your body needs to work smoothly. Potassium not just makes muscles strong and helps them move, it also provides assistance to the muscle cells to get all the required nutrients. Mainly speaking of cells in the heart, Potassium keeps your heart strong. Additionally, Potassium also keeps your blood pressure under control.

What Leads to Hypokalemia?

There is no fixed reason that leads to Hypokalemia. Instead, there are many causes of this disease, some of which are mentioned below:

An extreme case of vomiting

Nausea

Diarrhea

Kidneys are not functioning properly

Excessive intake of strong medications

Excessive consumption of Alcohol

Too much sweating

Deficiency of Folic Acid in the body

Excessive intake of antibiotics

History of diabetes

Excessive consumption of tobacco/cigarette

Taking frequent asthma medicines

Low levels of magnesium inside the body

Liddle Syndrome

Gitelman Syndrome and many more.

What Does Hypokalemia Lead To?

Some of the most common symptoms of Hypokalemia are:

Weakness in body

Frequent Muscle Cramps

Acidity (Constipation)

Fatigue

Tiredness, etc.

How Does Hypokalemia Affect Kidneys?

So far, we have discussed every significant detail related to Hypokalemia. In this section of the article, we will explain how Hypokalemia affects the kidneys.

Just like every other organ, Kidneys also need various nutrients and minerals for smooth functioning. However, patients suffering from the possible case of Hypokalemia might have impaired kidneys which reduce kidneys' ability to concentrate urine by filtering out excess water from the body. As a result, it could result in a condition known as Polyuria, where a kidney patient urinates excessively. Moreover, it could also lead to Polydipsia, where a kidney patient suffers from excessive thirst.

Since Potassium provides required electrolytes to the kidneys, its deficiency in the body could damage kidneys. As a result, the kidneys would not perform all the functions they are meant to, which could give rise to various other problems.

Hypokalemia Ayurvedic Treatment

Now you might have understood that Hypokalemia harms our kidneys along with other areas in the body. This condition might not come under notice at its initial stage; however, it could turn fatal and life-threatening with time. This is why health experts worldwide advise getting its treatment before it becomes too late.

Though there are other treatments, taking Hypokalemia Ayurvedic Treatment is the best thing one could do to get complete relief from the problem. Since Hypokalemia affects the kidneys, it is better and more convenient to take its cue from Ayurveda.

Ayurveda focuses on three areas or doshas: Pitta, Kapha, and Vata, which means the energy of digestion or metabolism, the energy of lubrication and structure, and the energy of movement, respectively.

By working on these doshas and bringing all the required changes in the diet and lifestyle of individuals, Ayurveda does not leave any stones unturned and offers the best cure to the problem. Some of the changes in the Diet and Lifestyle of patients recommended by Ayurveda include:

Exercising daily

Eating foods rich in Potassium

Reducing consumption of Alcohol

Avoiding non-veg items like red meat, fish

Eating more plant-based proteins

Drinking plenty of water, etc.