The Student Who Ate 5-Day Old Pasta And His Liver Shut Down

Summary

视频脚本讲述了一个大学生因食用存放五天的意大利面而导致严重肝衰竭的案例。该案例探讨了食物中的细菌如何产生毒素，影响线粒体功能，导致脂肪代谢紊乱和急性肝衰竭。视频详细解释了线粒体在能量代谢中的作用，以及毒素如何干扰这一过程，最终导致患者需要肝脏移植。

Takeaways

• 🍝 视频中讨论了一个案例，一名学生因食用存放了五天的意大利面而导致肝脏完全衰竭。
• 💸 许多美国大学生通过接受大额贷款来支付高等教育费用，这在1990年代后可能成为终身债务的潜在机制。
• 🏫 大学生为了节省食物开支，可能会一次性准备一周的餐食，这可能导致食物安全问题。
• 🩺 该学生因低血糖、急性肝衰竭、黄疸、弥漫性出血等症状被送往急诊室。
• 🧬 肝脏是高度代谢的器官，负责分解化学物质、分泌胆汁、制造凝血因子等多种功能。
• 🔍 通过患者肝脏样本的分析，发现微泡性脂肪变性，这与常见的由酒精滥用、糖尿病和肥胖引起的大泡性脂肪变性不同。
• 🦠 导致肝衰竭的细菌是土壤中常见的蜡样芽孢杆菌，其产生的毒素专门针对线粒体，阻止其使用脂肪产生能量。
• 🔋 线粒体是细胞的能量工厂，蜡样芽孢杆菌产生的毒素（cereulide）导致线粒体内钾离子异常流入，破坏了能量生产过程。
• 🚨 由于线粒体功能障碍，肝脏无法正常处理脂肪，导致急性肝衰竭，如果不及时治疗，可能会导致死亡。
• 📚 视频还提到了医学教育中关于食物中毒的教训，强调了正确理解食物处理和保存的重要性。

Q & A

为什么大学生可能会选择吃存放了五天的意大利面？

大学生可能会因为经济原因选择吃存放了五天的意大利面，因为意大利面价格便宜，而且提前准备一周的餐食可以节省时间和金钱。

在视频中提到的学生因为吃了五天前的意大利面而出现了什么健康问题？

学生因为吃了五天前的意大利面而出现了急性肝衰竭，导致他的肝脏完全停止工作。

为什么吃了五天前的意大利面会导致急性肝衰竭？

五天前的意大利面上生长的细菌产生了一种名为cereulide的毒素，这种毒素专门针对线粒体，阻止线粒体使用脂肪产生能量，导致脂肪在肝脏中迅速积累，最终导致急性肝衰竭。

线粒体在细胞中扮演什么角色？

线粒体是细胞的能量工厂，负责产生大部分ATP（三磷酸腺苷），这是细胞能量的主要来源。

cereulide毒素是如何影响线粒体功能的？

cereulide毒素是一种钾离子载体，它与线粒体内膜结合，允许钾离子自由流入线粒体基质，这会干扰线粒体的氧化磷酸化过程，导致ATP合成受阻，线粒体肿胀并破裂，引起肝细胞坏死。

为什么在视频中提到了Pepto-Bismol（胃乐）？

在视频中提到了Pepto-Bismol是为了简要说明水杨酸盐（salicylates）的作用，它是一种氧化磷酸化的解偶联剂，在过量摄入的情况下可能会导致微泡性脂肪肝，因为它消耗了辅酶A（CoA），从而影响了脂肪的活化和β-氧化。

为什么视频中提到了ATP合成的电子传递链？

电子传递链是ATP合成的关键过程，它通过一系列复杂的蛋白质复合体将电子从高能状态传递到低能状态，同时推动质子（氢离子）通过ATP合酶，释放能量合成ATP。

在视频中提到的微泡性脂肪肝（microvesicular steatosis）与常见的大泡性脂肪肝（macrovesicular steatosis）有何不同？

微泡性脂肪肝的特点是脂肪在肝细胞中以小泡的形式积累，而大泡性脂肪肝则是脂肪在肝细胞中以大泡的形式积累，通常与酒精滥用、糖尿病和肥胖有关。

为什么视频中提到了20岁男性的健康问题？

视频中提到20岁男性的健康问题是为了强调在这个年龄段，慢性疾病并不常见，因此急性肝衰竭更可能是由于某种特定的原因，如摄入了某种有害物质。

在视频中，为什么提到了肝脏的功能和它在代谢中的作用？

肝脏是高度代谢活跃的器官，负责分解化学物质、分泌胆汁、制造凝血因子、处理蛋白质等多种功能，了解这些功能有助于理解为什么肝脏受损会导致如此严重的后果。

Outlines

00:00

📚 深入探讨教育贷款与健康问题

Dr. Bernard（别名Chubby Emu）介绍了他的第二频道Heme Review，该频道深入讨论主频道未涉及的话题，并提供音频播客格式。他回顾了2019年的一个案例，涉及一名大学生因食用五天前的意大利面而导致肝脏衰竭。这名学生的案例反映了许多美国年轻人为了高等教育而背负巨额贷款的现象，这可能成为他们一生的债务。Dr. Bernard讨论了大学生为节省开支而提前准备一周食物的普遍做法，以及这种习惯如何导致食物中毒的风险。他详细描述了该学生的病状，包括低血糖、肝脏衰竭的征兆，以及紧急情况下的医疗响应。

05:00

🍝 五天意大利面与肝脏衰竭的联系

Dr. Bernard讨论了五天意大利面如何可能导致肝脏衰竭。他解释了肝脏的代谢功能，包括处理食物、分泌胆汁、制造凝血因子和处理蛋白质。他提到，肝脏需要大量能量来执行这些功能，而脂肪是细胞的能量来源。通过患者肝脏样本的分析，发现微泡性脂肪变性，这是脂肪在肝脏细胞中的异常积累。Dr. Bernard推测，由于细胞无法处理脂肪，导致能量生产受阻，最终导致肝脏衰竭。他进一步解释了细菌如何在五天的意大利面上生长，并产生针对线粒体的毒素，阻止能量的产生，导致急性肝脏衰竭。

10:02

🧬 线粒体功能障碍与ATP产生

Dr. Bernard深入探讨了线粒体在细胞能量生产中的作用，特别是电子传递链和ATP合成酶如何协同工作以产生ATP。他解释了NADH如何在线粒体中产生，以及它如何参与脂肪酸的β-氧化过程。他讨论了脂肪酸如何转化为乙酰辅酶A，这是进入三羧酸循环（TCA循环）的关键步骤。Dr. Bernard还提到了由于线粒体功能障碍导致的ATP产生减少，以及这如何导致肝脏细胞的坏死和肝脏衰竭。

15:02

🏥 肝脏衰竭的临床影响与治疗

Dr. Bernard描述了肝脏衰竭的临床影响，包括凝血因子的减少导致的广泛出血、氨在血液中的积累导致的脑水肿和颅内高压。他讨论了如果没有及时进行肝脏移植，患者将无法存活。他还回顾了之前视频中添加的关于患者服用Pepto-Bismol（含有水杨酸铋）的情况，这种药物在过量时可能导致线粒体功能障碍和微泡性脂肪变性。Dr. Bernard强调了在医学实践中，必须基于当前信息做出决策，因为情况往往是复杂的，并且存在许多未知因素。

Keywords

💡急性肝衰竭

急性肝衰竭是指肝脏在短时间内突然失去功能，通常伴随黄疸、低血糖和脑病等症状。在视频中，主角因食用了放置五天的意大利面而导致急性肝衰竭，突出细菌感染和毒素对肝脏的严重影响。

💡Bacillus cereus

Bacillus cereus是一种常见的土壤细菌，通常会导致自限性的食物中毒。在视频中，这种细菌产生了一种特别的毒素，导致了患者的急性肝衰竭。这个细菌的毒素攻击了线粒体，干扰了脂肪代谢。

💡线粒体功能障碍

线粒体功能障碍是指线粒体无法正常进行能量代谢。在该视频中，Bacillus cereus产生的毒素影响了线粒体的功能，阻止了ATP的生成，从而导致肝细胞的死亡。这是急性肝衰竭的直接原因。

💡五天的意大利面

视频中的患者吃了放置了五天的意大利面，导致了致命的食物中毒。由于食物长时间暴露在室温下，Bacillus cereus细菌生长并产生了有毒的cereulide，这种毒素破坏了患者的肝脏功能。

💡低血糖

低血糖是指血糖水平过低，可能导致昏迷和其他危及生命的并发症。患者在急性肝衰竭时表现出低血糖，这是肝脏功能失调的早期症状，表明肝脏无法维持正常的代谢过程。

💡脑病

脑病是由于肝功能衰竭导致的脑功能异常，通常表现为昏迷或意识模糊。在视频中，患者的脑部受到了毒素和肝脏失调的影响，最终因脑水肿而死亡。

💡肝脏代谢功能

肝脏代谢功能指的是肝脏在体内分解化学物质、产生能量和处理废物的能力。在视频中，患者的肝脏由于Bacillus cereus的毒素失去了代谢脂肪的功能，导致脂肪在肝细胞中积聚，最终引发急性肝衰竭。

💡cereulide毒素

cereulide是一种由Bacillus cereus产生的毒素，它会破坏线粒体，导致细胞无法产生ATP。在视频中，这种毒素是导致患者急性肝衰竭的主要原因。它干扰了肝脏的代谢过程，使肝脏细胞迅速崩溃。

💡微脂滴性脂肪变性

微脂滴性脂肪变性是指小脂肪囊在肝细胞中异常积累，通常与线粒体代谢功能障碍有关。视频中，患者的肝脏在显微镜下显示出这种现象，表明肝细胞无法正常代谢脂肪。

💡能量代谢

能量代谢是指细胞通过分解营养物质产生ATP的过程。在视频中，患者的肝细胞无法通过正常的能量代谢来生成ATP，这主要是因为Bacillus cereus毒素破坏了线粒体的功能，导致肝脏衰竭。

Highlights

Dr. Bernard（Chubby Emu）在Heme Review频道深入探讨了在主频道未涉及的话题。

2019年讨论了一个案例，一名学生吃了五天前的意大利面后肝脏完全衰竭。

许多美国大学生接受大额贷款支付高等教育费用，这可能成为他们一生的债务。

意大利面价格便宜，大学生为了节省食物开支，有时会准备一周的餐食。

患者因食用五天前意大利面导致严重肝衰竭，朋友曾开玩笑说他可能会死于食物中毒。

肝衰竭的初步症状包括低血糖，但不足以确定为急性肝衰竭。

患者是一名20岁的大学生，因腹痛、恶心、呕吐和全身出血被送往急诊室。

20岁的男性不太可能患有常见于65岁以上人群的慢性疾病。

急性肝衰竭通常需要长时间发展，但在年轻人中可能因不同原因迅速发生。

患者血液中的AST和ALT水平高，出现神经症状和黄疸，但之前没有肝脏疾病。

患者可能摄入了导致急性肝衰竭的物质，考虑到年龄和社会人口统计学特征，可能是在大学环境中。

患者没有饮酒或使用刺激剂的迹象，呼吸正常，因此排除了某些药物的影响。

患者可能食用了导致急性肝衰竭的食物，特别是五天前的意大利面。

肝脏是高度代谢的器官，负责分解化学物质、分泌胆汁、制造凝血因子等。

患者的肝脏样本显示微泡性脂肪变性，与常见的大泡性脂肪变性不同。

微泡性脂肪变性与线粒体功能障碍有关，可能是由于细胞内脂肪处理和能量产生的障碍。

患者食用的五天前意大利面上的细菌是导致肝衰竭的原因，特别是产毒的芽孢杆菌。

芽孢杆菌产生的毒素专门针对线粒体，阻止其使用脂肪产生能量，导致脂肪积累和急性肝衰竭。

线粒体是细胞的能量工厂，其功能障碍会导致ATP合成减少，进而影响细胞功能。

患者因线粒体功能障碍导致肝细胞坏死，最终导致功能性肝衰竭。

患者因肝衰竭导致全身出血，因为肝脏无法产生足够的凝血因子。

患者因肝衰竭导致氨在血液中积累，流向大脑，引起脑水肿和颅内高压。

患者最终因急性肝衰竭死亡，尸检发现其肠道内容物、肝脏和加热意大利面的锅中有芽孢杆菌。

Dr. Bernard在视频中提到，患者还服用了大量Pepto-Bismol，这可能与肝衰竭有关。

Pepto-Bismol中的水杨酸盐可能干扰线粒体功能，导致ATP合成减少和脂肪积累。

Dr. Bernard强调，医学中存在许多未知和时间敏感的因素，需要基于当前知识做出决策。

Transcripts

hi everyone dr bernard here you might

know me as chubby emu this is my second

channel heme review where i go more in

depth on topics that aren't otherwise on

the main channel these episodes are also

available in audio only podcast format

link in the description below i post

here when i can sometimes alongside

chubby emu videos so if you subscribe

you'll get notifications when i do in

2019 i discussed a case about a student

who ate five-day-old pasta and his liver

completely shut down link to that video

is in the description below

aj the student was like a lot of

american people his age who went to

college in his time accepted a large

loan to pay for higher education that

depending on career choice where they

land who they met along the way or knew

beforehand and elements of luck and hard

work could serve the main purpose of

upwards socioeconomic mobility based on

scholastic merit but after the 1990s

served as a potential mechanism to

indebt someone for their entire life the

association with this machinery might be

something completely unknown to people

hundreds of years down the line but what

we do know is that pasta is cheap one

can save money on food that's a heavy

driving factor for college students and

some people like to prepare all of their

meals for the week in advance so they

don't have to think about it the

patient's practices led his friends to

joke that one day he would die of food

poisoning except this time it wasn't

going to be a joke when i started to

describe the liver failure i started

with hypoglycemia

that tells you a little probably not a

lot it's a non-specific description and

by itself it's not enough to know that

someone has acute hepatic failure i

spent maybe a whole week writing that

part and the entire video couldn't

proceed until i rectified it it really

could have gone several different ways

but starting with low sugar presence in

blood i found was the quickest way to

get to the point that i needed to for

general audience blood sugar as an idea

is in common language and it's easier to

grasp by a majority of people than

encephalopathy the word itself being

intimidating and the idea of

international normalized ratio there's

an overhead that's associated with going

that route that'll make the video longer

what's inr or prothrombin time what's

hepatic encephalopathy why does it

happen how does it happen how about

liver enzymes what's an enzyme that's

the overhead it's all technical okay so

in context of liver failure in the very

beginning of the case i tell you some

really big details aj is a 20 year old

man presenting to the emergency room

with abdominal pain nausea and diffuse

bleeding

paramedics were scrambling because he

kept vomiting in the ambulance until he

fell unconscious abdominal pain with

extreme nausea vomiting something

abdominal falling unconscious something

neurological diffuse bleeding he didn't

just get a cut somewhere it's diffuse so

he's bleeding in many different places

why would he be bleeding like that this

is someone who also has jaundice first

two sentences of the video tells you a

lot this is not a borderline case it's

an extreme one neuro exam unconscious

unarousable unresponsive to pain diffuse

bleeding so something systemic something

is wrong airway is fine breathing is

okay circulation all right heart rate

and rhythm normal in that first sentence

i also tell you that he's a 20 year old

man who is described as a student in the

title 20 is a little too old to be in

high school so this is someone at the

university undergraduate level what can

you tell me about health problems in 20

year old men

20s pretty young to have chronic

diseases that are common in people over

65 years old if we're looking at heart

attacks a 20 year old having a heart

attack is more often than not going to

have one for a different reason than a

70 year old liver damage usually takes a

long time to happen so liver failure

happening between the two age groups is

likely going to be for very different

reasons and this is acute liver failure

high ast alt in the blood neurologic

signs and symptoms jaundice hypoglycemia

no known prior liver disease so what

would be a cause of liver failure in a

previously healthy 20 year old man i

could go into all the things like

autoimmune hepatitis or ischemic

hepatopathy or scorpion sting right in

the middle of winter outside of

baltimore everything put together this

is very likely something happening due

to this person ingesting and putting

something in their body what are some

things that a 20 year old might ingest

okay heart rate and rhythm are normal so

it doesn't look like there's stimulant

use he's breathing normally so probably

not opioids because that would be

respiratory depression so what else

would you think of did he drink

something maybe that could be likely

given age and social demographic being

in college setting if it was to the

point of causing acute liver failure you

might be able to smell it off of his

breath if it happened recently enough

but in this case we know he didn't drink

any liquor did he eat something now

we're talking

one thing that i find interesting in

looking at tweets that come up randomly

about this case and the associated ones

is that this case is often met with a

lot of fear it's something that's taught

in medical pharmacy and nursing schools

because of its nature students tend to

remember that reheating pasta and rice

is dangerous

unfortunate that that ends up being the

takeaway because that's not what this

case is about

very generally reheating pasta and rice

after a day or two or three and it's

been refrigerated the whole time within

a couple of hours after it was made is

not going to cause problems so with that

how would sketchy five-day-old pasta

that was left out for at least a whole

day cause liver failure so severe that

the person eating it will die from it i

set this line in the chubby emu video

you see the liver is a highly metabolic

organ you can't live for very long

without one everything that enters your

mouth ends up in the liver as it breaks

down chemicals and red blood cells

secretes bile for digestion makes blood

clotting factors that stop you from

bleeding and processes proteins among

other functions and it maintains blood

sugar levels bringing us back to

metabolism when you think of something

being metabolically active you think of

metabolism of heat of movement the

breaking and creation of chemical bonds

involving a lot of energy being produced

and consumed an energy factory could be

called a powerhouse and because we know

that the mitochondria is the powerhouse

of the cell

now we're talking a sample of the

patient's liver revealed microvesicular

steatosis microbe meaning small vesicle

referring to a sac or a vacuole a space

and steat referring to fats or lipids

and osis meaning a disorder of a

disorder of fat contained in small sacs

this is different from

macrovesicular steatosis where the sacs

are big and they're so big that the

nucleus of the cell gets pushed off to

the side you can see that underneath a

microscope macro vesicular steatosis is

common and associated with alcohol

misuse diabetes and obesity

microvesicular

is not as common so we're talking about

the liver the liver needs a lot of

energy to function this patient had

liver failure cells use fats as an

energy source but in these samples we

see an inappropriate presence of fat in

the liver from this information we can

take one guess that fats entered the

liver cells like how they normally do

but something happened so that those

cells couldn't process and handle the

fats causing them to quickly build up

without being able to produce energy

from fats some machinery in the cell was

disturbed and couldn't make up for this

loss resulting in the big picture result

of the liver shutting down in the

extreme case that a hundred percent of

the liver no longer functions wastes in

the blood that are normally processed by

the liver accumulate quickly among them

is ammonia from gut bacteria processing

proteins and this causes disturbances in

cerebral osmolytes this results in more

water entering the brain than is normal

causing cerebral edema intracranial

hypertension herniation and then it's

over so what was that something that

happened so that cells couldn't process

and handle the fats well it was bacteria

that grew on the five-day old pasta but

it was bacillus cereus which is commonly

found in soil if it causes an illness

from food it's usually self-limiting so

it's more than just the bacteria some

strains can produce a toxin that

specifically targets the mitochondria

preventing the mitochondria from using

fats to create energy causing the

buildup and causing the acute liver

failure

in the mitochondria we have atp

production a majority of it being the

product of the electron transport chain

where protons re-enter the matrix by

traveling through a pore in atp synthase

and the energy released in that process

is used to make atp for reference the

matrix is the innermost part of the

mitochondria the inter-membrane space is

inside the mitochondria but outside the

matrix going upstream the process if atp

production ends with protons re-entering

the matrix because a gradient was

created then something must have caused

them to be pushed out of the matrix and

into the inter-membrane space if protons

were moved and those are positive

charges then we could make a guess that

electrons which are negative charges

were involved and we know in the process

of atp production there's the electron

transport chain four complexes big

proteins starting with nicotinamide

adenine dinucleotide nadh the reduced

form and it gets oxidized so two

electrons are removed and transferred to

a compound called ubiquinone the quinone

moiety is a conjugated cyclic dione so

there's two carbon double bond o's in a

structure with delocalized electrons

gaining two electrons means that the

charge becomes negative so to neutralize

it two protons are accepted and

ubiquinone becomes ubiquinol and then it

diffuses across the membrane in the

united states you see commercials

everywhere on tv for coq10 supplement

and that is ubiquinol as this conversion

happens the electron current passing

through complex one powers the active

transport so remember it's creating a

gradient of four protons in the inter

membrane space but where does nadh come

from

going upstream the process we have the

tricarboxylic acid tca cycle which

reduces nad to nadh this is all the

stuff that you learned in school

multiple times and depending on where

you end up may or may not have applied

to you you have had to memorize it

multiple times for a test without any

context of why but really all of those

times that you learned it were for

situations like this where it absolutely

applies here and it's good that you know

about it even if you don't remember it

all from school to enter the tca cycle

you need acetyl coa where does acetyl

coa come from there's one pathway where

it comes from glucose but there's

another pathway where it comes from fats

and remember we know that there's a

dysfunction of creating atp and the

pathological findings show an

inappropriate accumulation of fats in

the form of microvesicular steatosis so

this brings us to how the toxin from the

bacteria in five day old pasta caused

feminine hepatic failure to get acetyl

coa from fatty acids the pathway is

going to appear boring but there's

important steps in between that entire

diseases are based off of triglycerides

and fatty acids get converted to acyl

coa by acyl coa synthetase acyl is a

general term describing a double bond

oxygen and carbon and an alkyl group so

the number of carbons is not specific it

could be a couple it could be a lot in

any given sample you're going to have a

wide variety of different quantities

really long fatty acids which have a lot

of carbons can't cross the mitochondrial

membrane on their own but there's a

shuttle for it mediated by carnitine

diseases can happen here if there's

something wrong with the carnitine

transporter a problem with the carnitine

palmitoyl transferase enzyme that places

the carnitine on the fatty acid in or

outside the mitochondria these are all

diseases of metabolism so you can expect

highly metabolic tissue like the liver

the heart the brain to be affected in

patients who have it carnitine is bound

to the fatty acid and shuttled into the

mitochondria where the carnitine is then

taken off and acyl co-a is reformed

again and this is where it's converted

to acetyl coa through beta oxidation

completing our cycle but if we're

looking at a problem where fat is

building up into vesicles and we're

assuming that the person didn't have any

deficiencies upstream of the cycle at

this point then it's here where the

problems can form and this is called

fatty acid beta oxidation beta referring

to the second carbon from the carbonyl

group or carbon number three if you're

counting carbons starting from the

carbonyl in that first step there's

three isozymes very long chain acyl coa

dehydrogenase medium chain acyl coa

dehydrogenase and short chain acyl coa

dehydrogenase you can be born with

deficiencies of these enzymes and it's

not that uncommon medium chain acyl-coa

dehydrogenase deficiency has a

prevalence of 1 in 20 000 live births so

what happens if someone has a deficiency

for medium chain they would have primary

inhibition of fatty acid beta oxidation

what does that look like let's say it's

a kid and he's a really picky eater

mom's not having any of it she says you

know what if you don't want to eat this

dinner i'm not cooking anything extra

and i'm not going to buy you mcdonald's

chicken nuggets guess you're just going

to have to wait until morning to eat so

the kid's liver will start tapping

glycogen stores to provide glucose to

make acetyl coa to feed into the cell

machinery to produce atp but as the

hours pass those sugar stores are

getting more and more depleted and it's

harder to get a quick source acetyl-coa

provides the acetyl group for ketones

and those can be used for energy but

acetyl-coa is the precursor the

medium-chain acyl-coa dehydrogenase

deficiency which is putting a hard limit

on acetyl-coa production

that limits atp production causing a

metabolic acidosis hypoglycemia is

happening because the kid hasn't eaten

but also can't use his fat stores

because of this inhibition of fatty acid

oxidation cytoplasmic fatty acids are

converted to triglycerides which

accumulate and produces microvesicular

steatosis in the liver bringing us back

to the student who ate five-day-old

pasta the toxin made by that strain of

bacteria is called cereulide again

uncommon strain that develops from the

right conditions on rice and pasta

cereulide from what we understand is a

potassium ionophore it's a cyclic

peptide that binds to the mitochondrial

inner membrane and allows potassium to

flow freely into the matrix on the

mitochondrial inner membrane there is a

hydrogen potassium exchanger that is to

pump potassium out of the matrix and

bring hydrogen into the matrix but

there's two problems with that as an

ionophore the amount of potassium let in

would overwhelm this exchanger and not

only that remember the electron

transport chain happens here the

electron transport chain pumps hydrogen

out so that it can flow through a pore

and atp synthase to make atp so

importing hydrogen into the matrix

because you need to get rid of excess

potassium would mean that you're

disturbing the gradient that's being

created by the electron transport chain

the introduction of a lot more potassium

than normal into the matrix starts to

raise the ph of the matrix because

protons are getting pumped out while

potassium flows in

remember the electron transport chain

happens because of proteins which are

adapted to certain ph

if this changes then you could guess

that the complex's ability to function

would change because proteins can change

in different ph and there's also some

evidence that ubiquinone would also

stabilize which would then not move

electrons impairing atp synthesis as

more and more potassium floods into the

hepatocyte mitochondria oxidative

phosphorylation becomes uncoupled

reactive oxidative species form because

oxygen is supposed to be the final

electron acceptor but it can't do that

anymore the mitochondria swell up and

rupture causing hepatocellular necrosis

extensive necrosis results in functional

liver failure before the cell lysis

blebs form in the cell membrane and

enzymes start leaking out as the blebs

coalesce the cell dies and leaks out all

its contents as the liver fails it

doesn't produce the right amount of

blood clotting factors which can result

in diffuse bleeding the liver doesn't

process the ammonia that's produced by

the gut breaking down the proteins as

the ammonia flows into the liver from

the portal circulation it's supposed to

be detoxified to glutamine and urea by

the urea cycle which happens to be

another branch of the acetyl-coa

breakdown pathway but the liver is

failing and the processes are all

overloaded and normal function is not

attained ammonia spills into the blood

and flows to the brain where glutamine

synthetase in the astrocytes convert

ammonia with glutamate into glutamine

which is a cerebral osmolite causing

cerebral edema and without a liver

transplant in time nothing can be done

enough and in time to prevent what will

happen because at autopsy the bacteria

from the patient's intestinal contents

his liver and also residue from the pan

used to reheat his pasta were cultured

and it was found to be bacillus serious

the final note that i want to add here

is that in the chubby emu video at the

time i added in that the patient drank a

whole bottle of pepto-bismol to the case

because i wanted to teach briefly about

salicylates pepto-bismol is bismuth

subsalicylate being an uncoupler of

oxidative phosphorylation in the setting

of overdose it appears that it could

lead to microvesicular steatosis because

it consumes co-a which would then mean

that acetyl-coa would have trouble being

produced so there would be a decreased

fatty acid activation from low coe

levels leading to decreased beta

oxidation adding in that dual blockade

in my mind was that there would be no

question that the liver failure was

complete from a dual blockade of the

same pathway

unfortunately i could see many comments

couldn't deal with that they would go so

far as to say that it was only the

bottle of pepto-bismol that caused that

liver failure that the pasta meant

absolutely nothing but that reveals to

me that those people commenting entirely

missed everything about cerealide about

a massive intra mitochondrial shift of

potassium from a cyclic peptide acting

as an ionophore causing mitochondrial

dysfunction it didn't help that the news

articles covering the story at the time

just said that it was food poisoning

without explaining that a special strain

of bacteria that's common produced a

toxin that made this food poisoning so

much worse than normal it taught me a

lesson that two ideas at the same time

that are interwoven and related

sometimes won't be processed my videos

since 2019 have reflected that lesson

learned but the reality is in medicine

there's a lot of ifs and there's a lot

of unknowns that are time sensitive at

that particular point in time the big

bucks are made because things more often

than not are borderline and you have to

make a decision on which way to go based

on what you know at that point in time

not very many things are so obviously

unipolar and in just one dimension but

that's a quick review of microvesicular

steatosis and feminine hepatic failure

that occurred because of someone who ate

five-day-old pasta by accident