(Terbutaline, ritrodine)
(Neostigmine, physiostigmine)
When we go to thorax or abdomen... It's hard to remember their relation... Are there any tips?
What sort of relation? The relation of structures that pass through the diaphragm?
Yep.
Ok I know one mnemonic for that.
I ate (8) ten eggs at twelve.
I: Inferior vena cava
aTe: T8!
Eggs: Esophagus (Vagus rhymes with it!)
Ten: T10
AT: Azygous vein, Thoracic duct! Twelve: T12
So to summarize:
IVC - T8
Esophagus, vagus - T10
Azygous, thoracic duct - T12
Hope this helps!
Does anyone know the name of retinopathy occurring in pancreatitis?
Purtscher's retinopathy!
What are it's characteristics?
Signs visible on fundoscopic examination include
pathognomonic Purtscher flecken and cotton-wool spots around the optic nerve n intraretinal h'age
Yes. The macula is affected too. Granulocyte deposition occurs in the posterior retinal artery.
Antimalarial that causes irreversible retinal toxicity??
Chloroquine?
Yes. It's hydroxychloroquine..!!
Also used in...??
DLE, rheumatoid arthritis!
Lepra reactions too!
Also in extra intestinal amoebiasis!
Skin lesions in dermatomyositis!
Okay, so what pathology in the eye does hydroxychloroquine cause..??
It accumulates there because of high volume of distribution?
It causes Bull's eye maculopathy..!!
And the pathogenesis?
It is said that the drug binds to melanin in the RPE, which could explain the persistent toxicity even if after discontinuation of the medication!!!
I remember the use of hydroxychloroquine (Plaquenil) in Behcet's Disease. Follow up with eye exam every 2-3 months.
What's Behcets disease?
Behcets syndrome is inflammatory, multi system disease of small vessels resulting in frequent aneurysms and rupture..!! Eyes, genitals and mucous membranes are involved.
It takes many months to treat genital ulcers!
What is that test to confirm behcets..??
Pathergy test
Pricking the skin with a needle = pathergy test. After one or two days, people with Behçet's can develop a lump or nodule where the needle broke the skin.
Correct!
I had a patient with several mouth ulcer's looking like Aphthous ulcer. No other symptoms, just episodic mouth ulcers!
Okay.. Could be due to stress and vitamin deficiency..
And it turned out to be Behçet's disease.
They have a lot Behçet's disease clinic's in Turkey! Must be genetic which is why it is so common.
The exact cause of the disease remains unclear. But Behçet's disease is thought to involve an autoimmune response. This means the body's defense mechanism begins to attack its own tissues. Something in the environment may trigger this abnormal immune response in susceptible individuals. Genetic factors may also play a role.
It is common in young men in Mediterranean area..
Our patient was a woman.
Oh nice to know, thanks!
Cutaneous signs of insulin resistance and lipoproteinemia
Electrolyte abnormalities that cause constipation
Aspirin
Cycloserine
Morphine and atropine
Drug for neurological manifestations of Wilson's disease
ACE in lung diseases
Central trachea in pleural effusion
Walking pneumonia
Aortic regurgitation
Pressure and volume reservoir in the human body
HOCM
Cardiac embryology and fetal heart sounds
Atrial septal defects - Why do they present late?
Gallstone ileus
Hepatic encephalopathy
Kartageners syndrome
Haemosiderosis and haemochromatosis
Thyroid surgery practicals viva questions
Venous ulcer
Pre-eclampsia and HELLP syndrome
Differentials of discharge in a pregnant woman
Glycogen storage diseases mnemonic
Cytochrome c
Agranular cytoplasmic reticulum
Colorful amino acids and pH
Difference between antibody and anti-toxin
Lymph nodes in various diseases
It's been a crazy busy week, especially with group 3 and all, I stay on my toes!
-IkaN
Differences between haemosiderosis and haemochromatosis?
Haemochromatosis is iron overload primary and secondary, iron overload is within cells and interstitium, causes tissue damage. Hemochromatosis is primarily genetic!
Where as haemosiderosis is a form of secondary hemochromatosis due to repeated blood transfusions, deposition of haemosiderin in the cells, with reversible accumulation of iron in RES. I hope its clear!
So heamochromatosis is irreversible?
The tissue damage, I agree, will have consequences. But you can chelate the excess iron?
Yes! But reversible if in the form of secondary- haemosiderosis
Blood letting! Pts encouraged to donate blood it seems, and iron chelating agents would help.
Those untreated develop HCC
Even cardiomegaly
And endocrine issues.. Especially, pituitary and the adrenals
Yeah I think they continuously need to get their iron chelated
So it can be counted as reversible then?
Not reversible..But manageable.
Yes that's a good term actually
Controllable I would say!
Heart failure cells are macrophages laden with haemosiderin in LVF OR pulmonary odema.
Was an episode in house MD. The girl was suspected to have it cause her skin tone had changed several tones darker.
There was this one more episode where they diagnosed Wilson's disease based on the colour change of nailbed on rubbing it with nail remover! I so want to try that.
Really ?
The blood copper level wasn't raised.. No kf rings in cornea.
The lady was a mean woman.. She couldn't feel emotions.. Was manipulative. And the change in personality happened when she was a teenager.
Interesting!
They applied nail remover and behold.. The nail turned blue.
I had a suspected case of Wilson's disease in my college.. She took discharge before I could experiment this.
There is even one more episode on Wilson's in season 1. They diagnose it by observing KF ring over the cornea.
Also, an another episode on Hemochromatosis with a mean chess playing lad.
Yup.. I remember both the episodes! The alcoholic mom with schizophrenia had Wilson's. And the jerk xD
Yeah! Actually, she did not have schizophrenia. They were the manifestations of Wilson's itself.
It was pretty cool how House figures that self sacrifice isn't a symptom of Schizophrenia
Yeah! I love the way House has epiphanies leading to diagnoses.
Differences between haemosiderosis and haemochromatosis?
Haemochromatosis is iron overload primary and secondary, iron overload is within cells and interstitium, causes tissue damage. Hemochromatosis is primarily genetic!
Where as haemosiderosis is a form of secondary hemochromatosis due to repeated blood transfusions, deposition of haemosiderin in the cells, with reversible accumulation of iron in RES. I hope its clear!
So heamochromatosis is irreversible?
The tissue damage, I agree, will have consequences. But you can chelate the excess iron?
Yes! But reversible if in the form of secondary- haemosiderosis
Blood letting! Pts encouraged to donate blood it seems, and iron chelating agents would help.
Those untreated develop HCC
Even cardiomegaly
And endocrine issues.. Especially, pituitary and the adrenals
Yeah I think they continuously need to get their iron chelated
So it can be counted as reversible then?
Not reversible..But manageable.
Yes that's a good term actually
Controllable I would say!
Heart failure cells are macrophages laden with haemosiderin in LVF OR pulmonary odema.
Was an episode in house MD. The girl was suspected to have it cause her skin tone had changed several tones darker.
There was this one more episode where they diagnosed Wilson's disease based on the colour change of nailbed on rubbing it with nail remover! I so want to try that.
Really ?
The blood copper level wasn't raised.. No kf rings in cornea.
The lady was a mean woman.. She couldn't feel emotions.. Was manipulative. And the change in personality happened when she was a teenager.
Interesting!
They applied nail remover and behold.. The nail turned blue.
I had a suspected case of Wilson's disease in my college.. She took discharge before I could experiment this.
There is even one more episode on Wilson's in season 1. They diagnose it by observing KF ring over the cornea.
Also, an another episode on Hemochromatosis with a mean chess playing lad.
Yup.. I remember both the episodes! The alcoholic mom with schizophrenia had Wilson's. And the jerk xD
Yeah! Actually, she did not have schizophrenia. They were the manifestations of Wilson's itself.
It was pretty cool how House figures that self sacrifice isn't a symptom of Schizophrenia
Yeah! I love the way House has epiphanies leading to diagnoses.
Differences between haemosiderosis and haemochromatosis?
Haemochromatosis is iron overload primary and secondary, iron overload is within cells and interstitium, causes tissue damage. Hemochromatosis is primarily genetic!
Where as haemosiderosis is a form of secondary hemochromatosis due to repeated blood transfusions, deposition of haemosiderin in the cells, with reversible accumulation of iron in RES. I hope its clear!
So heamochromatosis is irreversible?
The tissue damage, I agree, will have consequences. But you can chelate the excess iron?
Yes! But reversible if in the form of secondary- haemosiderosis
Blood letting! Pts encouraged to donate blood it seems, and iron chelating agents would help.
Those untreated develop HCC
Even cardiomegaly
And endocrine issues.. Especially, pituitary and the adrenals
Yeah I think they continuously need to get their iron chelated
So it can be counted as reversible then?
Not reversible..But manageable.
Yes that's a good term actually
Controllable I would say!
Heart failure cells are macrophages laden with haemosiderin in LVF OR pulmonary odema.
Was an episode in house MD. The girl was suspected to have it cause her skin tone had changed several tones darker.
There was this one more episode where they diagnosed Wilson's disease based on the colour change of nailbed on rubbing it with nail remover! I so want to try that.
Really ?
The blood copper level wasn't raised.. No kf rings in cornea.
The lady was a mean woman.. She couldn't feel emotions.. Was manipulative. And the change in personality happened when she was a teenager.
Interesting!
They applied nail remover and behold.. The nail turned blue.
I had a suspected case of Wilson's disease in my college.. She took discharge before I could experiment this.
There is even one more episode on Wilson's in season 1. They diagnose it by observing KF ring over the cornea.
Also, an another episode on Hemochromatosis with a mean chess playing lad.
Yup.. I remember both the episodes! The alcoholic mom with schizophrenia had Wilson's. And the jerk xD
Yeah! Actually, she did not have schizophrenia. They were the manifestations of Wilson's itself.
It was pretty cool how House figures that self sacrifice isn't a symptom of Schizophrenia
Yeah! I love the way House has epiphanies leading to diagnoses.
In liver failure, what is the cause of hepatic encephalopathy?
They are not sure yet but they think it's ammonia.
Yes, NH3 and other substances.
They act as pseudotransmitters.
But how do ammonia levels rise?
Liver detoxifies ammonia by forming urea.. Failure to convert ammonia into urea.
Since liver is damaged.. Ammonia rises.
Does it occur on inhaling ammonia?
You mean, inhaling ammonia when liver is damaged or in normal people? Ammonia is an irritant to the 5th nerve, if I am not wrong. Why would anyone inhale it for a long time?
If by an accident?
Umm. I haven't heard of a situation like that
We inhale ammonia everytime we pass an unclean public toilet! :P
Argh.
Hahaha!
*a picture of an ulcer was posted on which this discussion took place in the group*
Which side is the lesion on? Medial or lateral?
If it is medial, it can be venous ulceration too! Mass obstructing the venous outflow.
Yup could be as it is superficial.. And also it could be venous ulcer because it looks like the ulcer is in gaiters area..above the medial malleolus..
What is gaiters area?
Gaiters area is where venous ulcers are usually seen. Above medial malleolus!
Where there is highest preasure in vein due to gravitational pull! And incompetent valve also in varicose vein
What's the name of the perforator in that area?
They are cockett boyd dodd and hunter from below upwards.
I have a mnemonic for the perforators
Do share!
http://medicowesome.blogspot.ae/2014/09/types-of-perforators-of-lower-limb.html
What is Kartagener syndrome?
Immotile cilia syndrome
May result in Situs inversus
Bronchiectasis
Sinusitis
Glue ear too!
Infertiliy? Sperm motility is also affected i guess
Sperm motility is affected.
The protein involved is 'dynein'.
I've seen a case of Kartageners in my hospital. The auscultation and looking at radiographs was fascinating!
*a picture of gall stone ileus was posted in the group as guess the diagnosis after which this discussion took place*
Commonest position of obstruction by gallstone in ileum
Ileocaecal junction?
Not ileocaecal valve. The position in books have been mentioned terminal ileum. A little proximal to the ileocaecal valve.
Most commonly, obstruction occurs at the distal ileum.
I didn't know gallstone ileus could be this big. I imagined them to be tiny!
Me too!
I've heard there has to be a fistula for the stone to be that big to obstruct the ileum. Something that connects the gall bladder to the intestine.. Because a stone this big wouldn't pass the common bile duct
I agree with IkaN
Yup I'm sure the patient suffered from a fistula too..
It enters the intestine through cholecystoduodenal fistula commonly..
I've heard my resident mention fistula once
Yep.. And the predisposed patients are those with Crohn's disease! Thanks, just wanted to confirm it :D
Large stones, >2.5 cm in diameter, are thought to predispose to fistula formation by gradual erosion through the gallbladder fundus...
Ohh that makes sense! The huge stone itself causes fistula formation which is why they are common!
"A fistula develops between a gangrenous gallbladder and the duodenum or other parts of the gastrointestinal tract, allowing passage of the stone. Occasionally the stone may enter the intestine through a fistulous communication between the bile duct and the gastrointestinal tract."
Colorful aminoacids?
Donno. Maybe tyrosine because they add pigment?
Trytophan phenylalanine tyrosine. Tryptophan is major!
They add color to us! Makes sense. At first, I have to admit, I was imagining colors of the rainbow xD
Yeah and remaining are colorless!
At physiological pH what is the charge of amino group and Carboxyl group?
Positive amino negative carboxyl
PANCard
That's a good mnemonic! Will never forget this!
I just remember histidine is the one who is neutral at physiological pH.
Name the positively charged amino acids!
Basic are positively charged I guess. Histidine lysine arginine.
Mnemonic! http://medicowesome.blogspot.ae/2013/11/amino-acids-with-electrically-charged.html
IkaN mnemonic wow <3
Lady gaga is always negative hahaha!
What is moonlight effect of cytochrome c?
Sounds interesting!
Cytochrome c in cytosol cause cell death by apoptosis. Cytochrome c in mitochondria helps in electron transport. This dual function!
Ooo.. Yes, the life maintainer and the killer! Why moonlight though?
Moon light means a job on the side, one that you wouldn't wanna disclose.
I have a question, what is the differences between cytochrome c1 and cytochrome c?
I think cyt c is mobile and the other is not.
Yep.
What are the functions of agranular cytoplasmic reticulum?
Synthesise lipids, transportation of proteins,enzymes for detoxification of drugs,enzymes of glycolysis.
Why do ASD present later in life?
You mean atrial septal defects?
Yup.
The left atria is stronger than the right, so it's a left to right shunt, initially (Oxygenated blood getting more oxygenated kind of shunt.)
This is why, ASD is acyanotic at birth. It won't present till there is pulmonary hypertension (The lungs get fed up of the excess blood!)
This will cause a reversal of shunt - turning it into right to left. (Now, the deoxygenated blood is getting thrown into circulation!)
This reversal is also known as Eisenmenger's syndrome.
This is why, ASDs present late in life.
Okay.. So I think the compensatory mechanisms make up for the disturbances in circulation in early years but fail later hence the features appear later..
Also the atria contribute very little as compared to the ventricles.
Atrial defects are usually very small thus, less complications in infancy. And also murmurs heard in ASD are not very loud, so its difficult for a physician to detect it.
I think, it becomes complicated due to development of Eisenmenger syndrome in later years.
Yes.. And the patient hardly survive 5-6 yrs after development of Eisenmenger syndrome..
Sometimes, ASDs never get severe enough to present as a heart disease. A paradoxical embolus is the initial presentation of an ASD in some cases!
Cardiac Embryology review question! Which blood vessel does the 6th arch artery give rise to?
Pulmonary arteries!
Common carotid artery derived from..??
3rd arch
Right!
Here's a mnemonic on the derivatives of arch arteries http://medicowesome.blogspot.ae/2013/11/aortic-arch-derivatives-mnemonic-images.html
The coronary arteries develop from which structure?
From aortic sinuses of valsalva..??
Endothelial tissue grows out of the aortic wall and connects with the subepicardial vessel plexus while the heart is developing to form coronary arteries.. Is that right??
Ya.. At first the cells are derived from venous sinus then they transform to become arteries.
When does heart start pumping ?
I am guessing its 4wks?
First heart beat by 4 weeks!
When does the fetal heart beat for the first time in utero? And when is the heartbeat detected by ultrasound? I know 4 weeks is when the heart starts pumping but is it the same time we detect through USG?
I think there are 2 different terms!!
Fetal heart motion around 5-6 weeks
Fetal heart sounds can be heard around 8-10 weeks
Ohh.
Fetoplacental unit establishes around 21-22 days following fertilization.
Fetal heart motion: 9 weeks by doppler USG.
Fetal heart sounds 18-20 weeks by stethoscope.
When does the fetal movements start?
18-20 weeks?
That's probably right. I know mothers start noticing moviments from 20th week on. a bit later if it is their first child and they don't how to recognise the sensation.
Yep. Multigravidas appreciate fetal movements earlier than primis
In 16 to 18 wks - That's for multigravida.
But fetal movements start at 8-9 weeks. They are perceived late I guess!
In what case foetal heart fails to mature enough such that we can't detect sounds even at 8w?
One case would be hydatidiform mole. No heart sounds heard.
I don't know what is a hydatidiform mole.
Hydatidiform mole isn't a fetus. It's a edematous condition of the Placental villi. You'll learn this is second year, Pathology!
There is no fetus or fetal parts. Not compatible with life... You'll have to read it up from books.
Here are some study links!
Embryology and gestational trophoblastic disease
Difference between complete and partial mole mnemonic
Hydatidiform mole (Complete vesicular mole) mnemonic
Why is such a gap between starting of heart beats and its detection by US ??
I mean heart starts beating at around 4w and heart beats are detected at around 8w .. why so ?
That's a very interesting question.. But I have no idea regarding that!
Theories:
Maybe because motion is there but structurally heart is immature so no sound is there (av valve)
I think we don't have equipment to detect faint sounds. We could detect heart sounds along with the motion if we had the technology!
Maybe you guys will invent a fetoscope that detects it earlier in the future! :D
A young, apparently healthy athlete, while playing collapses to the ground and dies.. Diagnosis?
Hypertrophic obstructive cardiomyopathy.
Right, as always!
Will probably also have family history!
Oh oh review question - what is the site of obstruction in HOCM?
Ventricular septal wall?
Interventricular septum.
Left ventricular outflow is obstructed.
Yup. Basically below the outflow tract of the aorta.
What will happen to the intensity of the murmur in HOCM during Valsalva maneuver?
It will increase. HOCM and MVP are the only two conditions in which a decrease in blood volume to the heart increases the intensity of the murmur.
What's Brugada syndrome??
In Brugada syndrome there's risk of sudden cardiac death.. And it's also genetic..
Oh.. Didn't know. What is the defect in brugada syndrome? In HOCM it is beta myosin I guess.
Some defect in sodium or calcium channels I guess.. Not sure.
Ohh okay. Thanks!
Differentials of 28 week primi presenting with white discharge?
You wanna see for pooling of fluid in the fornices and check for pH.
It could be premature rupture of membranes. It could be stress incontinence. It could also be a normal excessive discharge.
Could it be infection?
Yep, it could be.
Depends on the quantity of discharge.
Um okay..
I had a case on this in my final year university exam
The entire viva went on it!
Mine was normal physiological discharge with oligohydramnios.