PLEASE help me improve these videos! Take this quick survey about how the videos help you learn: goo.gl/BjU8bk Description of pathophysiology of type 1 and type 2 diabetes, and a discussion of complications.
Mr. Wolf.. You are the sole reason why I am passing Patho right now. I don't even listen to my teacher in class. I jot down some notes of diseases and processes that we cover, and then when I get home...I pray to god that you have covered them in a tutorial! THANK YOU!
You are a great lecturer and easy to understand. Wonderfully helpful explanation of the pathophysiology behind diabetes. I am a 2nd year nursing student your videos are really helping me. Thank you.
Mr. Wolf great lecture and explanation for the DM.. Plus the expected outcomes of both are an added bonus!! Cellular K and serum differences are awesome!! Thank you
You are very good at explaining this. I didn't feel like you were talking over-my-head, so I was able to enjoy this video and come away with a really good understanding of the material. I really appreciate that!
I always have difficulty understanding Type 1 and type 2 diabetes especially in-depth of pathos. Watching your video makes it so much easier to understand and fun to watch. Thank you so much for your great videos.
Amazing video!! I think this is my first time that I've actually enjoyed pathophysiology! Regards from a Kuwaiti PhD student, cardiac rehab specialist, at Swansea University, UK Fatimah
GOOD. I learnt more in this 25 minute video than I did in my entire semester for cardiometabolic (4th year uni) about diabetes. Failed my practical because I gave a dismal answer to the client in why they are at risk of diabetes (with PAD, HTN and dyslipidemia). I guess I would answer that now as; as you have high levels of circulating fatty acid due to your dyslipidemia diagnosis, this causes increased inflammatory hormones which damage 2nd messenger system that works to release insulin. How would I link this back to HTN and PAD though?
Mr. Wolf, You said FFA causes increased cytokines and inflammation which may be cause for inhibiting the second messenger system. My question is, why wouldn't anything that causes increased levels of cytokines and inflammation do the same thing? How can you pinpoint only Free Fatty Acids as the cause and in the same note claim it's from the processes that FFA induce? Multiple other stimuli have the same inflammatory affect, no?
Late clinical complications are:1 Macrovascular complications, eg larger blood vessels like coronary and cerebral arteries may become prone to occlusion. 2 Microvascular complications-damage to small vessels eg fine capillaries in eye and kidney causing retinopathy and nephropathy respectively. 3 Microvascular damage to blood vessels in skin may cause lesion- dermopathy and 4 Peripheral nueropathy where peripheral nervous tissue mainly sensory nerves can become progressively damaged.
The third main type of diabetes is gestationaI diabetes, which is a condition that women can get when they are in the second trimester of pregnancy. About 4 percent of aII pregnant women wiII deveIop gestationaI diabetes. UnIike Type 1 and Type 2 diabetes, gestationaI diabetes wiII disappear after the baby is born ..........
Triglycerides are derived not only from fats in the diet but also sugar (carbs and simple), alcohol, and excess calories in general. I think it's important to note this so as not to demonize fats in the diet specifically. Please correct me if I'm wrong.
I did appreciate the video, but don't forget the simple stuff. like osmotic effects. No mention of the three "P's"??? The typical early indicators of diabetes are Polyurea, Polydipsia, and Polyphagia. (Urinating frequently, Thirst, and hunger). Another osmotic effect is increased intra-ocular pressure.
wow...you are an excellent educator and i like your explanation really. would you mind please telling my how to access to your power points or handouts? Thank you very much
i wish my teacher is YOU !! .. this would be soo much easier for me not sleeping in classes.... and understanding everything!! thanks for ur videos really help... please post some more!! =)
Great video. Type 1 diabetes is due to HLA chromosome 6. Type 2 is due to uterine malnutrition (Barker hypothesis). Can I feauture this in my educational youtube channel?
hello there i was wondering if you could explain the reason why ketoacidosis is more pronounced in type I diabetics rather then type II, i was think because of complete lack of insulin in type I the patient is more likely to burn the fats while in type II even though there is insulin resistance some tissues in the body show some response to the insulin so ketoacidosis doesn't manifest to the same extent. hope you can clear up my understanding
Is there a known mechanism for Type 1 diabetic patients that do not have viral infections, pancreatic tumors, pancreatitis, and have consistently normal fasting glucose till the age of 30+?
C-peptide, a component of proinsulin (precursor to insulin) declines in DM1. It apparently plays a protective role in preventing beta cell destruction; therefore less C-peptide will accelerate decline in beta cells. The autoantibodies and cytotoxic T cells will continue to destroy beta cells unabated. McCance & Huether, 2010 - pathophysiology: a biologic basis for disease in adults and children - pg. 748
The high glucose level will form plaques on the wall of blood vessel and it makes blood vessel hard (arteriosclerosis), this will cause poor blood circulation, and high glucose concentration serves as food to the bacteria.
I thought type 1 one was juvenile diabetes and was diagnosed in childhood, therefore I did not believe people whe claimed to have a combination of both type 1 and 2 especially when the type 2 lifestyle was glaring evident and the diagnosis came in late teen or adult years. However, from what you have said I can see the possibility. Can a Pt have both types and do adults get type 1
Hi Dr. Wolf, These videos are so helpful! I am trying to get ready for my final in Patho and can't figure out what pathway is activated in the kidneys to increase urine and excrete the additional serum K+ during DKA? Is it the RAAS? Thank you!
insulin is secreted from beta cells in the form of pro-insulin (insulin+c-peptide) then it splits into insulin & c-peptide so,estimation of c-peptide level in the blood can be an indicator for endogenous insulin level as estimation of insulin level cant determine whether it is the insulin secreted from pancreas(endogenous) or it is insulin therapy (exogenous)
hello sir!!..thankyou for ur video.i have a doubt.sir,how can hyperinsulinemia compensate the high blood glucose levels when the problem is with secondary messenger system? i mean,the high or low levels of insulin are not gonna regulate glucose levels as the problem is with insulin resistance.
I am trying to fend off diabetes type 2 by taking cholesteroff (Naturesway brand)and tricalcium (my bones are clacifying and Ca is important to 2d messenger signaling)
G'day, can you recommend a good text/journal with more in detailed analysis of the destruction of the beta cells (the exact physiological response). Every source i have found skims across this area. Is this because of a lack of knowledge of just its low level of importance.
Dear Andrew, i'm a bit lost here.. Shouldn't it be the other way? Hyperosmolarity stimulates vasopressin secretion and therefore the patient will experience polydipsia, with polyuria as a consequence? thanks for yor support! btw.. i love the twix bar guy! he rocks!!! thank u!
This is a very good video Mr Wolf, but I have the same question with Sara Leland. If the second messenger system of the liver cells in prediabetic condition (type 2 DM) is blocked, how the patient can compenzate just fine? Since the glucose transporters on the plasma membrane of the hepatocytes do not brink the glucose molecules in the cytoplasm. How the patient can have a normal glucose level in the blood at this prediabetic state? I am looking forward for your reply... Thank you :-)
I really appreciate that! But sir, why the video doesnt continue till the end ?!! when somebody enters your room & u say Hold on Please, the video ends, but u didnt explain the CONTROL... !!!
Apparently, animation is too difficult for pharmacy school professors. Wish you would have taught our class! Diabetes does not have to be so difficult.
Dr. Wolf: OK, I know to check for microalbumuria in Type II DM every six months or so. Then what, if a patient does have microalbuminuria? If they are already taking an ACE inhibitor, do we send to a nephrologist for evaluation promptly if there are no symptoms? Do we work on controlling blood sugars first, then refer if microalbumuria persists? I am participating in the care of a few patients that have been taking their meds intermittently (HbA1C 11, etc)
hello sir, how in patient with diabetes type 2 will be a block in second messenger ...you mentioned something about cytokines and fatty acid what is the relationship between them . thank you
I seem to be finding conflicting information on HHNK (or HHS). Is hyper or hyponatremia associated with this syndrome? Is it a false hypernatremia d/t hemoconcentration? I am confused on the levels of Na+ in DKA and HHNK. Please help. Thanks!
Andrew, as always legendary videos. You should add more information on about me section ... give more info of who you are and what you did ... just saying
It seems like even if the body was making extra insulin you would still have diabetes if the cell isn't able to uptake the glucose... I don't understand how the increased insulin is useful at taking care of the glucose.
Hi Andrew, I found your explanation of the effect of insulin on the Na/K pump to be succinct and informative, thank you. However, can you explain the role of the liver. My understanding is the liver increases glucose secretion in an effort to somehow supply cells starved of glucose? What triggers this response? Does DKA lipolysis result in lactic acid by-product; further augmenting H production? Are there other by-products of protein and fat breakdown?
Interesting to listen to this now. Ten years later! The liver generates the 5 grams(one teaspoon) of glucose that your body needs at any one time for body function. ALL OTHER INTAKE OF CARBS , SUGAR, OTHER TYPES OF SUGAR,(dextrose, Maltrose etc.) is excess and triggers insulin response. High carb load equals high insulin production. And that leads into all the complications the video goes on to list. Since this video came out, there has been large increase of interest in low carb high fat diets, (Atkins diet but lower protein) .
hello Mr, Wolf, i wanted to thank you for explaining the patho beyond diabetes and i truly appreciate it! i am currently trying to answer this essay question, and i wanted to know what would be your input in regards to this question? A 28 yo Caucasian male with a history of Type I Diabetes presents to the clinic for his annual physical exam. While taking his history he states that he took 10 units of Regular Insulin prior to leaving for the clinic but forgot to eat lunch. what would you do?
