Diffuse glomerulosclerosis

Kimmelstiel–Wilson nodule (blue arrows) are pathognomonic for diabetic nephropathy

AGE is a bitch
صارلي ساعة أريد أتذكر هالإختصار يرمز لشنو

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طبعًا اني جنت مقرر أغلس على الهستو والباثو لباقي حياتي، لحدما طلع النفرولوجي كله معتمد عليهن...

حرفيًا إنجبرت أحبهن، بالنعال هم...

Unrelated, but kinda related:

C-peptide is the connecting peptide that is cleaved in the production of insulin from pro-insulin. It can be readily measured in blood and urine by sensitive immunoassays.
Serum C-peptide is a marker of endogenous insulin secretion (a synthetic insulin does not contain C-peptide) and is particularly useful if a patient is on exogenous (injected) insulin treatment, when insulin assays would simply detect the injected insulin.

Serum C-peptide can help clarify the differential diagnosis of diabetes, as it is usually very low in long-standing type 1 diabetes and very high in severe insulin resistance.

Glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) are released from gastrointestinal L cells and K cells, respectively, following a meal, and act via receptors on the pancreatic β cells to augment insulin secretion.
Thus, for a given glucose stimulus to the β cell, there is greater insulin secretion with oral glucose administration (where the gut peptides are released) compared to intravenous glucose administration (which does not stimulate gut peptide release).
This enhanced insulin secretion following oral administration of glucose is termed the ‘incretin’ effect, and GLP-1 and GIP are known as incretin hormones.

Btw, Whipple's triad is a clinical cluster of signs and symptoms that indicate insulinoma.

When a detective solves a case of murder, he doesn't jump blindly to the conclusion. First, he finds the usual suspects. Same applies to diagnosis

In COPD B2-agonists and anticholinergic agents produce similar effects or a greater response from anticholinergics. The combination may be helpful. In contrast, in asthma B2-agonists produce a greater effect.

Without treatment, 25% to 42% of uncomplicated acute cystitis (UTI) cases in women will resolve spontaneously. Even without effective treatment, the likelihood that uncomplicated acute cystitis will progress to pyelonephritis is only around 2%

The preferred agents for empiric therapy of acute simple cystitis are:
• Nitrofurantoin
• Trimethoprim-sulfamethoxazole (TMP-SMX)
• Fosfomycin

Antimicrobial selection for acute simple cystitis depends on the risk of infection with a multidrug-resistant (MDR) gram-negative infection.
We generally consider patients to be at risk for an MDR gram-negative infection if they have any of the following within the prior 3 months:


• An MDR gram-negative urinary isolate or a fluoroquinolone-resistant Pseudomonas aeruginosa urinary isolate.

• Inpatient stay at a health care facility (eg, hospital, nursing home, long-term acute care facility).

• Use of a fluoroquinolone, trimethoprim-sulfamethoxazole, or broad-spectrum beta-lactam (eg, third- or later-generation cephalosporin).

• Travel to parts of the world with high rates of MDR organisms.

Diabetic foot ulcer (DFU)

It's caused by a combination of peripheral neuropathy & peripheral artery disease (PAD)

الفكرة هي أنّ السكري يسبب neuropathy وهذا الشي يخلي الشخص يفقد إحساسه برجله ومفاصله، وممكن يدوس عليها ويأذيها بشكل طفيف وية كل حركة بدون ما يشعر causing micro-trauma (بالإضافة لأشياء أُخرى). هاي الإصابات الصغيرة لما تتجمع تدريجيًا، رح تؤدي لتشوه مفاصل وعظام الرجل (charcot joints).

وبنفس الوقت السكّري يسبب PAD اللي ممكن نعرّفه ببساطة على أنّه:
Narrowing/occlusion of peripheral vessels due to atherosclerosis (or other causes such as spasm).
بحالة السكّري فالـ PAD يصير بسبب الـ atherosclerosis (لأن كل السكر الزايد رح يتحول لدهون تتجمع بالجسم وبالأوعية الدموية) وهالشي رح يقلل وصول الدم للأطراف وبالأخص للقدم ويسبب ischemia.
كل هالعوامل تزيد إحتمالية الإصابة بتقرحات القدم السكّرية diabetic foot ulcer.