Diabetes mellitus
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Diabetes mellitus
Endocrine system
Adrenal gland disorders
Congenital adrenal hyperplasia
Primary adrenal insufficiency
Waterhouse-Friderichsen syndrome
Hyperaldosteronism
Adrenal cortical carcinoma
Cushing syndrome
Conn syndrome
Thyroid gland disorders
Thyroglossal duct cyst
Hyperthyroidism
Graves disease
Thyroid eye disease (NORD)
Toxic multinodular goiter
Thyroid storm
Hypothyroidism
Euthyroid sick syndrome
Hashimoto thyroiditis
Subacute granulomatous thyroiditis
Riedel thyroiditis
Postpartum thyroiditis
Thyroid cancer
Parathyroid gland disorders
Hyperparathyroidism
Hypoparathyroidism
Hypercalcemia
Hypocalcemia
Pancreatic disorders
Diabetes mellitus
Diabetic retinopathy
Diabetic nephropathy
Pituitary gland disorders
Hyperpituitarism
Pituitary adenoma
Hyperprolactinemia
Prolactinoma
Gigantism
Acromegaly
Hypopituitarism
Growth hormone deficiency
Pituitary apoplexy
Sheehan syndrome
Hypoprolactinemia
Constitutional growth delay
Diabetes insipidus
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Gonadal dysfunction
Precocious puberty
Delayed puberty
Premature ovarian failure
Polycystic ovary syndrome
Androgen insensitivity syndrome
Kallmann syndrome
5-alpha-reductase deficiency
Polyglandular syndromes
Autoimmune polyglandular syndrome type 1 (NORD)
Endocrine tumors
Multiple endocrine neoplasia
Pancreatic neuroendocrine neoplasms
Zollinger-Ellison syndrome
Carcinoid syndrome
Pheochromocytoma
Neuroblastoma
Opsoclonus myoclonus syndrome (NORD)
Endocrine system pathology review
Adrenal insufficiency: Pathology review
Adrenal masses: Pathology review
Hyperthyroidism: Pathology review
Hypothyroidism: Pathology review
Thyroid nodules and thyroid cancer: Pathology review
Parathyroid disorders and calcium imbalance: Pathology review
Diabetes mellitus: Pathology review
Cushing syndrome and Cushing disease: Pathology review
Pituitary tumors: Pathology review
Hypopituitarism: Pathology review
Diabetes insipidus and SIADH: Pathology review
Multiple endocrine neoplasia: Pathology review
Neuroendocrine tumors of the gastrointestinal system: Pathology review
Assessments
Diabetes mellitus
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USMLE® Step 1 questions
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Diabetes mellitus
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Reproduced from: Wikimedia Commons
Synchronized electrical cardioversion is attempted; however, the patient loses a pulse immediately afterwards. After 10 rounds of cardiopulmonary resuscitation, the patient is pronounced dead. Which of the following processes was the most likely contributor to this patient’s cause of death?
Memory Anchors and Partner Content
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2016
Atherosclerosis p. 302
diabetes mellitus and p. 346
β -blockers p. 246
diabetes and p. 246
Cataracts p. 535
diabetes mellitus and p. 346
Cerebrovascular disease
diabetes mellitus p. 346
Coronary artery disease
diabetes mellitus and p. 346
Diabetes mellitus p. 346-352
acanthosis nigricans p. 483
atherosclerosis and p. 302
atypical antipsychotics p. 573
β -blockers and p. 246
binge eating disorder p. 566
carpal tunnel syndrome p. 449
cataracts and p. 535
chronic renal failure and p. 603
CN III damage p. 541
diabetic ketoacidosis p. 350
diabetic retinopathy p. 537
endometrial cancer risk p. 648
Friedreich ataxia p. 531
fungal infections p. 186
glaucoma and p. 536
glucagonomas p. 350
glucosuria in p. 584
hemochromatosis p. 395
hepatitis C p. 173
hypertension and p. 301, 316
Klebsiella p. , 145
neonatal respiratory distress syndrome p. 661
nephropathy with p. 594, 595
neural tube defect association p. 491
opportunistic infections p. 153
pancreatic cancer p. 395
polyhydramnios and p. 642
preeclampsia and p. 643
in pregnancy p. 300
pyelonephritis and p. 600
readmissions with p. 272
renal papillary necrosis and p. 602
sexual dysfunction p. 567
tacrolimus and p. 120
teratogenic potential p. 614
type 1 vs type p. -19, 352
urinary incontinence with p. 599
urinary tract infections p. 181
UTIs and p. 600
Diabetes mellitus management p. 352-352
Diabetes mellitus type p. -20, 352
autoantibody p. 115
HLA subtypes with p. 100
Diabetes mellitus type p. -19, 352
amyloidosis p. 218
hyperosmolar hyperglycemia nonketotic syndrome p. 350
Diabetic glomerulonephropathy p. 595
Gangrene
diabetes mellitus p. 346
Glaucoma p. 536
diabetes mellitus and p. 346
Glucocorticoids
diabetes mellitus p. 346
Growth hormone (GH) p. 334, 356
diabetes mellitus p. 346
Kimmelstiel-Wilson nodules
diabetes mellitus p. 346
Maternal diabetes
cardiac defect association p. 300
Myocardial infarction (MI) p. 304
diabetes mellitus p. 346
Nephropathy
diabetes mellitus p. 346
Neural tube defects p. 491
maternal diabetes p. 614
Neuropathy
diabetes mellitus p. 346
Polyuria p. 599
diabetes mellitus p. 346, 350
Pregnancy p. 633
Proteinuria p. 595
diabetes mellitus p. 346
Renal failure
diabetes mellitus p. 346
Retinopathy
diabetes mellitus p. 346
Transposition of great vessels p. 298
maternal diabetes and p. 300
Weight loss
diabetes mellitus p. 346
External Links
Transcript
Contributors
Tanner Marshall, MS
In diabetes mellitus, your body has trouble moving glucose, which is a type of sugar, from your blood into your cells.
This leads to high levels of glucose in your blood and not enough of it in your cells, and remember that your cells need glucose as a source of energy, so not letting the glucose enter means that the cells starve for energy despite having glucose right on their doorstep.
In general, the body controls how much glucose is in the blood relative to how much gets into the cells with two hormones: insulin and glucagon.
Insulin is used to reduce blood glucose levels, and glucagon is used to increase blood glucose levels.
Both of these hormones are produced by clusters of cells in the pancreas called islets of Langerhans.
Insulin is secreted by beta cells in the center of the islets, and glucagon is secreted by alpha cells in the periphery of the islets.
Insulin reduces the amount of glucose in the blood by binding to insulin receptors embedded in the cell membrane of various insulin-responsive tissues like muscle cells and adipose tissue.
When activated, the insulin receptors cause vesicles containing glucose transporters that are inside the cell to fuse with the cell membrane, allowing glucose to be transported into the cell.
Glucagon does exactly the opposite, it raises the blood glucose levels by getting the liver to generate new molecules of glucose from other molecules and also break down glycogen into glucose so that it can all get dumped into the blood.
Diabetes mellitus is diagnosed when the blood glucose levels get too high, and this is seen among 10% of the world population.
Sources
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
- "Harrison's Endocrinology, 4E" McGraw-Hill Education / Medical (2016)
- "Hyperglycemic Crises in Adult Patients With Diabetes" Diabetes Care (2009)
- "MECHANISMS IN ENDOCRINOLOGY: Seizures and type 1 diabetes mellitus: current state of knowledge" European Journal of Endocrinology (2012)
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