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A student with a ‘hangover’
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
Additionally if the DKA has been caused by serious illness, the patient may present with the symptoms relating to that condition (e.g. myocardial infarction, pneumonia, sepsis). Such symptoms and the associated signs may mask those associated with ketoacidosis. This is particularly true of renal and cardiac causes, which, if volume-retaining, can counteract the usual volume depletion.
Pathophysiology of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Neonatal diabetes affects infants and their ability to produce or use insulin. It is a monogenic condition that is controlled by a single gene. Neonatal diabetes develops within the first 6 months of life. Since there is not enough insulin produced, the glucose levels increase. This rare disease only occurs in 1 of every 100,000–500,000 live births. It can be mistaken for type 1 diabetes. There are two types of neonatal diabetes. The permanent form is lifelong, while the transient form disappears during infancy. However, the transient form can recur later in life. Onset of neonatal diabetes can be linked to abnormal pancreatic development and the speeds of beta cell dysfunction. The condition can be genetically linked between patients and offspring. Symptoms include polydipsia, polyuria, dehydration, dry mouth, tiredness, and dark-colored urine. When dehydration is severe, signs include hypotension, sunken eyes, weak pulse, tachycardia, and fatigue. Ketoacidosis develops if the disease is severe. Related to neonatal diabetes is intrauterine growth restriction, with the fetus not growing to reach a normal weight within the womb. After birth, the infant may have hyperglycemia or hypoglycemia. Permanent and transient neonatal diabetes are both genetically inherited from the mother or father.
Diabetes in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Preexisting diabetes mellitus complicates approximately 0.3% of all pregnancies in the United States (1), while gestational diabetes mellitus (GDM) complicates 5% to 10% (2). Type 2 diabetes, characterized by the typical clinical presentation of obesity and insulin resistance, is roughly 10 times more prevalent in the American population than type 1 diabetes; in recent years, as the nationwide epidemic of obesity and type 2 diabetes has impacted younger and younger individuals, type 2 diabetes is becoming proportionally more common in pregnancy. Individuals with type 1 diabetes are prone to ketoacidosis whereas those with type 2 diabetes rarely manifest this complication.
Comparative safety of sodium-glucose co-transporter 2 inhibitors in elderly patients with type 2 diabetes mellitus and diabetic kidney disease: a systematic review and meta-analysis
Published in Renal Failure, 2023
Yi Liu, Chuan An, Peilong Liu, Fan Yang, Quanlin Zhao
A total of 58489 patients (32530 in the SGLT2 inhibitors group and 25959 in the placebo group) participated in 9 studies on the hypoglycemic outcome. Meta-analysis results showed no significant difference in the incidence of hypoglycemia between patients on SGLT2 inhibitors and those on placebo (RR: 0.97; 95%CI [0.93–1.01], p = 0.18, I2=44%) (Figure 4(a)). 11 studies reporting data related to adverse events of urinary tract infections (UTIs), the meta-analysis showed no significant difference in the probability of UTIs using SGLT2 inhibitors compared with placebo (RR: 1.06; 95%CI [1.00–1.11], p = 0.04, I2=35%) (Figure 4(b)). We extracted data on events consistent with genital mycotic infections from baseline to end of follow-up from 10 studies. The results showed that the SGLT2 inhibitor group was significantly different from placebo, and genital mycotic infections are more likely to occur with SGLT2 inhibitors (RR: 3.47; 95%CI [2.97–4.04], p < 0.00001, I2=26%) (Figure 4(c)). 7 studies reported diabetic ketoacidosis. Participants who were treated with SGLT2 inhibitors had a significantly higher risk of diabetic ketoacidosis than those treated with placebo (RR: 2.25; 95%CI [1.57–3.24], p < 0.0001, I2=0%) (Figure 4(d)). Results of meta-analysis showed that the use of SGLT2 inhibitors did not increase the incidence of fractures (RR: 1.07; 95%CI [0.99–1.16], p = 0.08, I2=0%) (Figure 5(a)).
Association of Candida esophagitis with acute esophageal necrosis
Published in Baylor University Medical Center Proceedings, 2022
Muhammad Sheharyar Warraich, Bashar Attar, Shazaq Khalid, Muhammad Ali Khaqan
A 53-year-old man with a history of uncontrolled type 2 diabetes mellitus, chronic kidney disease, necrotizing pancreatitis complicated by chronic pancreatitis, and alcoholic Child B cirrhosis presented to the emergency department with 1 week of nausea, nonbloody and nonbilious vomiting, and diffuse abdominal pain. On admission, his blood pressure was 135/80 mm Hg; heart rate, 106 beats/min; respiratory rate, 30 breaths/min; and temperature, 34.4°C. The blood glucose was 675 mg/dL; bicarbonate, 16 mEq/L; anion gap, 26; pH, 7.30; urea, 36 mg/dL; creatinine, 1.4 mg/dL; hemoglobin, 8.3 g/dL; and white cell count, 17 k/μL. Blood cultures were obtained. Computed tomography of the abdomen with contrast revealed gastric distension with fluid-filled distal esophagus and changes of portal hypertension and chronic pancreatitis. The patient was diagnosed with diabetic ketoacidosis and admitted to the intensive care unit. Treatment was initiated with intravenous fluid and an insulin drip, and the patient’s condition improved.
An evaluation of empagliflozin and it’s applicability to hypertension as a therapeutic option
Published in Expert Opinion on Pharmacotherapy, 2020
Lakshini Y Herat, Vance B Matthews, Aaron L Magno, Marcio G Kiuchi, Revathy Carnagarin, Markus P Schlaich
Similar risk factors including hypertension are responsible for the development of CVD and renal disease in T1D [100]. Recently, the EASE-1 and -2 programs investigated Empagliflozin in T1D subjects and showed clear beneficial effects on HbA1c, body weight, BP, glucose variability, and total daily insulin use with minimal adverse events [101,102]. The EASE-3 program only used a very low dose of Empagliflozin (2.5 mg) but still revealed beneficial effects on metabolic and BP outcomes including HbA1c, body weight, total daily insulin dose, and SBP. Interestingly, a lower risk of hypoglycemia and diabetic ketoacidosis was observed. These metabolic benefits suggest a novel role for Empagliflozin in the setting of T1D. However, given the higher risk of diabetic ketoacidosis for people with T1D, the 2.5 mg Empagliflozin dose warrants further investigation [102].