Diabetes mellitus (Type 1): Clinical sciences

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Diabetes mellitus (Type 1): Clinical sciences

cardio

cardio

Introduction to the cardiovascular system
Introduction to the lymphatic system
Cardiovascular system anatomy and physiology
Coronary circulation
Lymphatic system anatomy and physiology
Abnormal heart sounds
Normal heart sounds
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Cardiac cycle
Cardiac work
Changes in pressure-volume loops
Pressure-volume loops
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac afterload
Cardiac contractility
Cardiac preload
Frank-Starling relationship
Law of Laplace
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Cardiac conduction velocity
Cardiac conduction system
ECG basics
ECG normal sinus rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Control of blood flow circulation
Microcirculation and Starling forces
Blood pressure, blood flow, and resistance
Compliance of blood vessels
Laminar flow and Reynolds number
Pressures in the cardiovascular system
Resistance to blood flow
Action potentials in myocytes
Action potentials in pacemaker cells
Cardiac excitation-contraction coupling
Excitability and refractory periods
Adrenergic antagonists: Beta blockers
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Lipid-lowering medications: Fibrates
Lipid-lowering medications: Statins
Miscellaneous lipid-lowering medications
Positive inotropic medications
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Atrial fibrillation
Atrial flutter
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Wolff-Parkinson-White syndrome
Brugada syndrome
Long QT syndrome and Torsade de pointes
Premature ventricular contraction
Ventricular fibrillation
Ventricular tachycardia
Endocarditis
Myocarditis
Rheumatic heart disease
Cardiac tumors
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Atrial septal defect
Coarctation of the aorta
Patent ductus arteriosus
Ventricular septal defect
Hypoplastic left heart syndrome
Tetralogy of Fallot
Total anomalous pulmonary venous return
Transposition of the great vessels
Persistent truncus arteriosus
Cor pulmonale
Heart failure
Cardiac tamponade
Dressler syndrome
Pericarditis and pericardial effusion
Shock
Arterial disease
Aneurysms
Aortic dissection
Angina pectoris
Coronary steal syndrome
Myocardial infarction
Prinzmetal angina
Stable angina
Unstable angina
Abetalipoproteinemia
Familial hypercholesterolemia
Hyperlipidemia
Hypertriglyceridemia
Conn syndrome
Cushing syndrome
Hypertension
Hypertensive emergency
Pheochromocytoma
Polycystic kidney disease
Renal artery stenosis
Hypotension
Orthostatic hypotension
Lymphangioma
Lymphedema
Peripheral artery disease
Subclavian steal syndrome
Nutcracker syndrome
Superior mesenteric artery syndrome
Angiosarcomas
Human herpesvirus 8 (Kaposi sarcoma)
Vascular tumors
Behcet's disease
Kawasaki disease
Vasculitis
Chronic venous insufficiency
Deep vein thrombosis
Thrombophlebitis
Acyanotic congenital heart defects: Pathology review
Aortic dissections and aneurysms: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
Cardiomyopathies: Pathology review
Coronary artery disease: Pathology review
Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
Endocarditis: Pathology review
Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
Arteriole, venule and capillary histology
Artery and vein histology
Cardiac muscle histology
Development of the cardiovascular system
Fetal circulation
Anatomy of the coronary circulation
Anatomy of the heart
Anatomy of the inferior mediastinum
Anatomy of the superior mediastinum
Anatomy clinical correlates: Heart
Anatomy clinical correlates: Mediastinum
Introduction to pharmacology
Chest X-ray interpretation: Clinical sciences
Electrolyte disturbances: Pathology review
Anatomy clinical correlates: Breast
Anticoagulants: Heparin
Thrombolytics
Congestive heart failure: Clinical sciences
Approach to ascites: Clinical sciences
Approach to dyspnea: Clinical sciences
Approach to lower limb edema: Clinical sciences
Coronary artery disease: Clinical sciences
Chronic obstructive pulmonary disease: Clinical sciences
Tobacco use: Clinical sciences
Approach to chest pain: Clinical sciences
Approach to hypertension: Clinical sciences
Acute coronary syndrome: Clinical sciences
Carotid artery stenosis screening: Clinical sciences
Diabetes mellitus (Type 1): Clinical sciences
Diabetes mellitus (Type 2): Clinical sciences
Dyslipidemia: Clinical sciences
Essential hypertension: Clinical sciences
Peripheral arterial disease and ulcers: Clinical sciences
Abdominal aortic aneurysm: Clinical sciences
Aortic dissection: Clinical sciences
Approach to bradycardia: Clinical sciences
Approach to postoperative hypotension: Clinical sciences
Approach to tachycardia: Clinical sciences
Atrioventricular block: Clinical sciences
Cardiac tamponade: Clinical sciences
Central line-associated bloodstream infection: Clinical sciences
Hypovolemic shock: Clinical sciences
Infectious endocarditis: Clinical sciences
Pericarditis: Clinical sciences
Ventricular tachycardia: Clinical sciences

Decision-Making Tree

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Diabetes mellitus is a chronic condition where tissue cells can’t properly absorb and use glucose, so it stays and builds up in the blood. Normally, pancreatic islet beta cells produce insulin, which acts on insulin receptors on tissue cells to promote uptake and storage of glucose, amino acids, and triglycerides, as well as stimulate glycolysis, protein synthesis, and lipogenesis.

Now, there are two types of diabetes, type 1 and type 2. In type 1 diabetes, there’s autoimmune destruction of the pancreatic islet beta cells, resulting in severe insulin deficiency and, ultimately, hyperglycemia. This is in contrast to type 2 diabetes mellitus, where the pancreatic islet beta cells stop properly responding to stimulation to produce insulin, combined with insulin resistance, meaning that the tissue cells aren’t able to appropriately respond to the little insulin that’s still being produced.

In either disease type, the resulting hyperglycemia can cause clinical manifestations ranging from prediabetes and diabetes mellitus, to severe life-threatening conditions, like diabetic ketoacidosis, or DKA, most commonly seen in patients with type 1 diabetes, and, hyperosmolar hyperglycemic state, or HHS, most commonly in type 2 diabetes.

Now, if you suspect type 1 diabetes mellitus, you should first perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable, stabilize the airway, breathing, and circulation. This means that you might need to intubate the patient. Next, obtain IV access and, if your patient is hypotensive, start IV fluids for volume resuscitation. Finally, put your patient on continuous vital sign monitoring, such as pulse oximetry, blood pressure, and heart rate.

Next, you want to assess for DKA or, less frequently, HHS. Obtain a focused history and physical exam, and order labs, such as point-of-care blood glucose, serum osmolality, BMP, urinalysis, hemoglobin A1c, as well as ABG or VBG.

Patients typically present with fatigue, headache, or dry mouth, polyuria, and polydipsia. They may also be so confused they cannot give an accurate history, so be sure to speak with caretakers and review the chart thoroughly to get an accurate history. Your patient may also have had a precipitating illness or infection, or have a known history of diabetes mellitus with or without disruption to their diabetes treatment plan.

On the other hand, physical exam might reveal tachypnea, tachycardia, and hypotension in a confused, somnolent patient. The mucous membranes are often dry. Let’s start by using our labs to help us distinguish between DKA and HSS. In HHS, lab results typically reveal a significantly elevated random blood glucose, more so than DKA, often exceeding 600 milligrams per deciliter. BMP may reveal hyponatremia and hypokalemia, as well as elevated BUN and creatinine. The serum osmolality is high, usually greater than 320 milliosmoles per kilogram. Finally, there will be an elevated hemoglobin A1c.

On the other hand, DKA, lab results reveal a significantly elevated random blood glucose, exceeding 250 milligrams per deciliter. BMP may reveal hyponatremia and hypokalemia, as well as elevated BUN and creatinine. There is a normal serum osmolality. Finally, there will be an elevated hemoglobin A1c, and the ABG or VBG will confirm elevated anion gap metabolic acidosis. You may also see decreased bicarbonate, hinting at a metabolic acidosis. Urinalysis will show ketones.

In either case, HHS or DKA, management of these individuals includes IV fluid resuscitation to correct dehydration and hyperosmolality, as well as electrolyte repletion. Additionally, you can start an IV insulin drip, if indicated, and carefully monitor potassium levels. Don’t forget to treat any underlying or precipitating causes!

Now that we're done with unstable patients, let’s go back to the ABCDE assessment and discuss stable ones. If your patient is stable, first obtain a focused history and physical examination. Your patient might report unintentional weight loss, polydipsia, polyuria, and blurred vision, while family history often reveals autoimmune disorders such as thyroid disease or celiac disease.

On physical exam, you may notice oral thrush or dry mucous membranes. At this point, you should suspect diabetes mellitus, and proceed with labs, such as hemoglobin A1c, a fasting blood glucose, a 2-hour oral glucose tolerance test, or OGTT, and a random blood glucose test. Keep in mind that not all patients require an OGTT; this is often used when the other values are inconclusive or unclear in making a diagnosis.

Now let’s look at lab results to determine a diagnosis. Now, if the hemoglobin A1c is less than 5.7%, fasting blood glucose is less than 100 mg/dL, blood glucose after the 2-hour OGTT is less than 140 mg/dL, and random blood glucose is less than 200 mg/dL, then you should consider an alternative diagnosis.

On the other hand, you should consider prediabetes if the hemoglobin A1c is between 5.7 and 6.5%, fasting blood glucose is between 100 and 126 mg/dL, or blood glucose after the 2-hour OGTT is between 140 and 199, and a random blood glucose is under 200 mg/dL. Keep in mind that prediabetes typically precedes type 2 diabetes mellitus, and only rarely precedes type 1.

Sources

  1. "American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update" Endocr Pract (2022)
  2. "The Management of Type 1 Diabetes in Adults. A Consensus Report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD)" Diabetes Care (2021)
  3. "Type 1 diabetes" Lancet (2018)
  4. "Harrison's Principles of Internal Medicine, 21e." McGraw Hill (2022)