Endocrine Patho Flashcards
What do cells need/use as a source of energy?
Glucose
What is a hormone that increases the amount of glucose in your blood?
Glucagon
What is a hormone that decreases the amount of glucose in your blood?
Insulin
What produces insulin?
B cells in the pancreas
What patient population typically has Type 1 DM?
- Once of most common childhood diseases
- Peak onset = 11-13 years
- 1.5-2x higher in whites
- Genetic component: 5-10% risk to siblings and 2-5% to offspring
What is the pathophysiology of Type 1 DM?
- Absolute insulin insufficiency
- Autoimmune attack on the beta cells of the pancreas
- Typically destroy 90% of B cells before s/s occur
3 Major clinical manifestations of Type 1 DM
- Polyuria: increased pee because sugar in urine and water follows sugar
- Polydipsia: increased thirst, hypovolemic
- Polyphagia: increased hunger, weight loss r/t fluid loss, fat/protein store breakdown
Other clinical manifestations of Type 1 DM
Fatigue, weakness, blurred vision, nausea, slow wound healing, tingling in hands, increased infection
Evaluation of Type 1 DM
- History and physical
- Ketones and glucose in urine
- Blood glucose
- HgA1C over 6.5
How do we evaluate blood glucose?
- Random sampling of blood glucose above 200 mg/dl with classic s/s of diabetes
- Fasting blood glucose over 126 mg/dl
- Blood glucose concentration over 200 mg/dl 2 hours after 75 g oral glucose load
Type 1 DM Treatment
- Insulin therapy: main treatment
- Diet/meal planning
- Activity and exercise
Monitor for complications of Type 1 DM
- Acute hyperglycemia
- Diabetic ketoacidosis
- Hypoglycemia
- Chronic changes
Hypoglycemia
T: tachycardia I: irritable R: restless E: excessive hunger D: diaphoresis and depression
Diabetic Ketoacidosis
- One of most common reasons for diabetic hospitalization
- Causes: stress, ineffective management of diabetes
- Result of increased lipolysis and conversion to ketone bodies
- Clinical symptoms: metabolic acidosis (increased breathing and depth of breathing, fruity smelling breath, hyperkalemia)
Patient population with Type 2 DM?
- Accounts for most cases of diabetes
- Mostly non-caucasian (especially blacks and native Americans) and elderly
- Risk factors: aging, sedentary, obesity, genetics, metabolic syndrome, HTN, dyslipidemia
Pathophysiology of Type 2 DM
- Body is resistant to the action of insulin on peripheral tissues
- Requirement for more insulin and glucose utilization is lowered
Evaluation of Type 2 DM
- H and P but more subtle
- Glucose in urine
- Blood glucose
- HgA1C above 6.5
Treatment of Type 2 DM
- Primarily lifestyle changes: diet, exercise, weight loss improve glucose tolerance
- Meds: oral, insulin over time
Monitor for complications of Type 2 DM
- Chronic changes from hyperglycemia
- Eyes, kidneys, CV, cerebrovascular, neuropathy, peripheral vascular, infection
What is gestational diabetes?
Glucose intolerance during pregnancy
What causes gestational diabetes?
- Placental hormones and weight gain during pregnancy cause insulin resistance and inability to produce increased amount of insulin needed during pregnancy
- Risk factors: advanced maternal age (35-40+), family history of diabetes, previous GDM, previous LGA babies
- All pregnant women screened around 28 weeks
Treatment of GDM
- Nutritional counseling and exercise
- Insulin if not controlled with above
Complications of GDM
- Babies: weight over 4 kg, neonatal hypoglycemia, stillbirth
- Mom: higher chance of developing DM in next 10-20 years
What are the adrenocortical hormones?
Produced by adrenal cortex (too much or too little)
- Glucocorticoids: cortisol (energy, immune response, inflammatory, stress)
- Mineralocorticoids: aldosterone (retain sodium and fluids)
- Androgens: sex hormones
What is Addison’s disease?
- Adrenal insufficiency
What are causes of Addison’s disease?
- Destruction of adrenal cortex leads to decreased secretion of adrenal hormones
- Causes: removal of adrenal gland, autoimmune disease (most common), Neoplasms, TB, histoplasmosis, cytomegalovirus
What are clinical manifestations of Addison’s disease?
- Decreased cortisol: hypoglycemia
- Decreased aldosterone: sodium and water loss = hypotension
- Hyperkalemia = acidosis
- Decreased androgens: changes in body hair distribution
- ACTH not suppressed: pigmentation changes
What is evaluation of Addison’s disease?
- History and physical
- Labs: plasma cortisol level
- ACTH stimulation test: would cause cortisol in normal person but no or little rise in person with this
How do we treat Addison’s disease?
- Replacement hormones
- Stress dosing: increase during times of stress
What is Cushing’s disease?
- Cluster of clinical abnormalities caused by excessive adrenocortical hormones or related corticosteroids
- Excess of cortisol
What are causes of Cushing’s disease?
- Pituitary hypersecretion of ACTH
- Tumor
- Administration of synthetic glucocorticoids or steroids
What are clinical manifestations of Cushing’s disease?
- Moon face
- Fat deposits on back of shoulders
- Na and H2O retention
- Edema
- HTN
- Mood changes: depression
- Hyperglycemia
What is evaluation of Cushing’s disease?
- History and Physical
- Dexamethasone suppression test: cortisol stays high
How do we treat Cushing’s disease?
- Surgery/radiation for tumors
- Pharm: Anti-HTN, K+, diuretics
