Class 12/13 - Alterations in Endocrine Function Flashcards
Actions of Insulin
- Promote uptake of blood glucose by cells
- Promotes storage of glucose in the form of glycogen
- Prevents the breakdown of fats and glycogen
- Inhibits gluconeogenesis
- Increases protein synthesis, impacts metabolic processes
- Helps the movement of K+ into cells
- Building/metabolic protein
Diabetes Mellitus Incidence
Abnormal glucose regulation and nutrient storage. Insulin deficiency or insulin resistance
Name history “peeing a lot” and “sweet”
Type 1, Type 2, and Gestational. G increases the chance of developing 1 and 2 later in life
Incidence
- 11 million/ 36 mill Canadians live with diabetes and high risk
- 80% will die of heart disease or stroke
- Life span is decreased 5-15 years
- $15,000 dollars per year out of pock
Type 1 Diabetes Mellitus
Caused by the destruction of pancreatic beta cells
- Beta cells produce insulin and amylin (inhibits glucagon secretion after meals). Less amylin = more glucagon, causes hyperglycemia
Etiology:
- Most commonly an auto-immune response
- Genetically predisposed
- Environmental trigger
Characteristics:
- 10% o diabetes
- Earlier age of onset than Type 2
- Diagnosis peaks at age 12
Hyperglycemia causes - Osmotic diuresis - Polyuria - Polydipsia - Glucose in urine Cells are starving, causes - Weight loss - Polyphagia - Breakdown fats for fuel (ketonemia, ketonuria, fruity breath) - Fatigue Other manifestations - Recurrent infections - Visual changes - Paresthesia's
Diagnosis
- History and physical exam
- Elevated plasma glucose (fasting, glucose tolerance test or random plasma glucose)
- HbA1C (glycosylated hemoglobin)
- Ketonuria
- Glucosuria
Type 2 Diabetes Mellitus
Pathophysiology
- Progressive impairment of beta cells
- Progressive insulin resistance (decreased ability of insulin, and higher amount of insulin required)
- Beta cells are exhausted, but can recover
Etiology:
- Unknown but most likely genetic plus environmental and lifestyle choices
- Later age of onset, more gradual onset
Risk factors
- Family history
- Age
- Obesity
- Indigenous, African, or Asian ethnicities
Insulin Resistance affected by:
- Central obesity
- High blood pressure
- High triglycerides
- Low HDL-cholesterol
- Insulin resistance
Manifestations
- Non-speicifc
- Polyuria, polyphagia, and polydipsia
- Fatigue
- Recurrent infections
Often associated with
- Obesity/ abdominal obesity
- Dyslipiideemia
- Hypertensive
Diagnosis
- History and physical exam
- Elevated plasma glucose (fasting, glucose tolerance test or random plasma glucose)
- HbA1C (glycosylated hemoglobin)
- Ketonuria
- Glycosuria
Management
- Diet and exercise
- Oral hypoglycemics
- Insulin
- Bariatric surgery
Acute Complications
- Hypoglycemia
- Diabetic ketoacidosis
- Hyperosmolar hyperglycaemic nonketotic syndrome
Chronic Complications
- Macrovascular disease
- Microvascular disease
- Neuropathies
- Infection
Hypoglycemia
Blood sugar less than 4 mmol/L
Causes
- Too much exercise
- Too much medication
- Not enough food
Speed of onset is fast
Manifestations
- Confusion
- Agitations
Treatment
- Increase blood sugar
Diabetic Ketoacidosis
Blood glucose > 14 mmol/L
Causes
- Lack of insulin to meet needs.
Onset
- Hours to days
- Usually in type 1 diabetics
Patho and Manifestations
- Hyperglycemia - glucose in urine - polyuria - polydipsia - hypotension - tachycardia
- Rapid weight loss, marked fatigue, seizures, coma
- Kussmaul respirations, fruity or acetones breath
- Metabolic acidosis, respiratory system will be compensating
Treatments
- Insulin
- Fluid replacement
- Monitor and correct electrolytes. It impacts potassium
Hyperosmolar Hyperglycemic Nonketotic Syndrome
Blood glucose is > 33mmol/L.
Peeing out a huge amount of sugar and water
Causes
- Insufficient insulin
- Stress, illness, infection
Speed of Onset
- Days to weeks
- Usually in type 2 diabetics
Manifestations
- Hyperglycemia
- Glucose in urine +++
- Polyuria +++
- Polyphagia
- Polydipsia
- Profound fluid loss (hypovolemic)
- No ketosis
- No acidosis
- Outcomes worse than ketoacidosis
Treatment
- Fluid replacement
- Correct blood sugar
- Correct electrolytes
Chronic Complications
- Chronic hyperglycemia affects Schwann cells, ion pumps, reduces antioxidants, attracts water into the lens of the eye
- Glucose binds with proteins in blood vessel walls, traps LDL and triggers inflammation
- Macrovascular disease
- Microvascular diease
- Neuropathies
- Infection: impaired WBC function, high glucose function
Macrovascular Disease
Chronic complication of HHNS
Disease in any large blood vessel in the body
- Atherosclerosis
- MI, stroke, peripheral artery disease, foot ulcers
- Bad circulation, neuropathy, bacteria loves to live in sugary places.
Microvascular Disease
Chronic Complication of HHNS
- Ischemia of the eyes and kidneys
- Retinopathy (like looking through a hole punched piece of paper), glaucoma, cataracts
- Neuropathy
Neuropathies
Chronic Complication of HHNS
- Ischemia to the nerves, causes demyelination
- Paresthesias (numbing, tingles, numbness)
- Impaired pain sensation
- Gastric atony (impaired peristalsis)
- Paralytic bladder
- Impotence
Posterior Pituitary Gland
Releases ADH/vaspresin and Oxytocin
Syndrome of Inappropriate Antidiuretic Hormone Secretions (SIADH)
- Too much ADH
Caused by
- Pituitary tumour
- Stroke
- Traumatic brain injury
Results in the reabsorption of water
- Urine output decreases
- Serum sodium decreases (hyponatremia)
- Hypotonic body environment
Hyposecretion of ADH
Not enough ADH
Eg. Diabetes Insipidus
Caused by
- Pituitary tumour
- Traumatic brain injury
- Stroke
Results in the excretions of water
- Urine output increases
- Serum sodium indcreases
- Hypertonic
Thyroid Gland
Secretes Thyroxin (T4) and Triiodothyronine (T3) which increases metabolic rate. Regulated by Thyroid Stimulating Hormone (TSH). TSH is regulated by Troponin Releasing Hormone (TRH)
Thyroid hormones needed for physical growth and intellectual development
Hypothyroidism
Decreased levels of thyroid hormone
Most common cause is Hashimoto’s thyroiditis
- Autoimmune
- Destruction of thyroid glands by T cells
- Female gender link
Manifestations
- Fatigue
- Weakness
- Slower heart rate
- Slower respiratory rate
- Constipation
- Mental acuity slows down, trouble remembering
- Cold intolerance
- Edema of the extremities
- Link to depression/mental health
- Periorbital edema
- Myxedema
Diagnosis
- Blood testing for TSH levels
- TSH will be elevated
- Levels of T3 and T4 will be decreased
Treatment
- Synthetic form of thyroid hormone
In children there is Cretinism
- Stunted growth
- Delayed intellectual development
