Lecture 26 (diabetes) Flashcards
Diabetes (basic + main symptom)
problems with body’s regulation of serum glucose levels or antidiuretic hormone (ADH) levels
- both cause polyuria
2 main forms of diabetes (name + basic difference)
diabetes mellitus: lots of sugar in urine
diabetes insipidus: urine is unconcentrated (lack of ions + compounds)
Diabetes insipidus (types, causes, treatment)
both: increased urination, unconcentrated urine
Central diabetes insipidus (most common)
- decrease or lack of ADH caused by pituitary tumours, pituitary/hypothalamus infection…
- lack of ADH causes pour filtrate (made by kidney) reabsorption into blood
- treatment is ADH supplements (eg: nasal spray)
Nephrogenic diabetes insipidus (less common)
- kidney becomes insensitive to ADH
- often caused by drug use (not recreational)
- treatment is increase fluid + electrolyte intake (no real ‘fix’)
How posterior pituitary regulates ADH
Hypothalamus:
- produces ADH
- high blood osmolarity triggers release of ADH into
PPG:
- releases ADH into bloodstream
Kidney:
- ADH signals kidney to reabsorb water
Also:
- inhibits sweating, urination and increases blood pressure
(low blood osmolarity inhibits ADH)
blood osmolarity (what it is, what alters it, what it alters)
Concentration of dissolved particles in the blood, high osmolarity leads to higher blood pressure if there is water to be released into blood
increased by:
- increase in ion concentration (eg: Na+)
- decrease in water content (decrease blood volume, dehydration)
Insulin (traits + purpose)
- hydrophillic hormone released by beta cells of pancreas
- binds to cells with intrinsic tyrosine kinase activity
Causes (lower blood glucose): - increased diffusion of glucose into cells
- convert glucose into glycogen & slow glycogen breakdown
- synthesis of fatty acids & proteins
Pancreas hormones
alpha cells: glucagon
beta cells: insulin
Pancreas anatomy (location, structures, blood supply)
Anterior to duodenum
- head (right side of body)
- body (middle)
- tail (left)
Blood supply (from abdominal aorta):
- splenic artery
- hepatic artery
- superior mesenteric artery
HA and SMA form anastomosis through pancreaticoduodenal arteries
Pancreas (histology)
exocrine acinar cells (99% of pancreas volume)
- secrete bicarbonate + digestive enzymes
islets of endocrine (Langerhans) cells
- alpha cells: secrete glucagon when BG low or SNS active
- beta cells: secrete insulin when BG high or PNS active
Diabetes mellitus (types, causes, treatment)
both: high BG, increased urination, glucosuria (sugar in urine)
Type 1 (insulin dependent DM) IDDM
- caused by inadequate production of insulin (dysfunctional beta cells)
- treated with insulin
- more common in young adults (juvenile onset diabetes)
Type 2 (non-insulin dependent DM) NIDDM
- caused by inadequate response to insulin
- leads to overproduction of insulin
- more common in adults (adult onset diabetes) and obese individuals
- treatment: diet, exercise and oral hypoglycemics
GDM: gestational diabetes mellitus (appears Type 2)
- when diabetes occurs during pregnancy
- screened for using oral glucose challenge test
symptoms of type 1 diabetes
- cells which rely on insulin for sugar begin to starve
- fat burns in large quantities, causing production of ketone bodies –> ketoacidosis
- lowers blood pH
- causes fruity breath
- circulating fat deposits on blood vessels, damaging them
- gangrene can occur in hands and feet (foot ulcers) can lead to amputation
- person loses weight and begins to starve
symptoms of type 2 diabetes
- typically does not cause ketoacidosis (insulin response is enough)
- hyperglycemia
Long term: - beta cells wear out from producing insulin
- can develop type 1 diabetes
glucose regulation during pregnancy
- fetus constantly requires glucose regardless of XX need for glucose
- hypoglycemia during sleep/fasting periods
- glucose in XX blood decreases during fasting
- hormones produced during pregnancy can cause insulin resistance (typically later in pregnancy)
- insulin levels are 30% higher in third trimester relative to non-pregnant
- insulin resistance allows BG to be high for fetus
- more likely to develop Type 2 diabetes
effects of high maternal glucose on newborn
- fetus secretes large amounts of insulin (maternal insulin destroyed by placenta)
- can cause excess fat (lipogenesis)
- high insulin stimulates insulin-like growth factors (IGFs) –> large newborn (but not more developed)
- increased death rate, C-section rate
- increased rate of brachial plexus injury and clavicular fractures* (because they’re bigger)
- develops hyperinsulinemia (high insulin)
glucose challenge response
normal: sharp increase and decrease
normal (pregnancy-tri 3): lower starting BG, sharp increase, slow decrease
abnormal (Type 2): higher starting BG, sharp increase, slow decrease
*normal (pregnancy) and abnormal are difficult to distinguish
