First Lecture: Endocrine Disorders
☆ Diabetes Mellitus
- Patients with DM usually have a variety of comorbidities, such
as heart disease, HTN, and history/risk of stroke
- Leading cause of blindness, ESRD (end stage renal disease),
lower limb amputations
- Acute S/S
- Polyuria, polydipsia, polyphagia (excessive hunger)
- Fatigue (lack of E), prolonged wound healing and recurrent
infections (microorganisms feed off the blood glucose),
visual changes (blurry vision)(prolonged high blood
glucose = absorption, leading to changes in shape of the
lenses), fluid imbalance (osmotic diffusion from excess
glucose, drawing out electrolytes from cells)(may worry
about elevated K+; insulin IV will decrease K+ levels)
- Paresthesias, peripheral neuropathy, lethargy, weakness
- Late long-term S/S
- PVD (peripheral vascular disease; vessels narrow),
intermittent claudication from occlusions, angina and MI,
disease of eyes (cataracts), kidneys, and NS
- Type I Diabetes
- Insulin dependent; caused by insulin deficiency r/t
destruction of pancreatic beta cells
- Autoantibodies destroy these cells; S/S abrupt when
a majority are destroyed
- Unique S/S
- Weight loss, initial DKA before diagnosis,
- Type II Diabetes
- Insulin independent; can be managed with diet and
hypoglycemics (sometimes requires insulin as well)
- Insulin resistance or reduced insulin sensitivity,
combined with reduced insulin secretion, r/t
, - Insulin resistance (glucose stays up and
pancreas reacts by producing even more
insulin; reactors become less sensitive)
- High level of blood glucose
- B cell fatigue (dysfunction)
- Inappropriate release of glucose by liver
- Unique S/S
- Obesity, elevated LDL
- Gestational Diabetes
- Resembles Type II DM
- Occurs during pregnancy, and may develop
post-pregnancy
- Unique S/S: macrosomia, congenital anomalies of the
CNS/cardiac system, inhibit surfactant production of fetus,
hyperbilirubinemia, skeletal m. malformations
- ☆ DKA (Diabetic Ketoacidosis)
- Diabetic emergency more frequent in Type I DM
- Presents with hyperglycemia, ketosis and acidosis, and
dehydration
- Body has little to no insulin and is breaking down fats to
create energy, which also produces ketone bodies (acidic)
- S/S
- Polydipsia, polyuria, polyphagia, hypovolemic shock
(hypotension, tachycardia, kussmaul respirations
(rapid deep breathing), >300 glucose, ketone (fruity)
breath, N/V, confusion
- Interventions
- Monitor VS and restore fluids with normal saline
(raise B/P, restore output)
- Begin insulin drip after checking K+ levels
- Insulin drives K+ into cells; can cause
hypokalemia
- Continue to monitor e-, glucose, ketones in urine,
blood and urine pH, breath sounds
,- Hyperglycemia
- Treatment includes proper nutrition, regular physical
activity, insulin, and antihyperglycemic meds
- Type I DM requires insulin while Type II DM don’t
always need insulin
- Nutritional therapy
- Type I DM
- Usually NOT obese: increase caloric intake to
restore body weight
- Diet AND insulin needed
- NPH insulin: uniform timing of meals (no
skipping)
- 20g/hr of CHO (carbohydrates) when exercising
(bcs of insulin; blood sugar may run low)
- Type II DM
- Usually IS obese: reduce calorie intake
- Diet alone may be sufficient
- Timing of meals, snacks, and CHO may be
necessary if using insulin
- Insulin Therapy
- Rapid, short (Regular), intermediate (NPH), and long
acting (Lantus) insulins available
- Combination therapy: clear before cloudy
- ☆ Insulin Complications
- Lipodystrophy (lipoatrophy or lipohypertrophy)
- Somogyi effect (hypoglycemia during sleep; body
puts glucose in reserves causing rebound
hyperglycemia -> DKA)
- TX: less insulin
- Dawn phenomenon (Hyperglycemia upon waking;
growth hormone the main culprit)
- TX: adjustment in insulin timing
- Hypoglycemia
, - Oral Diabetic Medications
- Sulfonylureas: Lowers blood glucose by alerting
pancreas to produce more insulin
- Often in combo with biguanides
- Meglitinides: similar MOA as above, faster onset
- Alpha-glucosidase inhibitors: slows absorption of
CHO; not good for fasting hyperglycemia
- DPP-4 inhibitors: -gliptin drugs that prevents DDP-4
from breaking down incretin (hormone causing
insulin release in pancreas)
- ☆ Hypoglycemia
- “Insulin reaction” more common in DM I
- Insulin overdose
- Omitting meals
- Overexertion / too much exercise
- Alcohol intake (ineffective liver = less glucose
release)
- Blood glucose level < 70mg/dL (bad bcs brain needs
constant glucose supply)
- S/S: LOC, poor concentration, HA, tachycardia,
palpitations, sweating, nervousness, irritability
☆ MED SURG STUDY GUIDE
- Somogyi effect, diabetic diet, exercise on blood sugar, peak
action of different insulins
☆ Diabetes Mellitus
- Patients with DM usually have a variety of comorbidities, such
as heart disease, HTN, and history/risk of stroke
- Leading cause of blindness, ESRD (end stage renal disease),
lower limb amputations
- Acute S/S
- Polyuria, polydipsia, polyphagia (excessive hunger)
- Fatigue (lack of E), prolonged wound healing and recurrent
infections (microorganisms feed off the blood glucose),
visual changes (blurry vision)(prolonged high blood
glucose = absorption, leading to changes in shape of the
lenses), fluid imbalance (osmotic diffusion from excess
glucose, drawing out electrolytes from cells)(may worry
about elevated K+; insulin IV will decrease K+ levels)
- Paresthesias, peripheral neuropathy, lethargy, weakness
- Late long-term S/S
- PVD (peripheral vascular disease; vessels narrow),
intermittent claudication from occlusions, angina and MI,
disease of eyes (cataracts), kidneys, and NS
- Type I Diabetes
- Insulin dependent; caused by insulin deficiency r/t
destruction of pancreatic beta cells
- Autoantibodies destroy these cells; S/S abrupt when
a majority are destroyed
- Unique S/S
- Weight loss, initial DKA before diagnosis,
- Type II Diabetes
- Insulin independent; can be managed with diet and
hypoglycemics (sometimes requires insulin as well)
- Insulin resistance or reduced insulin sensitivity,
combined with reduced insulin secretion, r/t
, - Insulin resistance (glucose stays up and
pancreas reacts by producing even more
insulin; reactors become less sensitive)
- High level of blood glucose
- B cell fatigue (dysfunction)
- Inappropriate release of glucose by liver
- Unique S/S
- Obesity, elevated LDL
- Gestational Diabetes
- Resembles Type II DM
- Occurs during pregnancy, and may develop
post-pregnancy
- Unique S/S: macrosomia, congenital anomalies of the
CNS/cardiac system, inhibit surfactant production of fetus,
hyperbilirubinemia, skeletal m. malformations
- ☆ DKA (Diabetic Ketoacidosis)
- Diabetic emergency more frequent in Type I DM
- Presents with hyperglycemia, ketosis and acidosis, and
dehydration
- Body has little to no insulin and is breaking down fats to
create energy, which also produces ketone bodies (acidic)
- S/S
- Polydipsia, polyuria, polyphagia, hypovolemic shock
(hypotension, tachycardia, kussmaul respirations
(rapid deep breathing), >300 glucose, ketone (fruity)
breath, N/V, confusion
- Interventions
- Monitor VS and restore fluids with normal saline
(raise B/P, restore output)
- Begin insulin drip after checking K+ levels
- Insulin drives K+ into cells; can cause
hypokalemia
- Continue to monitor e-, glucose, ketones in urine,
blood and urine pH, breath sounds
,- Hyperglycemia
- Treatment includes proper nutrition, regular physical
activity, insulin, and antihyperglycemic meds
- Type I DM requires insulin while Type II DM don’t
always need insulin
- Nutritional therapy
- Type I DM
- Usually NOT obese: increase caloric intake to
restore body weight
- Diet AND insulin needed
- NPH insulin: uniform timing of meals (no
skipping)
- 20g/hr of CHO (carbohydrates) when exercising
(bcs of insulin; blood sugar may run low)
- Type II DM
- Usually IS obese: reduce calorie intake
- Diet alone may be sufficient
- Timing of meals, snacks, and CHO may be
necessary if using insulin
- Insulin Therapy
- Rapid, short (Regular), intermediate (NPH), and long
acting (Lantus) insulins available
- Combination therapy: clear before cloudy
- ☆ Insulin Complications
- Lipodystrophy (lipoatrophy or lipohypertrophy)
- Somogyi effect (hypoglycemia during sleep; body
puts glucose in reserves causing rebound
hyperglycemia -> DKA)
- TX: less insulin
- Dawn phenomenon (Hyperglycemia upon waking;
growth hormone the main culprit)
- TX: adjustment in insulin timing
- Hypoglycemia
, - Oral Diabetic Medications
- Sulfonylureas: Lowers blood glucose by alerting
pancreas to produce more insulin
- Often in combo with biguanides
- Meglitinides: similar MOA as above, faster onset
- Alpha-glucosidase inhibitors: slows absorption of
CHO; not good for fasting hyperglycemia
- DPP-4 inhibitors: -gliptin drugs that prevents DDP-4
from breaking down incretin (hormone causing
insulin release in pancreas)
- ☆ Hypoglycemia
- “Insulin reaction” more common in DM I
- Insulin overdose
- Omitting meals
- Overexertion / too much exercise
- Alcohol intake (ineffective liver = less glucose
release)
- Blood glucose level < 70mg/dL (bad bcs brain needs
constant glucose supply)
- S/S: LOC, poor concentration, HA, tachycardia,
palpitations, sweating, nervousness, irritability
☆ MED SURG STUDY GUIDE
- Somogyi effect, diabetic diet, exercise on blood sugar, peak
action of different insulins
