11/22/23, 5:21 PM Med Surg Exam 2 Study Guide 2
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
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, 11/22/23, 5:21 PM Med Surg Exam 2 Study Guide 2
- 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
about:blank 2/35
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
about:blank 1/35
, 11/22/23, 5:21 PM Med Surg Exam 2 Study Guide 2
- 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
about:blank 2/35
