Summary
Summary NUR 324 Exam 3 Study Guide
- Course
- NUR 324
- Institution
- Gwynedd Mercy University
This is a comprehensive and detailed summary on Exam 3. *Essential!!
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● Hyperplasia of a gland: more of the cells that can make the hormone (i.e. hyperthyroid enlarged gland)
● Abnormal immune reactions: disruption of the cells in the thyroid (Hashimoto’s), leads to the
body thinking there is a deficit
● Vascular problems: hormones are released into the bloodstream and travel throughout the
body; if the blood is not getting to the gland and distributing the way it should, it is going to
manifest as a deficit of that hormone (hypo-)
Diabetes Mellitus Type I
Causes:
● Autoimmune
● Genetic
Patho:
● Absolute deficit (does not make insulin at ALL); destruction of beta cells (make insulin in the
pancreas)
Manifestations:
● Hyperglycemia (glucose cannot get into the cells, so it is in the vasculature)
● 3 P’s
● Polyuria (glucose in the filtrate pulls urine out frequent urination)
● Polydipsia (extreme thirst due to dehydration from excess urination)
● Polyphagia (body thinks the body is starving/cell starvation; excess hunger)
● Glycosuria (glucose in the urine)
● Dehydration (due to polyuria/fluid being pulled from the cells by the glucose)
Diabetes Mellitus Type II
Risk Factors:
● Metabolic syndrome
● Obesity
● Gestational diabetes
Patho:
● Insulin resistance at the target cell (insulin is unable to open the gateway into the cell for
glucose); decreased production (cells are still able to function to a certain extent)
Manifestations:
● Hyperglycemia
● 3 P’s (polyuria, polydipsia, polyphagia)
● Glucosuria
● Dehydration
Diabetes Mellitus Complications
, Acute:
● Hypoglycemia (insulin shock): too little glucose in the blood; mimics the symptoms of a
stroke (slurred speech, paresthesias, confusion, disorientation, shaking/tremors,
tachycardia, diaphoresis); if not treated, coma and death
● Diabetic ketoacidosis (DKA): not enough insulin (most common in type I); glucose
usually >250; compensates by breaking down fat for energy (because it cannot use the
glucose) diabetic ketones bind with HCO3 ions, reduces pH, decreases the HCO3
results in metabolic acidosis
● Manifestations:
▪ Hyperglycemia
▪ Dehydration
▪ Metabolic acidosis
▪ Fruity breath (from ketones)
▪ Kussmaul’s respirations
▪ Ketonuria
▪ Electrolyte imbalances (Na+, K+ and Cl-)
▪ Severe dehydration
● Compensations: lungs blow off CO2 (Kussmaul’s respirations; deep and fast)
● Hyperosmolar hyperglycemic nonketoic syndrome (HHNKS): no ketosis, high glucose in
the blood; not using fat metabolism so they are not producing ketones (type II); glucose
>600 (cells are still getting a little insulin); typically in elderly with an infection and
decreased fluid intake, acute pancreatitis (enzymes prematurely activated and digesting
itself); overindulgence in carbs (using more insulin than is available); kidneys are unable
to get rid of the glucose through urine
● Manifestations:
▪ Polyuria
▪ Polydipsia
▪ Severe dehydration
▪ Electrolyte imbalance
▪ Seizures
▪ Coma (brain swelling cerebral edema)
Chronic
, ● Vascular Problems: thickening of the walls of vessels that are supplying the nerves with blood
demyelination of the nerve (myelin sheath around nerve makes sure impulses travel the right
direction); loss of sensation/touch
● Microvascular:
● Neuropathies
● Nephropathies: thickening of capillary basement membrane; occlusions/ruptures
(Diabetes is the number one reason for kidney failure)
● Retinopathy: leading cause of blindness (microaneurysms that form; hemorrhaging and
scarring)
● Macrovascular
● Coronary artery disease (HTN)
● Peripheral vascular disease (amputation)
● Neurovascular disease (CVA)
● Gastric motility problems
● Gastroparesis “paralyzed stomach” (delayed emptying of the stomach because of the
nerves that innervate the GI tract is damaged)
● Infections
● Glucose provides a petri dish for any microorganism leading to increased risk of infection
Diagnostic Tests-Diabetes Mellitus
● UA glucose and ketones (do not belong in urine)
● Hemoglobin A1C average glucose levels for the past 8-12 weeks
● DKA ABG (to test for metabolic acidosis)
Parathyroid Hormone: holds onto calcium; located at the back of the thyroid (in the neck)
Hypoparathyroidism: when there is too little calcium in the blood, it is secreted and will help the
absorption of calcium from the gut (prevent calcium from being secreted from the kidneys); help calcium
get to the bones
● Causes:
● Lack of parathyroid glands
● Autoimmune
● Radiation treatment in the neck
● Patho: decreased levels of calcium
● Manifestations:
● Tetany
● Paresthesias
● Chvostek and Trousseau Sign
● Cardiac dysrhythmias
Hyperparathyroidism: excess of calcium in the blood; excessively pulling calcium out of the bone (Ca+
keeps bones healthy and strong)
● Causes:
● Adenoma
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