Pathophysiology for Exam 3
Week 9: Renal/Urinary System Disorders
Anatomy of the Kidney
- Kidneys are involved with…
o Acid-base regulation
o Electrolyte balances
o Blood pressure
o Maintaining overall fluid balance
o Regulating and filtering minerals from blood
o Filtering waste materials from food, medications, and toxic substances
o Creating hormones that help produce RBC, promote bone health and regulate
blood pressure
- Nephrons: functional units of kidneys (has the renal corpuscles which is the filtration
unit of blood and renal tubules which secrete of waste body doesn’t need)
o Bowman’s capsule (glomerular capsule) form the filtration unit for blood (GFR is
calculated through the volume filtered through here)
o GFR: glomerular filtration rate (large volume of fluid passes from the blood into
the tubule)
 Cells and proteins stay in the blood
 Permeable to water and impermeable to large molecules
o When the filtration pressure increases, more filtrate forms, and more urine is
produced
Hormones Involved in Reabsorption
- Antidiuretic Hormone (ADH)
o Reabsorption of water in distal convoluted tubules and collecting ducts
- Aldosterone
o Sodium reabsorption in exchange for potassium or hydrogen
- Atrial Natriuretic Hormone
o Reduces sodium and fluid reabsorption
Kidney Function Labs (NORMAL)
- GFR: 90-120
- Creatinine: 0.6-1.2 and BUN
- Check electrolytes in CMP
- RBCs (due to epo)
- Urine tests check
o Urinalysis
o 24 hr creatinine clearance collection
o Elevated albumin or protein? Kidneys NOT good
What is BUN and creatinine?
- Blood urea nitrogen is excessive amino acids that are filtered by liver; a nitrogen waste
- Creatinine is a chemical waste product generated from muscle metabolism
DIAGNOSTIC TESTS FOR KIDNEY FAILURE
- Elevated BUN and Creatinine
o Indicate failure to excrete nitrogen wastes
 Caused by decreased GFR
- Metabolic Acidosis
o Failure of tubules to control acid-base balance
 Indicates decreased GFR
- Anemia
o Indicates decreased erythropoietin secretion and or bone marrow suppression
- Electrolytes
- Elevated renin levels (RAAS System)
o Indicate kidney as a cause of hypertension due to lack of kidney perfusion
NEPHROSCLEROSIS
- Thickening and hardening of the walls of arterioles and small arteries (can occur
normally with aging)
- Narrowing of the blood vessel lumen
o Reduction of blood supply to the kidney
o Stimulates renin (RAAS)  increased BP
o Continued ischemia  destruction of renal tissue, chronic renal failure
RENAL FAILURE
- Anything that leads to reduced GFR  reduced urine output can cause kidney failure
o Uncontrolled hypertension damages renal arteries and reduces blood supply to
kidney tissue
o Can be caused reduced blood flow to the kidneys
o Inflammati0on and necrosis of the tubules caused by obstruction and back
pressure
- Acute Kidney Injury/Failure (can be reversible)
o Sudden decline in renal function
o Decrease GFR and accumulation of nitrogenous wastes
o Can cause metabolic acidosis and hyperkalemia
o From slight renal changes to complete failure
CHRONIC KIDNEY INJURY/FAILURE (slower and over time) IRREVERSIBLE
o Progressive loss of renal function related to systemic diseases or intrinsic kidney
disease (HTN, CAD, DM)
 Decreased Reserve (60% of nephron loss) GFR goes down, Creatinine
goes up

Decreased GFR, creatinine ‘normal high’, BUN is normal, no
clinical signs
 Renal Insufficiency (75% of nephron loss)
 GFR is decreased to 20% of normal, BUN elevated, large volumes
of dilute urine due to decreased tubule function, erythropoiesis is
decreased and BP is elevated (anemia)
 End stage renal failure (more than 90% nephron loss)
 GFR is negligible, F&E and wastes are retained, and body organs
are affected, marked oliguria or anuria develops, dialysis or
transplant are necessary to maintain life
 Three A’s: Azotemia, anemia, and acidosis
o Makes it difficult to maintain homeostasis of acid-base balance, fluids,
electrolytes, dysrhythmias, and can eventually affect all other organ systems
(pulmonary edema, etc.)
CKD: Early Signs
 Increased urinary output
 General signs  anorexia, vomiting, N/V, anemia, fatigue, unintended
weight loss, exercise intolerance, HTN
 Bone marrow depression and impaired cell function due to increased
wastes and altered blood chemistry
 Elevated BP
CKD: Progression
 GFR decreases as BUN and Creatinine go up
 When GFR decreases to 25%, obligatory water and sodium losses
 Electrolyte imbalances: hyponatremia and hyperkalemia,
hypocalcemia, and hyperphosphatemia
 Loss of ability to concentrate urine
 Kidney will lose ability to regulate sodium and water and retention
will occur (edema, hypertension)
CKD: Manifestations
 Anemia, metabolic acidosis
 Reduced renal phosphate excretion hypocalcemia, stimulation of
parathyroid hormone = migration of calcium out of bone into serum
(osteoporosis and fractures)
 Serum protein levels decrease  loss of muscle mass
 Impaired glucose tolerance
 Azotemia: accumulation of nitrogenous wastes (BUN, creatinine)

Uremic syndrome: systemic symptoms from buildup of nitrogenous
wastes and toxins in blood
Complete Failure Symptoms (chronic renal failure)
 Oliguria
 Dry, hyperpigmented skin, easy bruising, uremic pruritis, peripheral
neuropathy
 Impotence in men, menstrual irregularities in women
 Encephalopathy
 CHF, dysrhythmias
 Failure to activate vitamin D
 Possible uremic frost on the skin
 Systemic infections
PRE-RENAL FAILURE (problem effects GFR)
- Sudden onset
- Causes
o Acute bilateral kidney diseases
o Hypoperfusion of kidneys
o Severe, prolonged circulatory shock
o GFR declines because of decrease in filtration pressure (hemorrhage,
hypovolemia, hypotension, low cardiac output CHF)
o Nephrotoxins
o Mechanical obstruction (calculi, blood clots, tumors
- Blood tests
o Elevated BUN and creatinine
o Metabolic acidosis and hyperkalemia
- Treatment
o Identify and remove or treat primary problem (to minimize risk of necrosis and
permanent kidney damage)
o Dialysis (to normalize body fluid and maintain homeostasis)
Intrarenal  problems within the kidney
- Acute tubular necrosis (ATN) from post-ischemic and nephrotoxic materials
- Acute glomerulonephritis
- Bacterial toxins
Post Renal  problems below the kidneys that back up into the kidneys because of obstruction
- Urinary tract obstructions that can affect the kidneys bilaterally (bladder obstruction,
BPH, calculi, blood clots, tumors)
- Symptoms: urinary retention, flank pain, polyuria, N/V, fever
Causes of Renal Failure  Nephrotoxins
- Filtrate becomes concentrated and tubule wall becomes swollen and necrotic
- Filtrate has high back pressure bc of obstructed lumen (stenosis almost)
- Decreased GFR and oliguria
Causes of Renal Failure  Ischemia
- Severe shock leads to vasoconstriction and decreased blood flow
- Tubule has ischemia, swelling, necrosis, and obstruction which leads to high back
pressure
- Oliguria present
Causes of Renal Failure  Pyelonephritis
- From bacteria
- Purulent exudate and abscesses block flow of urine and blood
- Oliguria present
Acute Kidney Failure: Goals of Therapy
- Correct fluid and electrolyte imbalance
- Treat infections or main reason
- Maintain nutrition
- Caution with drugs: reduced or no excretion
- Dialysis if necessary
Signs and Symptoms of Kidney Damage
- May be multisystemic depending on severity
- Abdominal pain, confusion, constipation
- Costovertebral angle (CVA) tenderness
- Flank pain
- Hematuria (from renal calculi or infection)
- Proteinuria (microalbuminuria)  protein in urine, urine looks foamy; no more than 150
mg)
- Tea colored urine
- Jaundice
Diagnostic Tests
- Metabolic acidosis becomes decompensated
- Azotemia
- Anemia becomes severe
- Serum electrolyte levels vary on water retention in the body (hyponatremia,
hyperkalemia, hypocalcemia, and hyperphosphatemia)
Treatment
- Difficult to maintain homeostasis of fluids, electrolytes, and acid-base balance
- Drugs that stimulate erythropoiesis (epogen)
- Drugs to treat cardiovascular problems (for hypertension and cardiac dysrhythmias)
- Intake of fluid, electrolytes, protein must be restricted
- Dialysis or transplantation
UREMIC SYNDROME (uremic frost)
- A serious complication of acute and chronic kidney disease
o It occurs when urea and other waste products build up in the body because are
unable to eliminate them
o Substance become poisonous (toxic) to the body in high levels
o More common in final stages of chronic failure (ESRD)
- Signs and Symptoms of Uremic Syndrome
o GI: N/V, anorexia, and weight loss
o Neuro: confusion, reduced LOC, agitation, psychosis, seizures, and coma
o Hematologic: abnormal bleeding, spontaneously
o Cardiac: irregular heartbeat, inflammation, pericarditis, and increased pressure
o Pulmonary: pleural effusion
o Integ: Uremic frost
DIALYSIS: HEMODIALYSIS AND PERITONEAL DIALYSIS
- Provides filtration and reabsorption
o Peritoneal and hemodialysis
- Sustains life during kidney failure
- Used to treat patients with acute kidney failure (until preliminary problem reversed)
- For patients in end-stage renal failure
o Until kidney transplants becomes available and is successful
Hemodialysis (Papi)
- In hospital, dialysis center, or home with special equipment and training
- Patient’s blood moved from an implanted shunt or catheter in an artery to machine (AV
fistula)
o Exchange of wastes, fluids, and electrolytes
o Semipermeable membranes between blood and dialysis (dialysate)  blood cells
and proteins remain in blood
- After exchange is completed, blood returned to patient’s vein
- Usually required three times a week (3-4 hrs)
- Potential complications (Assess for bruit and thrill)
o Shunt may become infected
o Blood clots may form
o Blood vessels involved in shunt may become sclerosed or damaged
o Patient has increased risk of infection with hep B, hep C, or HIV, if standard
precautions are not followed
Peritoneal Dialysis (Mama Celeste)
- Usually done on outpatient basis
- May be done at night (during sleep) or while patient is ambulatory
-
Peritoneal membrane serves as the semipermeable membrane
Catheter with entry and exit points is implanted into the peritoneal cavity
Dialyzing fluid is instilled into cavity
Dialysate is drained from cavity via gravity into container
*takes more time than hemodialysis
Requires loose clothing to accommodate bag of fluid
Major complication
o Infection resulting in peritonitis
***With both types of dialysis… prophylactic antibiotics with either form of dialysis
- Any additional problem occurring in patient such as infection may alter dialysis
requirements
- Caution is required with many drugs because toxic level buildup can occur
Renal Medications (drug notes)
- Aluminum Hydroxide (Amphojel)
o For hyperphosphatemia; is a phosphate binder
- Polystyrene Sulfate (Kayexelate)
o To treat hyperkalemia; excretes K+ in feces
- Diuretic Drugs  Furosemide (Lasix)
o To reduce edema caused by renal disease; promotes loss of K+
- Ferrous Sulfate (Feosol)
o For anemia; binds to hemoglobin
- Epoetin Alfa (Procrit)
o For anemia from renal failure; stimulates RBC production
Week 10: Glandular Issues
Endocrine System
- Endocrine glands secrete hormones directly into blood
o Hormones are chemical messenger that are classified by action, source, or
chemical structure
- Chemical factors  such as blood glucose or calcium levels
- Endocrine factors  a hormone from one endocrine gland controlling another
- Neural control  ANS directly stimulating of pancreas to secrete insulin
Hormone Release
- Happens when metabolic needs of the body are greater than normal
- Most often controlled by negative feedback mechanisms
o Endocrine and nervous system work together to regulate metabolic activities
(after the demands are met, it turns off)
o After release from an endocrine gland, hormones circulate to target cells or tissues
o Secretion may be controlled by more than one mechanism
-
After acting on specific receptors on/in target cells, the hormones are metabolized or
inactivated by the tissues or liver and excreted by the kidneys
o This prevents an accumulation in the body over time
- Most often controlled by a negative feedback loop aka “inhibitory feedback loop”
Negative Feedback Loop Blood Glucose
- An insensitivity to this system is Type 2 Diabetes
- Look at pictures
Negative Feedback Loop  TRH and TSH
- Look at pictures
Endocrine Disorders
- Two categories an excessive amount of hormone or a deficit
- Inadequate hormone synthesis
- Failure of feedback systems
- Inactive hormones
- Dysfunctional delivery system
- Inappropriate response by target cell (organ)
Gland
Anterior Pituitary
Hormone
TSH, ACTH, FSH, LH,
GH, PL
Posterior Pituitary
ADH, oxytocin
Thyroid
Parathyroid
Adrenal
Pancreas
T3, T4
PTH
Corticosteroids
Glucagon, insulin
TSH: stimulates thyroid gland (measurement can be used as diagnostic agent for thyroid
dysfunction)
ACTH: stimulate adrenal cortex to secrete cortisol and aldosterone (corticotropin used to
diagnose adrenal insufficiency)
ADH: increases reabsorption of water in kidneys
Insulin: secretes from beta cells in the pancreas; transport of glucose and other substances into
cells, lowers blood glucose
Glucagon: secretes from alpha cells in pancreas; glycogenolysis in liver and increases blood
glucose
T3 and T4: increases metabolic rate in all cells
PTH: increases blood calcium levels by stimulating bone demineralization and increasing
reabsorption of Ca+ in the digestive tract and kidneys
Aldosterone: from adrenal cortex; increases sodium and water reabsorption and excretes
potassium
Cortisol: from adrenal cortex; anti-inflammatory and decreases immune response, raises blood
sugar and you gain weight (stress response)
Norepinephrine: adrenal medulla; general vasoconstriction
Epinephrine: adrenal medulla; stress response, visceral and cutaneous vasoconstriction,
vasodilation in skeletal muscle, increases rate and force of heart contraction, bronchodilation
- Excess hormone levels
o Tumor produces high levels
o Excretion by liver or kidneys is impaired
o Congenital condition produces excess hormone
- Deficit of hormone or reduced effects
o Tumor produced too little hormone
o Inadequate tissue receptors present
o Antagonist hormone production is increased
o Malnutrition
o Atrophy, surgical removal of gland
o Congenital deficit
PITUITARY DISORDERS:
- Anterior pituitary gland  TSH and ACTH
- Posterior pituitary gland  ADH
o Deficiency: large water output, fluid and electrolyte imbalances (lower BP)
 Diabetes Insipidus: large amount of water excreted can lead to severe fluid
deficit and electrolyte imbalances
 ADH replacement is treatment  vasopressin, desmopressin
acetate
o Increase: low/no output, fluid overload (increases BP, F&E)
 SIADH: excess amount of water retention
 Treatment? Fluid restrictions, hypertonic saline
o Meds: demeclocycline, conivaptan, tolvaptan
DIABETES INSIPIDUS (posterior pituitary) TOO LITTLE ADH
- Uncommon disorder that causes an imbalance of the fluids in the body
- Normally about 1-2 quarts of urine is excreted each day
- Those with DI can excrete 3-20 quarts a day of “insipid” (dilute and odorless) urine a day
- Results from DEFICIT OF ADH
o Primary (neurogenic): defect at pituitary gland (tumor, head injury, surgery,
infection, genetic)
o Nephrogenic: defect at renal tubule (CKD, hypokalemia, hypercalcemia,
blockage in urinary tract)
o Drug-related; lithium
- Treatment? Replace ADH
- ***30 ml.hr is the normal rate of urine; 720 ml/day is the minimum rate of urine for the
day***
Signs and Symptoms of Diabetes Insipidus
- Polyuria
- Thirst
- Signs of dehydration
Complications of Diabetes Insipidus
- Headaches
- Weight loss
- Fatigue
- Low body temperature
- Chronic dehydration
- Tachycardia
- Hypovolemia
- Hypotension
- ** Long term: Kidney damage, circulation collapse, and CNS damage
Lab Assessment: Diabetes Insipidus
- Urine is DILUTE
o low specific gravity <1.005
o decreased osmolality pH, Na+, K+
o the more urine the patient passes, the less concentrated it is
- Serum (blood) is CONCENTRATED
o Increased osmolality, Na+, K+
o The more urine the patient passes, the more concentrated the blood is
- Vasopressin Test  inject vasopressin and if you see...
o The specific gravity increases, the disease is a primary cause (NOT nephrogenic)
Nursing Assessment: Diabetes Insipidus
- Assess patient for:
o High urine output (up to 20 L/day)
o High water intake
o Polydipsia, nocturia
o Fatigue
o Dehydration (know signs and symptoms)
Nursing Interventions: Diabetes Insipidus
- Lifelong vasopressin therapy for clients with permanent condition
o Teach daily weights
o Avoidance of caffeine
-
Monitor VS, I&O, labs
o Daily weight
o IV F&E replacement
o Encourage PO fluids (MUST!!!)
- ***Older adults are at great risk for dehydration
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION
(SIADH) (posterior pituitary) TOO MUCH ADH
- Condition in which the body makes too much ADH (little to no urine output)
- The results is too much water retention and electrolyte imbalance
o Hyponatremia (water intake exceeds output)
- Clinical manifestation related to enhances renal water retention, hyponatremia, and hypoosmolality
- *** There will be excess fluid in the blood stream with no edema
o Dilution of blood “hypo-osmolality”
o Seen in TBI and neurosurgery
- There is a breakdown in the normal feedback loop and vasopressin is excessively
secreted by pituitary gland even when plasma osmolality is low or normal
- ***Too much vasopressin = no pee pee (reduces or no urine output)
- Water is retained, resulting in hyponatremia secondary to excess of water rather than a
deficiency of sodium (bc its diluted)
Lab Assessment: SIADH (think opposite of diabetes insipidus)
- Urine is CONCENTRATED (due to not enough water being excreted)
o Increased osmolality, Na+
- Serum/blood is DILUTE (too much water in blood)
o Decreased Na+, osmolality
o Extra fluid, but decreased serum sodium
- Assessment: increased ADH in blood
Complications: SIADH
- Early
o Headache
o Muscle cramps
o Weight gain
o Weakness and fatigue
- Late
o N/V/D, oliguria
o Personality changed (irritability, combativeness, aggression)
o Confusion (due to hyponatremia)
o Seizures and coma (due to hyponatremia)
Nursing Interventions: SIADH
- Fluid restriction 500 to 1000 ml/day ACCURATE I&O!
- Daily weight, I&O, VITALS, URINE
- Assess mental status
- Safe environment
- Neurologic assessment every 4 hours
- Watch for S/S CHF
ADRENAL DISORDERS
The Adrenal Gland: Cortex and Medulla
- Cortex
o Glucocorticoids (cortisol; stress hormone)
o Androgens
o Mineralocorticoids (aldosterone)
- Medulla
o Epinephrine
o Norepinephrine
- Adrenal glands secrete…
o Aldosterone: water and sodium retention, potassium excretion
o Cortisol: glucose, protein, and fat metabolism, part of stress and immune response
o Sex hormones: androgens and estrogens (puberty and female sex characteristics)
ADDISON’S DISEASE (adrenal insufficiency) TOO LITTLE CORTISOL AND
ALDOSTERONE
- Rare
- Deficiency of adrenocorticotropic and cortisol secretions
- Autoimmune reaction is a common cause
- Adrenal gland may be destroyed by hemorrhage or infection (adrenals located above
kidneys)
- Secondary: pituitary tumor, adrenal tumor, meningococcal hemorrhage, viral, tubercular
or histoplasmosis infections
- ** Both result in decreased cortisol and aldosterone
Manifestations of Addison Disease
- Decreased blood glucose levels (due to low cortisol)
- Inadequate stress response (due to low cortisol)
- Fatigue (body out of homeostasis)
- Weight loss, frequent infections
- Low serum sodium concentration HYPONATREMIC
- Decreased blood volume HYPOVOLEMIC
- Hypotension
- High potassium levels HYPERKALEMIC
Complications of Addison’s Disease
- Hyperpigmentation (more common in primary)
- Weakness
- Dehydration
- Hyponatremia
- Hyperkalemia
- Hypoglycemia
- N/V
- Hypotension
- Weight loss
- Fatigue
- Frequent urination
Lab Assessment of Addison’s Disease
- Blood test
o May show hyperkalemia, hyponatremia, hypoglycemia
o Measures levels of cortisol and ACTH
o Measure antibodies associated with autoimmune Addison’s disease
- EKG
o Dysrhythmias on ECG related to electrolyte imbalances, hyperkalemia
- ACTH Stimulation Test
o This test measures the level fo cortisol in you blood before and after an injection
of synthetic ACTH
o Cortisol should be increased after injection of ACTH- in Addison’s, there will be
no to minimal rise
- Insulin-induced hypoglycemia test
o Measure blood glucose and cortisol levels after an injection of insulin
o Normally glucose levels fall and cortisol levels rise
- Imaging tests
o CT scan to view adrenals
o MRI to view pituitary
Nursing Interventions of Addison’s Disease
- Monitor VS, blood sugar, and electrolytes, weight
- Monitor I&O; assess for signs of dehydration
- Encourage fluids
- Monitor nutritional status
- Encourage a low stress environment
- EKG
ADDISON CRISIS
-
If it goes untreated
Adrenal crisis can be caused by
o Stress
o Steroid withdrawal
o Trauma
o Can precipitate system-wide responses
- Manifestations
o Severe abdominal pain
o Low BP and BS
o Hyperkalemia
- Can be life-threatening
- TX: dextrose IV fluids and glucocorticoid replacement are of emergent therapy
o 12-24 hours of crisis
o Dextrose lowers potassium because it pushes it into the cells because the dextrose
is in the blood
CUSHING’S SYNDROME (hypercortisolism) TOO MUCH CORTIOL
- Relatively rare condition that is the result of too much of the cortisol in the body
o Can occur due to:
 Adrenal hyperplasia
 Tumor
 Pituitary tumor
 Primary cancer
o also occurs from use of glucocorticoids other diseases:
 chemotherapy
 asthma
 organ transplant
 autoimmune disorders
- Cushing’s Disease
o Elevated ACTH, tumor in pituitary
- Cushing’s Syndrome
o Elevated cortisol, hyperfunction of adrenal cortex
- ***Exogenous steroids most common cause of Cushing’s syndrome***
- Changes associated with Cushing syndromes are changes in person’s appearance
o Round face, with ruddy color
o Truncal obesity, with fat bad between scapulae
o Thin limbs and hair
o Fragile skin, striae
o Women: hirsutism, male pattern hair growth, amenorrhea
o Puffy face called “moon face”
o Extra subcutaneous fat in the cervicothoracic area called “buffalo hump”
Manifestations of Cushing’s Syndrome
- Retention of sodium and water “moon face”
- Suppression of the immune response
- Stimulation of erythrocyte production
- Emotional lability and euphoria
- Increased catabolism of bone and protein
- Delayed healing
- Increased insulin resistance and possible glucose intolerance
Complications of Cushing’s Syndrome
- Hypertension
- Hirsutism
- Bruising and petechiae
- Changes in fat distribution (buffalo hum, moon face)
- Muscle wasting
- Emotional lability
- Decreased immune function
- Osteoporosis and fractures
- Impaired glucose tolerance (can lead to diabetic complications)
Lab Assessment of Cushing’s Syndrome
- Increased serum glucose and sodium HYPERGLYCEMIC, HYPERNATREMIC
- Decreased serum potassium and calcium HYPOKALEMIC, HYPOCALCEMIC
- Elevated serum cortisol levels
- 24-hour urine: elevated levels of cortisol in urine
THYROID DISORDERS
- Thyroid is butterfly shaped and is in front of the neck
- Thyroid produces the hormones T3 and T4, which regulate metabolism, temperature, and
HR
- Thyroid disorders can slow done or rev up metabolism by disrupting the production of
thyroid hormones
HYPOTHYROIDISM (underactive thyroid)
- Hypothyroid is when the thyroid gland does not produce enough thyroid hormones to
meet the needs of the body underactive
o Primary: dysfunction of thyroid; most common
 Subacute thyroiditis- mild form
 Hashimoto’s disease- autoimmune destructi0on of thyroid gland
 Myxedema coma- severe hypothyroidism that manifests with hypotension,
hypoglycemia, hypothermia LOC, and can be fatal
o Secondary: failure of the anterior pituitary gland
o Thyroid carcinoma/cancer
Complications of Hypothyroid
- Fatigue
- Cold intolerance
- Decreased bowel motility
- Weight gain
- Thin skin, thinning hair
- Depression
- Muscle pain
- Dry skin
- Edema in face, hands, and feet
- Slow thought process
- Abnormal menses
- ** sinus bradycardia (the main difference!!)
Diagnosis of Hypothyroid
- Labs: T3, T4, and TSH
- Thyrotropin
- Manifestations of patient reported symptoms
HYPERTHYROIDISM (overactive thyroid)
- Is a condition that occurs when thyroid gland produces too much of the hormone
thyroxine; overactive
o Accelerate your body’s metabolism causing unintentional weight loss and a rapid
or irregular heartbeat
- Excessive circulating hormones cause hypermetabolic state
o Primary: dysfunction of the thyroid
 Graves Disease is most common; autoimmune (AKA Thyrotoxicosis)
o Secondary: from issue with pituitary
o **Thyroid Storm: surge of thyroid hormone causing crisis (major complication)
 Hypothermia, hypertension, tachycardia, hyperglycemia
Complications of Hyperthyroidism
- Nervousness, irritability
- Exercise and heat intolerance
- Weight loss, increased appetite
- Insomnia
- Diarrhea
- Diaphoresis
- Vision changes, exophthalmos
- Tachycardia
THRYOTOXIC CRISIS (Thyroid Storm)  MEDICAL EMERGENCY
- Overwhelming release of thyroid hormones
- Stimulate metabolism
o High fever, tachycardia, agitation, psychosis
- Often precipitated by surgery or trauma
- ** medical emergency
- Lab Assessment: THS, T3, T4
o Lab values seem okay, but patients are not
DIABETES
TYPE 1 DIABETES “childhood diabetes”
- Autoimmune destruction of beta cells in pancreas e
- Insulin replacement required
- Acute onset in children and adolescents
- **Not linked to obesity
- Genetic factors may place a role
Metabolic Changes in Type 1 Diabetes
- Catabolism of fats and proteins
o Excessive amounts of fatty acids and metabolites
o Ketones in the blood
- Ketonuria
o Decreased serum bicarbonate
o Decrease in pH of body fluids
o Ketoacids excretes in urine
- Decompensated metabolic acidosis
TYPE 2 DIABETES
- Noninsulin-dependent
- Oral hypoglycemic medications may be used (metformin)
- Caused by decreased production of insulin and/or increased resistance by body cells to
insulin
- Onset is slow and insidious, usually in those older than 50 years
- Associated with obesity
- Component of metabolic syndrome
- Increasing incident in teens and young adults
- May be controlled by adjusting
o Dietary intake
o Increase body’s use of glucose (with exercise)
o Reducing insulin resistance
o Stimulating the beta cells of the pancreas to produce more insulin
Control of Type 2 Diabetes
- Monitoring blood glucose levels are ordered
- Medication to stimulate the beta cells of the pancreas to produce more insulin
- If insulin-dependent, proper administration of insulin to maintain glucose levels in
normal range
- Routine follow-up and blood testing
Initial Stage of Type 2 Diabetes
- Insulin deficit
o Results in decreased transportation and use of glucose in many cells
- Blood glucose levels rise (hyperglycemia)
- Excess glucose found in urine
- Large urine volume
- Fluid loss through urine, resulting in dehydration
- Dehydration causes thirst
General Manifestations of Type 2 Diabetes
- Polyphagia (excessive eating)
- Fatigue
- Hyperglycemia
- Glucosuria (dehydration happens)
- Polyuria (excessive urine)
- Polydipsia (excessive drinking)
Diagnostic Tests of Type 2 Diabetes
- Fasting blood glucose level
- Glucose tolerance test
- Glycosylated hemoglobin test (A1C)
o Clinical and subclinical diabetes
o Monitor glucose levels over several months
HYPOGLYCEMIA SUGAR TOO LOW
- BG less than 70mg/dl
o Excessive exogenous insulin
o Inadequate food intake
o Excessive physical activity
o Infection, illness, drug retention
- Compensatory response to raise BG
o epinephrine, glucagon, activation SNS
Manifestations of Hypoglycemia
- Sweating, hunger, dizziness, headache, heart palpitations, confusion (check blood
sugar!!)
-
Need action plan to address hypoglycemia
o Fast acting carbohydrates (15 grams)
o Avoid fats (delay glucose absorption)
o Recheck BS after intervention and if more carbs if needed
HYPERGLYCEMIA SUGAR TOO HIGH
- Imbalance among food, medication, and activity
Symptoms:
- BS >250
- Ketones (DKA!!)
- Polydipsia, polyuria, polyphagia
- Hyperventilation
- Dehydration
- Vomiting
- Fruity breath
- Coma
Treatment Principles
- Maintenance of blood glucose levels in normal range
o Helps reduce complications
- Diet and exercise
o Exercise reduces blood glucose level as skeletal muscle uses glucose
- Oral medication
o Increase insulin resistance
o Reduce blood glucose levels
- Insulin replacement
Complications
- Complications are directly related to duration and extent of abnormal blood glucose
levels
- Many factors lead to fluctuations in serum glucose levels
o Variation in diet and alcohol use
o Change in physical activity
o Infection
o Vomiting
- Complications may be acute or chronic
o Hypoglycemic Shock (insulin shock)
 More common with insulin replacement treatment
 Can occur because of excess oral hypoglycemia drugs
 Symptoms: decreased BS, decreased BP, confusion, decreasing LOC,
anxiety or change in behavior (immediate admin of glucose is required to
prevent brain damage)

Excessive insulin in circulation
 Glucose deficit in blood
 Can be life-threatening; cause brain damage if not treated
 Often follows strenuous exercise
 Dosage error
 Vomiting
 Skipping meal after taking insulin
 TREATMENT
 Conscious? Give sweet fruit juice, honey, candy, or sugar
 Unconscious? NPO, IV glucose 50% is required
DIABETIC KETOACIDOSIS (DKA) SUGAR TOO HIGH
- Occurs in insulin-dependent clients
- More commonly seen in type 1 diabetes
- Result of insufficient insulin in blood
- High blood glucose levels
- May be initiated by infection or stress
- May result from error in dosage, infection, change in diet, alcohol intake, or exercise
Diagnostic Criteria of DKA
- BG greater than 500
- pH (less than 7.3)  metabolic acidosis
- HCO3 (less than 15)
- Ketonuria
- Ketonemia
Manifestation of DKA
- N/V
- Dehydration
- Tachycardia; weak and thread pulse
- Hypotension
- Kussmaul’s respirations (deep and fast respirations)
- Ketone body odor
- Thirst
- Dry, rough oral mucosa
- Oliguria
Treatment for DKA: KNOW THIS! (diabetic coma or hyperglycemia)
- Insulin, fluids, and sodium bicarbonate!
- Assessment should be done to differentiate the cause
Ketoacidosis
- Kussmaul’s respirations
-
Acetone breath (sweet, fruity smell)
Lethargy and decreased responsiveness indicate depression of CNS owing to acidosis and
decreased blood flow
Metabolic Acidosis
- Decreased serum bicarb and pH
- Dehydration progresses, renal compensation is reduced, acidosis becomes decompensated
- Blood pH falls
- Loss of consciousness
- Electrolyte imbalances  abdominal cramps, N/V, lethargy and weakness
- TREATMENT  insulin admin, replacement of fluid and electrolytes
HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC COMA COMPLICATION OF
T2DM
- More common in type 2 diabetes; often occurs in older clients and assumes to be
cognitive impairment
- Results in severe dehydration and electrolyte imbalances
- Ketones not present, as some insulin present
o BG greater than 600
o pH greater than 7.3
o HCO3 greater than 18
o Blood osmolality greater than 320
- Hyperglycemia and increased plasma osmolality
Warning Signs of HHNK
- Blood sugar level over 600 mg/dl
- Dry, parched mouth
- Extreme thirst
- Warm, dry skin that does not sweat
- High fever over 101 degrees
- Sleepiness or confusion
- Loss of vision
- Hallucinations
- Weakness on one side of body
Manifestations of HHNK
- Hyperglycemia
- Severe dehydration
o Increased hematocrit
o Loss of turgor
o Increased HR and RR
- Electrolyte imbalances
o Neuro deficits
o Muscle weakness
o Difficulties with speck
o Abnormal reflexes
Difference between DKA and HHNK?
- DKA is sudden onset, from inadequate insulin dose, has ketones in blood and urine,
ketosis symptoms (kussmaul respirations, fruit breath, nausea, abd pain)
- HHNK is gradual onset, from poor fluid intake, altered CNS with neuro symptoms, no
ketones in blood or urine
- Both have dehydration and electrolyte imbalance symptoms: 3P’s, weight loss, dry skin,
sunken eyes, soft eyeballs, lethargy, coma
CHRONIC COMPLICATIONS OF DIABETES
- Vascular problems
o Increased incidence of atherosclerosis
o Changes may occur in small and large arteries
- Microangiopathy  changes in microcirculation
o Obstruction or rupture of small capillaries and arteries
 Tissue necrosis and loss of function
 Neuropathy and loss of sensation
 Retinopathy- leading cause of blindness
 Chronic renal failure- degeneration in glomeruli of kidney
- Macroangiopathy  affects large arteries
o Result in abnormal lipid levels
 High incidence of heart attacks, strokes, peripheral vascular disease
 May result in ulcers on feet and legs- slow healing
 Frequent infections and gangrenous ulcers
 Amputation may be necessary
- Peripheral neuropathy
o Common complication caused by ischemia in microcirculation to peripheral
nerves
 Impaired sensation, numbness, tingling, weakness, muscle wasting
- Infections
o Common and often sever in diabetics
o Infection in feet and legs
o Fungal infections common (in vagina or oral cavity)
o Dental caries
o Gingivitis and periodontitis
- Cataracts
o Opacity of lens in eye
o Related to abnormal metabolism of glucose
- Pregnancy
o Complication in both mother and fetus may occur
o Increased incidence of spontaneous abortions
o Infants born to diabetic mother
 Increased size and weight for date
 May experience hypoglycemia in first hours postnatally
DAWN PHENOMENON (increased BS in the morning)
- Surge of hormones around 4-5am
- The rise in glucose-body is making less insulin and more glucagon
- The less insulin made by the pancreas, the more glucagon the pancreas makes as a result
- Glucagon signals the liver to break down glycogen into glucose. This is why high fasting
blood glucose levels are common in people with Type 2
Preventing Dawn Phenomenon
- Avoid carbs at bedtime
- Adjust your dose of meds or insulin
- Switch to a different med
- Adjust the time when you take your medication or insulin from dinnertime to bedtime
SOMOGYI EFFECT (hypoglycemia followed by hyperglycemia)
- Is a pattern of undetected hypoglycemia followed by hyperglycemia
- Causes:
o Excess or ill times insulin
o Missed meals or snacks
o Inadvertent insulin administration
ORAL ANTIDIABETIC DRUGS (for type 2 diabetics)
- Stimulate pancreatic beta cells to secrete more insulin
- Increase tissue response to insulin
- Decrease glucose production
- Side effects/adverse reactions:
o Hypoglycemia, hyponatremia, blurred vision
o Nausea, diarrhea, weight gain
o Nervousness, tremors, confusion
Nursing Process: Oral Antidiabetics
- Concept: glucose regulation
- Assessment
o Determine patient’s knowledge of DM and use of meds
o Note vital signs and blood glucose levels
- Patient problems
o Reduced glucose regulation, hyperglycemia
-
Nursing Interventions
o Admin oral antidiabetics with food to minimize gastric upset
o Monitor blood glucose levels and report changes
o Teach patient to recognize symptoms of hyper and hypoglycemia
o Teach patient necessity to adhere to diet and drug regimen
Guidelines for Oral Antidiabetics Therapy for Type 2 Diabetes
- Onset of diabetes at age 40 or older
- Diagnosis of diabetes for less than 5 years
- Normal weight or overweight
- Fasting blood sugar 200 or less
- Less than 40 units of insulin required per day
- Normal renal and hepatic function
WEEK 11 INTESTINAL DISORDERS
Normal Functions of the GI System
- Stomach
o Temporary storage of food as it moves from the esophagus to intestine
o Mixing and breakdown of the food by contraction and relaxation of the layers of
the stomach
o Secretion of HCL and other enzymes to start digestion
- Small Intestine
o Major site for absorption of nutrients
 Complex carbs digested in the mouth and then intestines
 Proteins  peptides in the stomach amino acids in the intestines
 Fat soluble vitamins (A, D, E, K) are large molecules that do not require
digestion but are absorbed with fats (when there is an issue with fat
metabolism, these vitamins are not absorbed)
o Site of production of mucus and hormones
- Large Intestine
o Peyer patches
o Resident normal flora
o Vitamin K synthesis (risk for bleeding if it doesn’t work)
o Fluid and electrolyte reabsorption
o Formation of solid feces through the reabsorption of water
INFLAMMATORY BOWEL DISEASE  umbrella term
- Chronic inflammatory bowel disease that causes which are unknown
- All factors contribute to chronic inflammation
CROHN’S DISEASE (inflammation in the small intestine; interference with digestion and
absorption)
- May affect any area of the digestive tract
o Usually the small intestine affected
- Genetic mutation influence inflammation in flare patterns
o T cells, interleukins, and cytokines
- Characteristic distribution- “skip lesions”- affected areas separated by areas of normal
tissue
- Progressive inflammation and fibrosis may cause obstructed areas
o Damaged walls impair processing and absorption of food
o Inflammation stimulates intestinal motility reducing the time for absorption (food
passes too quick and little absorption happens)
- Interference with digestion and absorption
o Hypoproteinemia
o Avitaminosis
o Malnutrition
o Steatorrhea
- Other complications
o Adhesions between loops may form
o Ulcers may penetrate intestinal wall and cause abscesses
o Fistulas may develop due ulcer eroding through the intestinal wall
 Can occur in the intestine, bladder, or skin
o Children can have delayed growth and sexual maturation
Signs and Symptoms of Crohn’s Disease
- Exacerbations marked by diarrhea and cramping; abd pain and tender abd
- Stool is soft or semi-formed
- Melena may occur
- **Pain and tenderness in right lower quadrant!! REMEMBER!**
- Anorexia, weight loss, malnutrition, N/V/D
- Electrolyte imbalance
- Risk for obstruction due to narrowing
Treatment for Crohn’s Disease
- Diet management and vitamin supplements
o DIET: low fiber/low ‘bulk’, high protein, low fat, high vitamins, high calorie
- Antidiarrheals
- Abdominal cramping inhibitors
- Immunosuppressants
- Surgery: most patients will require surgery
- Treatment is step-up or top-down
ULCERATIVE COLITIS (inflammation in the rectum that goes to colon and large intestine)
- Inflammation starts in the rectum and progresses through the colon
o Most common in large intestine
-
Mucosa and submucosa are inflamed
o Tissue becomes edematous and friable (fragile)
- Individual ulcers can form into one, large areas are affected- tissue destruction interferes
with absorption of fluid and electrolytes in the colon
- Marked diarrhea, with up to 12 stools per day
o Contains blood and mucus
o Accompanied by cramping pain
- severe acute episodes- toxic megacolon may develop (stress and NSAID’s can trigger)
o can develop from severe inflammation  can lead to obstruction
o at risk for colon cancer and anemia
Signs and Symptoms of Ulcerative Colitis
- marked diarrhea- with up to 12 stools per day
o contains blood and mucus
o accompanies by cramping pain
o presence of tenesmus- persistent spasms of the rectum associated with need to
defecate
- rectal bleeding can be considerable leading to anemia
- fever and weight loss may be present
o can be from infection
- pseudopolips  can lead to food getting trapped and causing infections
What’s the difference between crohn’s disease and ulcerative colitis?
- Crohn’s: small intestine affected, skip lesions, loose and semi-formed stools, fistulas and
obstruction common, malabsorption and malnutrition
- Ulcerative colitis: colon, rectum, and large intestine affected, frequent watery stools (12
per day), no fistulas or obstructions, malnutrition not common, electrolyte imbalance
common
TREATMENT OF INFLAMMATORY BOWEL DISEASE Multi-modal approach
- Identify and remove physical and emotional stressors
- Anti-inflammatory meds (sulfa compounds and steroids)
- Anti-motility agents used for symptomatic relief
- Nutritional supplements and TPN If needed
o Recommended diet: high protein, vitamin, low fat and low fiber/bulk during
exacerbations
- Anti-microbials for secondary infection
- Immunotherapeutic agents
- Surgical resection
o Usually ileostomy and colostomy (can be reversed)
INTESTINAL OBSTRUCTION (medical emergency!!!)
- Lack of movement of intestinal contents through the intestines
o More common in small intestine
- Mechanical obstructions  tumors, adhesions, hernias, other tangible obstructions
- Functional or adynamic obstructions  result from impairment of peristalsis
o Spinal cord injury, paralytic ileus caused by toxins or electrolyte imbalance
- Gases and fluids accumulate proximal to the blockage, distending the intestine
- Increasingly strong contractions of proximal intestine (in order to more contents along)
- Pressure increases in lumen
o More secretions enter the intestine
o Compression of veins in wall
 Intestinal wall becomes edematous
 Prevention of absorption
- Intestinal distention leads to persistent vomiting
o Additional loss of fluid and electrolytes
o Hypovolemia can result
- Intestinal wall becomes ischemic and necrotic (from overgrowth of intestinal
bacteriaSEPTIC!!)
- Ischemia and necrosis  decreased innervation and cessation of peristalsis
- Paralytic ileus occurs if it is not a cause to begin with
- Obstruction promotes rapid production of intestinal bacteria (this is how you become
septic)
- Perforation of the necrotic segment may occur (generalized peritonitis and septic shock
OBSTRUCTION OF LARGE INTESTINE
- Develops slowly, with mild signs
- Constipation
- Mild abdominal pain, followed by abdominal distention
- Anorexia, vomiting, more severe pain
TREATMENT:
o Treatment of underlying cause
o Fluid and electrolyte replacement
o Surgery and antimicrobial therapy
OBSTRUCTION OF SMALL INTESTINE/SMALL BOWEL (MEDICAL EMERGENCY!)
- Mechanical obstruction of small intestine
o Severe colicky abdominal pain
o Intermittent or absent bowel sounds
- Paralytic ileus
o Pain is steady
o Bowel sounds decrease/absent
- **Vomiting and abdominal distention**
o Occurs quickly with obstruction of small intestine
o Vomiting is recurrent, eventually with bile-stained content
- Obstruction of the small intestine is a medical emergency
- *Vomiting, no bowel movements, abdominal pain and distention? Go to the hospital to
rule out small bowel obstruction!!*
TREATMENT OF INTESTINAL OBSTRUCTION
- Treatment of underlying cause
- Fluid and electrolyte replacement
- Surgery and antimicrobial therapy
TOTAL PARENTERAL NUTRITION (TPN)
- Is the administration of nutrients through the blood stream rather than the GI tract
- Used in cases where there is no functioning GI tract or in need of additional nutritional
support due to poorly functioning GI tract
- GI absorption of nutrients is always preferable so this is not the first option
- Fluid which contains high concentrations of glucose are irritating to peripheral veins so
should be administered through a central line
- Considered and often initiated in patients who have
o Lost 7% or more of body weight
o Been NPO for 5 days or greater
- Conditions that affect TPN
o Absorption
o Recovery time
o Metabolism
- Can be used for:
o Pancreatitis
o Peritonitis
o Burns
o Bowel obstructions
o Post op
o Severely malnourished
- Consists of amino acids, carbs, electrolytes, fats, vitamins, and water
- Hyperosmolar IV solution  approx. 700 cal/day
Administration of TPN
- Daily lab values determine concentration of solution (bags and tubing good for 24 hours)
- Central line; has a dedicated line
- Gradual titration to allow body to adjust
- Never stop abruptly- significantly affects glucose levels
- If given for less than 4 weeks, can use PICC line in brachial
- If more than 4 weeks, use subclavian or internal jugular vein
Glucose
- Check Q4-6 for at least the first day
- Sliding insulin scale
- **keep dextrose 10% in room to keep blood sugar stable if next bag not readily available
Sterile Procedure of TPN
- Change tubing and bag ever 24 horus
- Dedicated line for TPN
- IV filter
- Central line dressing
Complications of TPN
- Metabolic:
o Hyper or hypoglycemia
o Hypervolemia
o Vitamin deficiencies
- Air embolism
- Infection
B12 DEFICIENCY
- Basic problem is lack of absorption of vitamin B12 because of lack of intrinsic factor
o Intrinsic factor secreted by gastric mucosa
o Required for intestinal absorption of vitamin b12
- Characterized by very large, immature, nucleated erythrocytes
o Carry less hemoglobin
o Shorter life span
- Often due to intestinal problems/surgery
Manifestations of B12 deficiency
- Tongue is typically enlarged, red, sore, and shiny
- Digestive discomfort, often with nausea and diarrhea
- Feeling of pins and needles, tingling in limbs