CD #3

Diabetic Ketoacidosis

• Clinical features:
• 1. Hyperglycemia btwn 300-800
• 2. Dehydration and electrolyte loss
• 3. Acidosis

• Is an acute situation caused by an absence or markedly inadequate amount of insulin
• 3 main causes: illness, undiagnosed and untreated and decreased insulin
• Other causes include:
• pt error (ex: thought they took it but didn't)
• intentional skipping of insulin

• Polyuria - pee
• Polydipsia - thirst
• Polyphagia - hunger

• 3 P's
• Orthostatic hypotension (Must have change of pulse along with BP)
• Ketosis
• GI sx (N/V)
• Acetone breath
• hyperventilation

• BS btwn 300-800
• Acidosis
• Electrolyte abnormalities - usually due to dehydration
• Elevated BUN, creatinine and hct r/t dehydration

*is not necessarily related to the blood glucose level.

• Low serum bicarb (HCO3) < 15 mEq/L
• Low pH: 6.8 - 7.3
• Low partial pressure of carbon dioxide (PCO2 10 - 30 mm) which reflects respiratory compensation - hyperventilation - referred to as Kussmaul respirations
• Increased plasma ketones, urine glucose & potassium
• BUN/Creat elevated = dehydration

• Administer fluids to treat dehydration. NS to start till BS at 300, then can be changed to D5W to prevent a precipitous decline in the blood glucose level 
• Insulin
• Monitor fluid overload
• Strict I&O
• Major electrolyte of concern is K, must be monitored
• Monitored EKG's
• Monitor vitals and pt responses to tx

• 15/15 rule: Eat 15 grams of carbohydrate and wait 15 minutes.
• Recheck BS in 15 mins, same s/s then repeat.
• After improvement, then give cheese and crackers or milk
• *Extreme situations, give glucagon (can cause N/V) or D50W

• 2-3 tsp sugar or honey
• 6-10 hard candies
• 4-6 oz fruit juice or soda
• 3-4 commercially prepared glucose tablets

• Casual Test (no regard to last eating) is >200
• Fasting plasma glucose ≥ 126
• OGTT (Oral glucose tolerance test like in preg) 2 hours after at ≥ 200

• Lab test for DM
• Measures blood glucose levels over past 2-3 months
• High levels of glucose will attach to hemoglobin
• Helps to ensure pt glucometer is accurate

• Carbs 45 - 65% total daily calories
• Protein 15-20%
• Fats - less than 30% total which saturated only 10% total calories
• Fiber - lowers cholesterol, increase satiety. Slowing absorption time seems to lower glycemic index
• Teach consistent well balanced small meals several times per day
• Exchange system or counthing carbs

• Increases uptake of glucose by muscles & improves utilization, alters lipid levels, increases HDL and decreases Triglycerides
• In of insulin, eat 15 g snack before exercise
• Check BS before, during & after
• Avoid trauma to feet
• Avoid pounding activities which could cause vitreous hemorrhage
• Caution if CAD
• Baseline stress test may be indicated

• Pt on insulin should check sugars 2-4 x day
• Not on insulin, two or three x per week
• Should check before meals and 2 hr after
• Parameters from physician important

• Morning hyperglycemia
• involves nocturnal surges of growth hormone
• don't have normal insulin responses to adjust for this. body is making less insulin and more glucagon (a hormone that increases blood glucose) than it needs
• Give insulin at HS not before dinner

• *Opposite of Somogyi effect
• Dx w BS monitoring at night

• nocturnal hypoglycemia followed by rebound hyperglycemia
• tendency of the body to react to extremely low blood sugar by overcompensating, resulting in high blood sugar.

*opposite of Dawn phenomenon

• begins with a soft tissue injury of the foot, formation of a fissure between the toes or in an area of dry skin, or formation of a callus
• Pts don't feel injuries, may go unnoticed until serious infection

• Sensory neuropathy leads to loss of pain and pressure sensation
• autonomic neuropathy leads to increased dryness and fissuring of the skin (secondary to decreased sweating).

there may be demyelination of the nerves, which is thought to be related to hyperglycemia. Nerve conduction is disrupted when there are aberrations of the myelin sheaths.

Poor circulation of the lower extremities contributes to poor wound healing and the development of gangrene.

Hyperglycemia impairs the ability of specialized leukocytes to destroy bacteria. Therefore, in poorly controlled diabetes, there is a lowered resistance to certain infections.

• Hyperglycemic Hyperosmolar Nonketotic syndrome
• Chronic and more life threatening then DKA
• Body secretes just enough insulin to prevent ketosis
• BS usually over 600
• Blood osmolarity higher
• Profound diuresis
• When dehydration is severe, glucose is not filtered into urine
• Impairment of thirst center occurs
• *To maintain osmotic equilibrium, water shifts from the intracellular fluid space to the extracellular fluid space. With glycosuria and dehydration, hypernatremia and increased osmolarity occur

• Similar to DKA - fluid replacement, correction of electrolyte imbalances, and insulin administration.
• Close monitoring for fluid overload, heart failure and dysrhythmias

• BS falls to <70
• Severe hypoglycemia at <40

Consistent pattern of eating, administering insulin, and exercising

• Coronary artery disease
• Cerebrovascular disease
• Peripheral arterial disease
• *Result from changes in the medium to large blood vessels. Blood vessel walls thicken, sclerose, and become occluded by plaque that adheres to the vessel walls. Eventually, blood flow is blocked.

to become, or cause to become, hardened.

• Increases risk for heart disease, stroke, and DM
• Involves combination of:
• HTN
• increased cholesterol
• hyperglycemia
• increase fat around waist

• Take insulin regardless if N/V
• Test blood and urine ketones every 3-4 hrs
• May need supplemental doses of insulin Q3-4hr
• Call doc if BS can't be maintained, confusion or disorientation

• Results from suboptimal levels of thyroid hormone
• Most common cause is autoimmune thyroiditis (Hashimoto’s disease), in which the immune system attacks the thyroid gland

• Extreme fatigue 
• weight gain
• hair loss, brittle nails, and dry skin
• numbness and tingling of the fingers
• voice may become husky
• menstrual disturbances and effected libido

• rare life-threatening condition
• decompensated state of severe hypothyroidism in which the patient is hypothermic and unconscious
• can also happen if pt forgets to take thyroid meds

• subnormal body temp and HR
• mental process slows & pt appears apathetic
• Speech is slow, the tongue enlarges, the hands and feet increase in size, and deafness may occur.
• constipation :-(

• Too much thyroid
• Graves disease, the most common cause of hyperthyroidism, is an autoimmune disorder that results from an excessive output of thyroid hormones caused by abnormal stimulation of the thyroid gland by circulating immunoglobulins
• disorder may appear after an emotional shock, stress, or an infection, but the exact significance of these relationships is not understood.

• *Nervousness
• emotionally hyperexcitable, irritable, and apprehensive
• have palpitations
• increased appetite and dietary intake,
• weight loss
• fatigability and weakness
• no period
• changes in bowel function

• form of severe hyperthyroidism, usually of abrupt onset
• Almost always fatal is untreated
• Sx:
• High fever
• Extreme tachy
• GI - weight loss, diarrhea, abd pain
• Cardio - edema, chest pain, dyspnea, palpitations)
• Neuro - Altered neurologic or mental state, which frequently appears as delirium psychosis, somnolence, or coma
• *immediate management is reduction of body temperature and heart rate and prevention of vascular collapse.

• also called end stage renal failure
• Goal is to maintain kidney function and homeostasis for as long as possible
• All contributing factors & those which are reversible (e.g., obstruction) are identified and treated.
• At least 1/2 of all CRF will need dialysis

• Complications can be prevented or delayed by administering prescribed:
• phosphate-binding agents
• calcium supplements
• antihypertensive and cardiac medications
• antiseizure medications
• recombinant human erythropoietan

• careful regulation of protein intake, fluid intake to balance fluid losses, sodium intake to balance sodium losses, and some restriction of potassium.
• Protein is restricted because urea, uric acid, and organic acids which can build up in the blood.  allowed protein must be of high biologic value (dairy products, eggs, meats)
• fluid allowance per day is 500 mL to 600 mL more than the previous day’s 24-hour urine output.
• Calories are supplied by carbohydrates and fat to prevent wasting

• Dialysis becomes your pt's life! They get depressed and crazy
• Kidney disease diet is hard to live with
• Pt and family need support, let them express feelings, counseling as needed
• Listen & be involved
• Teach new way of life
• *provide explanations and information to the patient and family concerning ESKD, treatment options, and potential complications

• use of renal replacement therapies becomes necessary when the kidneys can no longer remove wastes, maintain electrolytes, and regulate fluid balance.
• can occur rapidly or over a long period of time
• the need for replacement therapy can be acute (short term) or chronic (long term)

• Temporary site
• AV fistula
• AV graft

• Surgeon constructs by combining an artery and a vein
• 3-6 months to mature

• Man-made tube inserted by a surgeon to connect artery and vein
• 2-6 weeks to mature

hemodialysis, CRRT, and PD.

• used for the acutely ill  and advanced CKD and ESKD 
• prevents death but does not cure kidney disease and does not compensate for the loss of endocrine or metabolic activities of the kidneys.
• objectives of hemodialysis are to extract toxic nitrogenous substances from the blood and to remove excess fluid
• Involves diffusion, osmosis, and ultrafiltration

• three times a week with an average treatment duration of 3 to 5 hours in an outpatient setting.
• can also be performed at home by the patient and a caregiver

• Continuous Renal Replacement Therapies
• May be indicated for patients with acute or chronic renal failure who are:
• too clinically unstable for traditional hemodialysis
• have fluid overload secondary to oliguria (low urine output) renal failure
• kidneys cannot handle their acutely high metabolic or nutritional needs.

• Type of CRRT
• often used to manage AKI
• Blood from a double-lumen venous catheter is pumped (using a small blood pump) through a hemofilter and then returned to the patient through the same catheter.

• similar to CVVH
• Blood is pumped from a double-lumen venous catheter through a hemofilter and returned to the patient through the same catheter.
• In addition to the benefits of ultrafiltration, CVVHD uses a concentration gradient to facilitate the removal of uremic toxins and fluid by adding a dialysate solution into the circuit.

• Peritoneal Dialysis
• the peritoneal membrane that covers the abdominal organs and lines the abdominal wall serves as the semipermeable membrane
• A sterile dextrose dialysate fluid is introduced into the peritoneal cavity through an abdominal catheter at established intervals
• Once the sterile solution is in the peritoneal cavity, uremic toxins such as urea and creatinine begin to be cleared from the blood. 
• Diffusion and osmosis occur as waste products move
• Less common

• Continuous ambulatory - CAPD
• Continuous cyclical
• Intermittent

• Continuous Ambulatory Peritoneal Dialysis
• type of PD
• second most common form of dialysis for patients with ESKD
• performed at home by the patient or a trained caregiver
• allows the patient reasonable freedom and control of daily activities but requires a serious commitment to be successful. 
• patient performs exchanges four or five times a day, 24 hours a day, 7 days a week, at intervals scheduled throughout the day

• Continuous Cyclic Peritoneal Dialysis
• uses a machine called a cycler to provide the fluid exchanges
• programmed to deliver an established amount of PD solution that will dwell in the peritoneal cavity for a programmed period of time before it drains from the peritoneal cavity via gravity.

• Dietary protein is restricted when renal insufficiency and nitrogen retention (elevated BUN) develop.
• Sodium is restricted when the patient has hypertension, edema, and heart failure.

• Excessive medial eval 
• Contradictions include infections, DM and HTN
• bringing the patient’s metabolic state to a level as close to normal as possible through diet, possibly dialysis and medical management, and making sure that the patient is free of infection

• postoperative pulmonary hygiene, pain management options, dietary restrictions, IV and arterial lines, tubes (indwelling catheter and possibly a nasogastric tube), and early ambulation
• Help pt deal with anxiety over surgery, possible rejection and need to return to dialysis

• Assess pt for s/s of organ rejection
• prevent infection - good hand washing
• Monitor I's & O's, 
• Address psychological concerns of pt & family.. fear of rejection and immunosuppression is big concern
• Monitor for complications

• type of renal failure characterized by increased glomerular permeability and is manifested by massive proteinuria
• Results in decrease albumin in blood, diffuse edema, high cholesterol & LDL's
• major manifestation is edema

• Treatment is focused on addressing the underlying disease state causing proteinuria, slowing progression of CKD, and relieving symptoms.
• Typical treatment includes diuretic agents for edema, ACE inhibitors to reduce proteinuria, and lipid-lowering agents for hyperlipidemia.

• Antidiuretic hormone - causes you to retain water
• Increases permeability of renal distal tubule and collecting ducts to water
• Less free water is excreted in urine
• Urine volume is decreased and concentration is increased

• A condition in which abnormally large volumes of dilute urine are excreted as a result of deficient production of vasopressin
• Deficit of ADH or kidneys resistance to effects of ADH
• Either don't have it or kidneys don't recognize ADH

• Goal is to prevent circulatory failure and hyperosmolar encephalopathy ( Brain swelling due to imbalance in electrolytes)
• Replace ADH (vasopressin)
• Fluid replacement
• Treat underlying cause ex: head injury or tumor, infections of the nervous system, failure of renal tubules to respond to ADH, and the use of specific medications

• Syndrome of Inappropriate Antidiuretic Hormone
• Clinical condition involving an excess of ADH secretion 
• Serious retaining of water, diluting electrolytes

Low urine output in absence of hypovolemia

• Hyponatremia (Na <135)
• Low serum osmolality (<285)
• High urine specific gravity (>1.020)
• N/V
• Mental status changes

• muscle tissue breakdown results in the release of a protein (myoglobin) into the blood. Myoglobin can damage the kidneys.
• Early treatment with aggressive fluid replacement reduces the risk of kidney damage.

• Vigilant monitoring and aggressive IV therapy
• Monitor for fluid overload
• Houry I's & O's and daily weights
• Check for JVD
• Abnormal breath sounds
• Limit use of nephrotoxic agents
• EKG

• Assess for meds which may be the cause
• Replace fluids to restore electrolyte balance
• Eliminate or bypass urinary tract obstruction
• Nutritional support with adequate calories

• Peritonitis is the most common and serious complication of PD.  first sign is cloudy dialysate drainage fluid, diffuse abdominal pain and rebound tenderness 
• Leakage from catheter insertion site
• Bleeding

• BUN (blood urea) and creatinine are renal function tests
• BUN should be at >20 & will increase in kidney failure
• Creatinine should be <1, and will also increase
• GFR should be over 100
• Phosphorus >4.5

• 2-g sodium diet- negative sodium balance to reduce fluid retention
• liberal use of powdered, low-sodium milk and milk products.

an accumulation of albumin-rich fluid in the peritoneal cavity

• Alcoholic cirrhosis
• Postnecrotic cirrhosis,
• Biliary cirrhosis

• scar tissue characteristically surrounds the portal areas.
• most frequently caused by chronic alcoholism  
• most common type of cirrhosis.

• broad bands of scar tissue.
• This is a late result of a previous bout of acute viral hepatitis.

• scarring occurs in the liver around the bile ducts.
• This type of cirrhosis usually results from chronic biliary obstruction and infection (cholangitis)
• it is much less common.

Same as hep b, but only those who have had hep b can get hep d

• B complex
• A
• C
• K
• D
• "Back Door"