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Block 3 M/S Test - Fluids, Electrolytes, Kidneys, Endorine, Diabetes > Test Review > Flashcards

Test Review Flashcards

1
Q

Explain what would be happening to the pH, CO2 and HCO3 in metabolic acidosis.

What can cause this?

A

pH - decreased
CO2 - decreased or normal
HCO3 - decreased

Severe diarrhea, renal disease d/t unable to absorb HCO3, DKA, Lactic acidosis, renal disease (unable to secrete HCO3)

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2
Q

What would happen in respiratory acidosis?

What disorders cause this?

A

pH - decreased
CO2 - increased
HCO3 - increased or normal

Hypoventilation (narcotics, sedation), COPD, pneumonia

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3
Q

What values would you see for metabolic alkalosis?

What could cause this?

A

pH - increased
CO2 - increased or normal
HCO3 - increased

Causes: vomiting, suction, diuretics, increased in HCO3 possible antacid or steroids)

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4
Q

Explain what would be happening in Respiratory Alkalosis?

What could cause this?

A

pH - increase
CO2 - decrease (not enough causes alkaline)
HCO3 - increase or normal

Hyperventilation (hypoxia, pain, anxiety, fear) You blew off all your CO2. Breathing too fast.

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5
Q

What is the most important thing to monitor for potassium?

A

Cardiac

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6
Q

Which electrolyte resulted in muscle weakness or excitability (TETANY). Explain the relationship.

A

Calcium
Hypocalcemia = muscle excitability (TETANY) Trousseau’s & Chvostek’s sign, seizures
Hypercalcemia = muscle weakness

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7
Q

Inverse relationship with Calcium is?

Explain the relationship related to muscle.

A

Phosphate
Hyperphosphatemia = muscle spasms
Hypophosphatemia = muscle weakness

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8
Q

Sodium

A

Related to fluid excess or fluid depletion.

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9
Q

What electrolyte has the same symptoms as calcium?

What are they?

A

Magnesium

HYPER
Severe Lethargy
Confusion
Fatigue/Weakness

HYPO
Spasms, tetany, seizures

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10
Q

Six functions of the kidneys:

A
  1. Urine production: waste of non essential nutrients
  2. Blood Pressure Regulation:
    Renin-angiotensin-aldosterone system = BP INCREASE
    AND
    Prostaglandins = BP DECREASES
  3. Acid/Base Balance: excretes or retains HCO3
  4. Electrolyte Balance: makes Vitamin D active for absorption of calcium from GI.
  5. Fluid Balance: ADH antidiuretic hormone signals the kidney to either retain or remove water from the body.
  6. RBC production - produces erythropoietin, which triggers the bone marrow to make red blood cells.
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11
Q

Caused by poor toileting hygiene and Foley catheters.

S/S …

A

UTI = Cystitis (inflammation of the bladder)

S/S = urgency, frequency, dysuria, burning with urination

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12
Q

Postrenal failure is …

Causes …

A

Backup of urine into the kidneys, often a result of a blockage in the urinary tract. Backs up to the renal pelvis and impairs kidney function. BLOCKAGE GOING OUT

Caused by = hyperplasia, prostrate cancer, calculus, trauma, extrarenal tumors.

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13
Q

Formation of stones in the urinary system.
Cause (pre, intra, post)
S/S …

A

Urolithiasis or renal calculi or kidney stones

Cause = Post renal failure

S/S = sudden sever wave-like pain, spreads to groin, pink, red or brown urine.

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14
Q

What is Pyelonephritis (Pie-lo-neph-ritis)
Pre, Intra or Post renal failure?
S/S

A

Inflammation (infection) of kidney d/t UTI
Intra renal failure
S/S = flank pain (costovetebral angle), high fever, malaise, N/V, increased urinary frequency, urgency, dysuria (painful urination), WBC and bacteria in urine.

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15
Q

Diabetes Insipidus - what is it?
What happens to these people?
Medication?
S/S

A

Lack of ADH (anti diuretic hormone)
Pee…lots of pee. Can’t retain water in the body.
Vasopressin

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16
Q

What is glomerulonephritis?
Cause (pre, intra, post)?
S/S …
Treatment …

A

Inflammation or infection of glomeulous.
Intra renal failure
S/S = dark cola colored urine (heraturia), foamy urine (proteniuria), HTN, fluid retention (swelling), fatigue, history of STREPTOCOCCUS infection

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17
Q

Polycystic kidney disease

S/S

A

S/S = dull heaven ache in back, HTN

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18
Q

How would you position a PT to drain a suprapubic catheter?

A

Sit the PT up so the urine does not have to work against gravity.
Also turn side to side for proper drainage. Prone to infection, use sterile irrigation if needed.

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19
Q

Nephrostomy tubes
Where are they placed?
How to prevent infection?

A

Inserted straight into the renal pelvis (holds 3-5 mL of urine)
Have a high risk of infection; must use sterile flush w/ 3-5 mL

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20
Q

Antispasmodic/Analegesic
Purpose?
Action?
Drug?

A

Relieve pain or incontinence
Relax smooth muscle
Oxybutynin (ditropan)

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21
Q

Antibiotics used for kidney infections

A

Nitrofurantion (Macrodantin)
Trimethoprim/sulfamethoxazole (TMP/SMX) (Bactrim)
Ampicillin, Amoxicillin, Cephalosporins
Fluoriquinolones (ciprofloxacin)

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22
Q

Are diuretics a treatment for renal problems?

What diuretics are used?

A

They are not a treatment, they only treat the SYMPTOMS.

Buses (bumetanide)-loop diuretic - inhibit Na and water reabsorption, increase K loss. Watch for hypokalemia.

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23
Q

Important teaching point regarding use of diuretics for PT.

A

Daily Weights - report sudden gains or losses
Take in AM - PM will disturbed sleep
S/S orthostatic HTN - get up slowly
Increased urine output
Unless fluid restricted drink 6-8 glasses of water each day

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24
Q

Nephrotoxic Drugs

A

Antibiotics (ex): amphotericin B, penicillin, vancomycin
NSAIDs (ex): ibuprofen, naproxen, aspirin, torodol
IV contrast dye
Diuretics
Chemotherapeutic agents
ACE inhibitors
Mannitol

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25
Explain pre renal failure. What is it caused by? Treatment?
Inadequate perfusion of blood supplying the kidney. The kidneys need adequate BP. Caused by low BP, or hypovolemia (not enough fluids), kidneys are unable to filter the blood adequately (ex: shock, sepsis, dehydration, severe blood loss, decreased cardiac output, heart failure) Treatment: fluids, increase BP, give blood if needed, treat the underlying condition
26
What happens with intra renal failure? Caused by? Treatment?
Actual injury or necrosis of tubular structures resulting in impaired nephron function Causes: infection from the inside of body (not UTI), trauma, nephrotoxic drugs, acidosis, anything that kills cells, glomulernephritis, pyelonephritis, thrombotic disorders (sickle cell), malignant hypertension, myogloneuria. Treatment: fix underlying cause, possible temporary dialysis while it heals.
27
Describe post renal failure. Causes? Treatment?
Obstruction to the OUTFLOW of urine from one or both kidneys. Causes: stones, tumor, prostrate, trauma. Results in back pressure which causes damage. Treatment: remove blockage
28
ALL renal failures lead to _________________. When determining pre, post or intra we are talking about the ______________ cause.
POST | INITIAL
29
Phases of acute kidney injury (AKI) LIST
1. Initiating 2. Oliguric 3. Diuretic 4. Recovery
30
Explain initiating Phase
Begins at time of renal insult, continues until S/S are apparent, lasts hours to days, no clinical manifestations at this time.
31
``` Oliguric Phase Urine production? When does it occur? Duration? What happens when this phase lasts a long time? Urinalysis shows? Proteinuria present? Y/N/M S/S of renal failure? Y/N/M ```
Urine <400 mL in 24 hours occurs 1-7 days of precipitating event 10-14 days, but can lasts months The longer in this phase the poorer the prognosis of regaining renal function Urinalysis = casts, RBC, WBC, (sloughing off of necrotic cells) Proteinuria, may be present if glomular dysfunction May show signs of renal failure
32
S/S of AKI
Fluid volume retention (edema, HTN, HF) Metabolic acidosis (cant excrete acid, HCO3 decreased) Sodium imbalance (hyponatremia, can conserve Na) Potassium excess (cant excrete K+) Hematologic disorders (leukocytosis, decreased RBC) Waste products increase (urea/nitrogen/creatinine) increased BUN Neurological disorders: range from fatigue and confusion to seizures, stupor and coma (buildup of waste)
33
``` Diuretic Phase (HEALING) but not out of the woods What do you see? Duration? What do the labs show? ```
What's going on? Kidneys have recovered the ability to excrete waste, but can not concentrate urine. Urine production occurs, but the nephrons are not fully functional. Initially urine 1-3 L/day, may increase 3-5 L/day. Duration: 1-3 weeks Acid/Base, BUN, creatinine, electrolyte values begin to normalize.
34
How do you know when they are in the diuretic phase? | What to watch for?
HYPOvolemia HYPOtension electrolyte loss Especially monitor for **hyponatrimia, hypokaleima And DEHYDRATION
35
Recovery Phase What is the signal that this phase has begun? What happens to BUN and creatinine? Duration? Do all patients get to recovery phase? Y/N
GFR increases BUN and creatinine plateau and then decrease Lasts up to 12 months Some PT will never get here, but instead progress to chronic renal failure.
36
Collaborative care for treating AKI.
ELIMINATE THE CAUSE (#1 GOAL) Treat S/S Prevent complications (such as infection) Ensure adequate intravascular volume & cardiac output Fluid restrictions (600 mL + output last 24 hours) Manage fluid, electrolyte and acid-base balances Calcium supplements or phosphate binding agents ( Diuretics in early stages (not high dose) Dialysis if indicated
37
Nursing Dx AKI
Excess fluid volume r/t kidney failure and fluid retention Risk for infection r/t uremic toxins and altered immune response secondary to kidney failure Fatigue related to anemia, metabolic acidosis and uremic toxins Anxiety r/t disease process Potential complication disrhythemias r/t electrolyte imbalances
38
Renal Diet
Adequate calories (30-35 cal/kg/day) Adequate protein (0.8 mg/kg/day) to prevent protein breakdown Na+ and P- restriction to prevent edema, HTN and HF Designed to cut down on the amount of waste in the blood. Limited fluids May limit K+ and Ca+ THEY WILL NOT NEED EXTRA VIT D. IT DOES NOT MAKE A DIFFERENCE if they can not convert it.
39
What is the #1 complication of peritoneal dialysis? | What are the S/S?
INFECTION S/S = cloudy drainage, rigid abdomen, high fever, possible low bowel sounds
40
What diseases are associated with the posterior pituitary gland?
``` Diabetes Insipidus (DI) SIADH - syndrome of inappropriate antidiuretic hormone secretion ``` ADH = PP = ADH = PP = ADH = PP = ADH = PP = ADH = PP = ADH
41
What problems are associated with the thyroid?
Hypothyroid | Hyperthyroid
42
What problems are associated with parathyroid?
Calcium imbalance
43
What problems are associated with the adrenal cortex? Adrenal Cortex (AC) = addison's and cushing's (AC)
Cushing's disease (too much stress steroid) | Addison's disease (too little stress steroid)
44
What problem is associated with the adrenal medulla?
Pheocromocytoma
45
What problem is associated with the pancreas?
Diabetes mellitus (DM)
46
Vasopressin is also _____________ It is a treatment for _____________
Antidiuretic hormone ADH DI - they are not producing enough, so we have to give them more.
47
SIADH - too much ADH (HYPER SECRETION) SI - soggy, holding on to fluids What would be administered (med and what type of fluid) WHY?
``` Loop Diuretics (Lasix {furosemide}, Bumex {bumetanide}) HYPERtonic solution (3% saline) Why? Remove the fluid from the cell, back to the vessels, so it can be excreted. (Water follows Na+) So you give a HYPERtonic solution to pull the water out of the cell. ```
48
What does the adrenal cortex produce?
Cortisol (glucocorticoid hormone) Functions: controls blood sugar, burns fat and protein, reacts to stress like major illness or injury. Aldosterone (mineralcorticoid hormone) Functions: acts on the kidney to regulate excretion of salt and maintain BP
49
What causes Addisons? What are the S/S of Addisons? What are the treatments? How long will they be on steroids?
Lack of corticosteroids. Hypoglycemia , hyperpigmentation, weakness, fatigue, anorexia, weight loss, N/V, diarrhea, irritability. ``` Treatment = steroids Steroids = corticosteroids = both glucocorticoids and mineralocorticoids ``` Glucocorticoids = hydrocortisone, cortisone, prednisone, methylprednisone (solu-medrol), dexmethasone Meneralocorticoids = fludrocortisone (Florinef) On steroids for life.
50
Corticosteroid patient teaching
``` Glucocorticoids - usually divided sides Mineralocortocoids - usually given once in the morning Must not be stopped abruptly Increase during times of stress Measures to reduce occurrence of osteoporosis Na+ restriction is edema occurs Monitor for hyperglycemia Notify HCP if epigastric pain develops Prevent injury/infection Inform all HCP ```
51
What occurs in an Addisonian crisis? | Treatment?
Insufficient or sudden sharp decrease in hormones Life threatening Same as addisons plus: pain in lower back, abdomenor legs, severe vomiting, diarrhea = dehydration, low BP, LOC, high K+ and low Na+ Treatment: Shock management = Fluids (NS + 5% dextrose), high doses of hydrocortisone replacement, VS, LOC, labs, cushings (too high)
52
Complications of steroids
``` HIGH Glucose Immunosuppression Low K+ and Ca+ Mood and bahevior changes Moon face, truncal obesity Delayed healing Susceptibility to infection Peptic ulcer disease Muscle atrophy/weakness Protein depletion Risk for acute adrenal crisis if therapy is stopped abruptly ```
53
Cushings disease? Causes? Symptoms? Nursing Interventions?
Excess corticosteroid production. Symptoms: increased susceptibility to infection, HYPERglycemia, fat deposits on face, and back of shoulders (truck obesity), bruises, osteoporosis. Nursing interventions: GLUCOSE, VS, Daily weights
54
Which hormone stimulates glucose production and decreases movement of glucose into the cell? Which hormone promotes transport of glucose into the cells and adipose tissue?
Glucagon (closes the gate) keeps glucose in the blood stream. Insulin (opens the gate) moves glucose out of the blood stream.
55
Classic Signs of Type 1 Diabetes Destruction of what type of cells?
3 P's Polyuria (frequent urination) Polydipsia (excessive thirst) Polyphasic (excessive hunger) Beta cells
56
Type 2 diabetes is characterized by ...
Insulin resistance Decreased insulin production by the pancreas Inappropriate hepatic glucose production Altered production of Hormones and cytokines by adipose tissue.
57
Two oral diabetic medications. TYPE 2 ONLY
Metformin (glucophage) - reduce glucose production by liver, enhance insulin sensitivity, improve glucose transport.TYPE 2. May cause weight loss, w/h for PT surgery or radiology w/ contrast. Contraindications: renal, liver, cardiac disease, excessive alcohol intake Glyburide: increases insulin production from pancreas. MAJOR SIDE EFFECT: HYPOglycemia
58
Normal Blood Glucose Number A1C Numbers
70-120 Goal less than 6.5-7%
59
Patient teaching for prediabetes
Undergo screenings Manage risk factors Monitor for symptoms of diabetes Maintain healthy weight, exercise and diet
60
S/S HYPOglycemia Think of how you feel when you don't eat for long periods of time. Treatment?
Mental status change: confusion, stupor, confusion Shakey, Sweating, N/V Treatments: RULE OF 15 Consume 15 g simple CHO (juice, soda) Recheck in 15 minutes (repeat if still <70) Avoid foods with fat, slows absorption of sugar Give complex CHO after recovery Explore why hypoglycemia occurred
61
Symptoms of DKA Occurs with what type of diabetes?
``` Dehydration Severe hyperglycemia (>300) with KEYTONES in urine Metabolic acidosis Kussmaul respirations Sweet, fruity breath odor ``` TYPE 1
62
Priority treatment for DKA
``` #1 - INSULIN (unless there is a specific O2 need) #2 - fluids ```
63
Who gets insulin?
Type 1 diabetics and Type 2 who are do not respond to oral medications or have a severe case.
64
``` Insulins (Professor groups these two together in short) Rapid acting (Names, Onet, peak, duration) Short acting (Names, Onset, peak, duration) ``` ``` (Professor groups these two together in long acting) Intermediate (Names, onset, peak, duration) Long Acting (Names, onset, peak, duration) ```
Rapid (take with food) - lispro, aspart, apidra Onset: 15 min, Peak 2 hours. Duration 3-5 hours. Short - (take with meals) Regular Insulin Onset: 30-60 min. Peak 3 hours. Duration 5-8 hours. ``` Long Acting Insulin glargine (Lantas) and Detemir (Levemir) Onset: 1 hour, peak: none - sustained release ``` NPH Onset: 2-3 hours, peak 8 hours
65
Hyperosmolar hyperglycemia syndrome (HHS) What is it? Who gets it? How do you treat it? How different from DKA.
High blood sugar causes severe DEHYDRATION, increases osmolarity, high risk of complications and death. Type 2 diabetics ``` #1. IV access, begin fluids, 0.45 or 0.9 NaCl #2. Continuous REGULAR insulin drip 0.1 units/kg/hour - CHECK THE DRIP RATE WITH ANOTHER NURSE ``` No Keytones in serum or urine
66
If the blood is thick (salty, sugary, proteins, electrolytes) what will happen to the water in the cells?
It will pull the water out of the cells - dehydration of cells.
67
``` HYPOvolemia Pulse BP Heart Rhythm O2 ```
Pulse - increased (trying to pump blood) BP - decreased (orthostatic changes) O2 - decreased (not able to get blood flow to extremities)
68
``` HYPERvolemia Breath Sounds Pulse BP O2 ```
Breath sounds = crackles, fluid Pulse- can be up or down BP - increased O2 - up or down
69
``` Normal Lab Values Na+ K+ Ca+ Mg+ PP4- ```
``` Normal Lab Values Na+ 135-145 K+ 3.5-5 Ca+ 9-11 Mg+ 1.8-3 PP4- 2.3-4.5 ```
70
What do dehydrated cells do with Na+ ? | Too much water what happens to Na+ ?
dehydrated cells bring in Na+ the water will follow the Na+ Overloaded cells get rid of Na+
71
Top 3 signs of Na+ imbalances.
1. Seizure/Coma 2. BP - dehydration will decrease, fluid overload will increase 3. Weight fluctuation
72
Potassium binder? What is the name? What do you give in an emergency to get K+ into the cell?
Kayexalate = binds and removed K+ from gut Emergency hypokalemia = Dextrose and regular insulin

Block 3 M/S Test - Fluids, Electrolytes, Kidneys, Endorine, Diabetes (1 decks)

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