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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
Q

Explain pre renal failure.
What is it caused by?
Treatment?

A

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

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26
Q

What happens with intra renal failure?
Caused by?
Treatment?

A

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.

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27
Q

Describe post renal failure.
Causes?
Treatment?

A

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

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28
Q

ALL renal failures lead to _________________. When determining pre, post or intra we are talking about the ______________ cause.

A

POST

INITIAL

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29
Q

Phases of acute kidney injury (AKI)

LIST

A
  1. Initiating
  2. Oliguric
  3. Diuretic
  4. Recovery
30
Q

Explain initiating Phase

A

Begins at time of renal insult, continues until S/S are apparent, lasts hours to days, no clinical manifestations at this time.

31
Q 
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
A

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
Q

S/S of AKI

A

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
Q 
Diuretic Phase (HEALING) but not out of the woods
What do you see?
Duration?
What do the labs show?
A

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
Q

How do you know when they are in the diuretic phase?

What to watch for?

A

HYPOvolemia
HYPOtension
electrolyte loss
Especially monitor for **hyponatrimia, hypokaleima And DEHYDRATION

35
Q

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

A

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
Q

Collaborative care for treating AKI.

A

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
Q

Nursing Dx AKI

A

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
Q

Renal Diet

A

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
Q

What is the #1 complication of peritoneal dialysis?

What are the S/S?

A

INFECTION

S/S = cloudy drainage, rigid abdomen, high fever, possible low bowel sounds

40
Q

What diseases are associated with the posterior pituitary gland?

A 
Diabetes Insipidus (DI)
SIADH - syndrome of inappropriate antidiuretic hormone secretion

ADH = PP = ADH = PP = ADH = PP = ADH = PP = ADH = PP = ADH

41
Q

What problems are associated with the thyroid?

A

Hypothyroid

Hyperthyroid

42
Q

What problems are associated with parathyroid?

A

Calcium imbalance

43
Q

What problems are associated with the adrenal cortex?

Adrenal Cortex (AC) = addison’s and cushing’s (AC)

A

Cushing’s disease (too much stress steroid)

Addison’s disease (too little stress steroid)

44
Q

What problem is associated with the adrenal medulla?

A

Pheocromocytoma

45
Q

What problem is associated with the pancreas?

A

Diabetes mellitus (DM)

46
Q

Vasopressin is also _____________

It is a treatment for _____________

A

Antidiuretic hormone ADH

DI - they are not producing enough, so we have to give them more.

47
Q

SIADH - too much ADH (HYPER SECRETION)
SI - soggy, holding on to fluids
What would be administered (med and what type of fluid) WHY?

A 
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
Q

What does the adrenal cortex produce?

A

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
Q

What causes Addisons?
What are the S/S of Addisons?
What are the treatments?
How long will they be on steroids?

A

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
Q

Corticosteroid patient teaching

A 
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
Q

What occurs in an Addisonian crisis?

Treatment?

A

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
Q

Complications of steroids

A 
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
Q

Cushings disease?
Causes?
Symptoms?
Nursing Interventions?

A

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
Q

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?

A

Glucagon (closes the gate) keeps glucose in the blood stream.

Insulin (opens the gate) moves glucose out of the blood stream.

55
Q

Classic Signs of Type 1 Diabetes

Destruction of what type of cells?

A

3 P’s
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphasic (excessive hunger)

Beta cells

56
Q

Type 2 diabetes is characterized by …

A

Insulin resistance
Decreased insulin production by the pancreas
Inappropriate hepatic glucose production
Altered production of Hormones and cytokines by adipose tissue.

57
Q

Two oral diabetic medications.

TYPE 2 ONLY

A

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
Q

Normal Blood Glucose Number

A1C Numbers

A

70-120

Goal less than 6.5-7%

59
Q

Patient teaching for prediabetes

A

Undergo screenings
Manage risk factors
Monitor for symptoms of diabetes
Maintain healthy weight, exercise and diet

60
Q

S/S HYPOglycemia

Think of how you feel when you don’t eat for long periods of time.

Treatment?

A

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
Q

Symptoms of DKA

Occurs with what type of diabetes?

A 
Dehydration
Severe hyperglycemia (>300) with KEYTONES in urine
Metabolic acidosis
Kussmaul respirations
Sweet, fruity breath odor

TYPE 1

62
Q

Priority treatment for DKA

A 
#1 - INSULIN (unless there is a specific O2 need)
#2 - fluids
63
Q

Who gets insulin?

A

Type 1 diabetics and Type 2 who are do not respond to oral medications or have a severe case.

64
Q 
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)
A

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
Q

Hyperosmolar hyperglycemia syndrome (HHS)

What is it?
Who gets it?
How do you treat it?
How different from DKA.

A

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
Q

If the blood is thick (salty, sugary, proteins, electrolytes) what will happen to the water in the cells?

A

It will pull the water out of the cells - dehydration of cells.

67
Q 
HYPOvolemia
Pulse
BP
Heart Rhythm
O2
A

Pulse - increased (trying to pump blood)
BP - decreased (orthostatic changes)
O2 - decreased (not able to get blood flow to extremities)

68
Q 
HYPERvolemia
Breath Sounds
Pulse
BP
O2
A

Breath sounds = crackles, fluid
Pulse- can be up or down
BP - increased
O2 - up or down

69
Q 
Normal Lab Values
Na+
K+
Ca+
Mg+
PP4-
A 
Normal Lab Values
Na+  135-145
K+  3.5-5
Ca+  9-11
Mg+  1.8-3
PP4-  2.3-4.5
70
Q

What do dehydrated cells do with Na+ ?

Too much water what happens to Na+ ?

A

dehydrated cells bring in Na+ the water will follow the Na+

Overloaded cells get rid of Na+

71
Q

Top 3 signs of Na+ imbalances.

A
  1. Seizure/Coma
  2. BP - dehydration will decrease, fluid overload will increase
  3. Weight fluctuation
72
Q

Potassium binder? What is the name?

What do you give in an emergency to get K+ into the cell?

A

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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