Hpii Exam #1

Front 1

How does the potassium level change to compensate for hydrogen ion level changes, in acidosis?

Back 1

Hydrogen ions from the ECF to the ICF. Potassium ions move from the ICF to the ECF. This creates a hyperkalemic environment.

Front 2

How does the potassium level change to compensate for hydrogen ion level changes, in alkalosis?

Back 2

Hydrogen ions move from the ICF to the ECF. Potassium ions move from the ECF to the ICF. This creates a hypokalmeic environment.

Front 3

What is the normal pH range?

Back 3

7.35 - 7.45

Front 4

What is the relationship between plasma pH and H+ concentration?

Back 4

They are inversely related.

The greater the H+ concentration, the more acidic the solution and the lower the pH and vice versa.

Front 5

What are the pH ranges compatible with life?

Back 5

6.8 - 7.8

Front 6

What regulates the bicarbonate level in the ECF?

Back 6

Kidneys regulate the bicarbonate level in the ECF.

Front 7

What controls the carbonic acid content of the ECF?

Back 7

The lungs control the CO2 and thus the carbonic acid content of the ECF.

Front 8

Acid-base balance in older adults

Back 8

-kidneys shrink

-if underlying lung disease exist regulation of acid-base balance is less efficient

-difficulty handling excess acid

Front 9

What are people with chronic acidosis at risk for?

Back 9

Kidney stones

*Bone represents an additional source of acid base buffering

Front 10

Renal Control Mechanisms

Back 10

Hydrogen/Bicarbonate Exchange regulates pH through the secretion of excess H+ and re-asorption of HCO3- by the renal tubules.

Front 11

What happens with compensation changes in pH?

Back 11

Occurs to maintain acid/base balance. It will always be from the opposing system. If the pH remains abnormal, the compensation is partial. If the pH returns to normal, the compensation is complete.

Front 12

PCO2 normal ranges

Back 12

35 - 45 mmHg

Front 13

HCO3 Normal Ranges

Back 13

22 - 26 mEq/L

Front 14

PO2 normal ranges

Back 14

80 - 100 mmHg

Front 15

Anion Gap

Back 15

Normal Range: 12 - 16 mEq/L

AG = [Na+] + [K+] - (Cl- + HCO-3)

Front 16

Acute & Chronic Metabolic Acidosis (Base Bicarbonate Deficit)

Back 16

low pH (increased H+ concentration) + low plasma bicarbonate concentration

Compensation = increase in respiratory rate

2 Clinical Manifestations: high anion gap acidosis and normal anion gap acidosis

Front 17

Normal anion gap acidosis

Back 17

-direct loss of bicarb (diarrhea, use of diuretics)

-early renal insufficiency

-excessive administration of chloride

-administration of parenteral nutrition w/o bicarb or producing solutes

Front 18

High anion gap acidosis

Back 18

-excessive accumulation of fixed acid

-ketoacidosis

-lactic acidosis

-ketoacidosis w/ starvation

Front 19

Clinical Manifestations of Metabolic Acidosis

Back 19

-Increased RR rate & depth (hypoventilation )

-may lead to hyperkalemia

Front 20

Acute & chronic Metabolic Alkalosis (Base Bicarbonate Excess)

Back 20

-High pH (decreased H+ concentration) and a high plasma bicarbonate concentration

-Can be produced by a gain of bicarb or a loss of H+

-Common cause = vomiting/gastric suction w/ loss of H+ and Cl-

Front 21

Clinical Manifestations Metabolic Alkalosis

Back 21

-decreased RR

-ph increases and hypokalemia develops

-decreased motility & paralytic ileus

-related to decreased calcium ionization

Front 22

Respiratory Acidosis (Carbonic Acid Excess)

Back 22

*Acidosis = hypoventilation

-pH < 7.35 and PaCO2 is >42 mmHg

-Inadequate excretion of CO2 w/ inadequate ventilation, resulting in elevated plasma CO2 concentrations and increased levels of carbonic acid.

Front 23

Acute respiratory acidosis

Back 23

-acute pulmonary edema

-aspiration

-pneumothorax

-severe pneumonia

-administration of oxygen to a pt w/ chronic hypercapnia

Front 24

Chronic respiratory acidosis

Back 24

-MD
-MS

-MG

-Guillian-Barre (neuromuscular diseases may cause hypoventilation b/c it affects breathing muscles)

*COPD: retain Co2 b/c of damaged alveoli & normally high level of CO2.

-Brain insensitive to CO2 stimulant, lack of O2 becomes stimulant to breathe (hypoxemia)

Front 25

Clinical Manifestations of acute respiratory acidosis

Back 25

-Increased pulse and RR

-increased BP

-mental cloudiness/confusion

-feeling of fullness in the head or decrease in LOC

Front 26

Clinical Manifestations of chronic respiratory acidosis

Back 26

As long the body's ability to compensate is not exceeded, the pt will be aymptomatic

Front 27

Respiratory Alkalosis (Carbonic Acid Deficit)

Back 27

Alkalosis = hyperventilating

-Arterial pH >7.45 and PaCO2 < 38 mmHg

-Always caused by hyperventilation with "blowing off" of CO2 and decrease in plasma carbonic acid concentration

Front 28

Causes of acute respiratory alkalosis

Back 28

-Fever

-Hyperventilation

-Hypoxia

-Hysteria

-Overventilation by mechanical ventilators

-Pain

Front 29

Causes of chronic respiratory alkalosis

Back 29

-chronic hypocapnia w/ resultant decreased serum bicarb levels

-predisposed by chronic hepatic insufficiency and cerebral tumor

Front 30

Clinical Manifestations of Respiratory Alkalosis

Back 30

-lightheadedness due to vasoconstriction & decreased cerebral blood flow

-numbness and tingling due to decreased calcium ionization

-cardiac effects: tachycardia, dysrhythmia

-pts with chronic respiratory alkalosis usually asymptomatic

Front 31

Mixed Acid-Base Disorders

Back 31

A normal pH in the presence of changes in the PaCO2 and plasma HCO3 concentration suggests mixed disorder.

-The pulmonary and renal systems compensate for each other to return the pH to normal -> the system not causing the problem tries to compensate by returning the ratio of bicarb to carbonic acid to normal 20:1.

*The only mixed disorder that cannot occur is mixed respiratory acidosis and alkalosis

Front 32

Compensation

Back 32

Front 33

Types of acid base imbalance

Back 33

Front 34

How does oxygen travel through the body?

Back 34

bound to hemoglobin

-Alkalotic: move O2 bound to hemoglobin

Acidosis: less O2 bound to hemoglobin (retain CO2)

Front 35

ABG Ranges

Back 35

Front 36

ABG Tic-Tac-Toe Example

Back 36

Front 37

Normal Values for Arterial & Mixed Venous Bloods

Back 37

Front 38

Oxyhemoglobin dissociation curve

Back 38

Front 39

Causes of metabolic acidosis

Back 39

-diabetes mellitus or dka

-excessive ingestion of aspirin

-high-fat diet

-insufficient metabolism of carbs

-malnutrition

-renal insufficiency, acute kidney injury, or chronic kidney disease

-severe diarrhea

Front 40

Causes of metabolic alkalosis

Back 40

-diuretics

-excessive vomiting or gastrointestinal

-hyperaldosteronism

-ingestion of and/or infusion of excess sodium bicarbonate

-massive transfusion of whole blood

Front 41

What happens as the glomerular filtration decreases?

Back 41

-Serum creatinine increases

-BUN increases

- Creatinine clearance decreases (Evaluates how well the kidneys remove creatinine from the blood)

*Creatinine Clearance Test provides the best estimate of GFR.

Front 42

What foods should be avoided to prevent kidney stones?

Back 42

➤Oxalate containing foods

(Tea, Spinach, Strawberries, Rhubarb, Peanuts, Wheat bran)

➤ Calcium containing food

(beans, fish, dried fruits)

➤ Purine containing foods

(Sardines, sweetbreads, organ meats, most meats)

*restrict protein intake to 60 g/day

*drink two glasses of water at bedtime

Front 43

Fluid Regulation Cycle

Back 43

Front 44

What is acute kidney injury (AKI)?

Back 44

Loss of kidney function due to ischemia or toxic substances. It occurs abruptly & can be reversible.

Front 45

What is azotemia?

Back 45

The retention of nitrogenous waste in the blood. Increases in BUN and creatinine.

Front 46

What is chronic kidney disease?

Back 46

The progressive ongoing deterioration in kidney function. It is irreversible and results in uermia, waste in the blood, or ESKD. Characterized by a GFR of <60 mL/min for a period of 3 months or longer.

*Dialysis or kidney transplant needed to maintain life

Front 47

What is dialysis?

Back 47

Blood filtering performed via the bloodstream (hemodialysis) or the peritoneal cavity (peritoneal dialysis).

Front 48

Risk factors for AKI

Back 48

-dehydration

-infection

-benign prostatic hypertrophy (hyperplasia)

-anemia

-alcoholism

Front 49

What is the function of Antidiurectic hormone (ADH)?

Back 49

Reabsorbs water. It is secreted by dehydration or high sodium intake and by a decrease in blood volume.

Front 50

What is the function of Aldosterone?

Back 50

Stimulates the distal convoluted tubules to reabsorb sodium and secrete potassium.

Front 51

Risk factors associated with Renal Disorders

Back 51

-chemical or environmental toxin exposure

-contact sports

-Diabetes Mellitus

-Liver dieases

-Family Hx

-Frequent UTIs

-Heart Failure

-Hypertension

-Nephrotoxic Substances (NSAIDs, antibiotics)

-Radiographic contrast dye

Front 52

Gerontologic Considerations for Renal Disease

Back 52

-Decreased GFR, blood flow & Renal mass

-Decreased ability to concentrate & dilute urine

-increased risk of hyperkalemia, hyponatremia volume depletion & dehydration

-Special drug and dye considerations

Front 53

Cardinal features of AKI

Back 53

-Decreased GFR

-Azotemia

-Oliguria

Front 54

Types of Acute Kidney Injury

Back 54

Front 55

Prerenal AKI Etiology

Back 55

Reduction in renal blood flow leading to reduced glomerular filtration & glomerular perfusion.

Front 56

Prerenal AKI Causes & S/S

Back 56

Outside the kidney

-Hypovolemia (Hemorrhage, Dehydration, GI losses)

-Hypotension

-Decreased cardiac output

-Decreased peripheral vascular resistance

-Prerenal infection

-Dehydration

-Shock, Sepsis

-Vasoactive meds (epinephrine, dopamine)

-IV contrast dye

Front 57

Postrenal Etiology

Back 57

Mechanical obstruction of urine flow

Ex: tumors, calculi, injury, benign prostatic hypertrophy

Front 58

Postrenal AKI Causes & S/S

Back 58

Between the kidney & urethral meatus

-Bladder neck obstruction (decreased GFR, abnormal nephron function)

-Bladder Cancer

-Calculi

-Postrenal infection

*May be reversed after removal of obstruction

Front 59

Intrarenal AKI Etiology

Back 59

Damage to the kidney causing impaired function of the nephron.

Front 60

Intrarenal AKI Causes & S/S

Back 60

-Ischemia

-Nephrotoxic exposure (contrast induced nephropathy)

-Acute tubular necrosis (ATN)

-Infection

-Acute glomerulonephritis

-Oliguria

-Nausea

-+2 Edema

-Crackles on Auscultation

Front 61

What is ATN?

Back 61

Most common type of intrarenal failure.

-damage of basement membrane to tubular epithelium

-necrotic tissue sloughs off

-tubules become blocked

Front 62

Causes of ATN?

Back 62

-prolonged pre-post failure

-ischemia

-increase in myoglobin (caused by muscle injury anywhere in the body)

-hemolyzed RBCs

Front 63

Risk Factors for contrast induced nephropathy

Back 63

-Dehydration, hypotension

-Advanced age

-Diabetse

-Concurrent use of nephrotoxic medications

-GFR <60 mL/min

-Administration of large amounts of contrast

Front 64

How is Contrast Induced Nephropathy diagnosed?

Back 64

-Increased Creatinine level

*Occurs between 48-72 hours of contrast administration

Front 65

Pathophysiology of Contrast induced Nephropathy

Back 65

-Contrast has a toxic effect on the renal tubule cells

-Reduced medullary blood flow causes injury

Front 66

AKI Clinical Progression

Back 66

Front 67

AKI Initiation Phase

Back 67

Beginning of renal deterioration following injury.

-Several hours up to 2 days

- ↓Urine output (oliguria)

-electrolyte imbalances

*potentially reversible (if recognized early)

Front 68

AKI Oliguric Phase (Maintenance)

Back 68

-Elevated BUN & Creatinine levels

-Decreased urine specific gravity (prerenal causes) or normal (intrarenal causes)

-Decreased GFR & creatinine clearance

- Hyperkalemia, Hypervolemia, Hypocalcemia, Hyperphosphatemia

-Normal or decreased sodium level

-signs of excess fluid volume: edema, hypertension, HF, dysrhthymias

-Signs of uremia: N/V, anorexia, pruritis

Front 69

AKI Diuretic Phase

Back 69

-Gradual decline in BUN & Creatinine but still elevated

-Continued low Creatinine clearance w/ improving GFR

-Hypokalemia, Hyponatremia, Hypovolemia

-Excessive urine output indicates that damaged nephrons are recovering ability to excrete waste

-urine output rises slowly, followed by diuresis

Front 70

AKI Recovery Phase

Back 70

-↑GFR

-Stabilization or continual ↓in BUN & creatinine levels toward normal

-Complete recovery (may take 1 - 2 years)

-urine volume returns to normal

-memory improves

-strength increases

Front 71

Prerenal Management

Back 71

Goal: Improve Renal Perfusion

Management:

-Volume replacement

-Increased cardiac output (vasoactive meds, hydration, hemodynamic monitoring)

Front 72

Postrenal Management

Back 72

Goal: Alleviate obstruction

Management:

-May require an indwelling urinary catheter (monitor for sepsis & S/S of UTI)

-Stent placement (temporary tube alleviate + increase urine formation)

Front 73

Intrarenal Management (ATN)

Back 73

Goal: Conserve kidney function; prevent and manage complications

Management:

-Pharmacologic (diuretic, kayexalate)

-Dietary (monitor phosphorus, potassium, sodium, calcium)

-Management of fluid & electrolyte imbalances

-Renal Replacement Therapy

-Psychosocial Support

Front 74

Risk factors for CKD

Back 74

♦Diabetes Mellitus

♦Hypertension

♦Cardiovascular disease

♦Obesity

Front 75

CKD Causes

Back 75

♦Chronic glomerulonephritis

♦Pyelonephritis or other infections

♦Obstruction of urinary tract

♦Vascular disorders

♦Medications or toxic agents

♦Nephrotic syndrome

*earliest sign is fatigue

Front 76

CKD

Back 76

Front 77

Stages of CKD

Back 77

Front 78

ESRD

Back 78

♦Renal function declines & require renal replacement therapy permanently

♦Progression & clinical manifestations depend on underlying disorder

♦Results when kidneys cannot remove wastes or perform regulatory functions

Front 79

Clinical Manifestations of ESRD

Back 79

♦Fluid & Electrolyte imbalances

♦Gas Exchange

♦Uremia

♦Metabolic Acidosis

Front 80

What does hyperkalemia have the most serious effect on?

Back 80

An elevated potassium level can cause tall, peaked T waves, flat P waves, a widened QRS complex, and a prolonged PR interval decreased cardiac output.

Front 81

Pharmacologic Therapy for CKD

Back 81

♦Epoetin Alfa (for Anemia)

♦Sodium polystyrene, Calcium gluconate (for Hyperkalemia)

♦Calcium Acetate (Hyperphosphatemia)

Front 82

CKD Dietary Management

Back 82

Goal: provide adequate energy, protein, micro-nutrients to maintain homeostasis

Possibly restrict:

♦Protein

♦Sodium

♦Potassium

♦Fluid intake (output 500- 1000 ml/day)

♦Phosphorus

♦Magnesium

Front 83

Renal Replacement Therapy

Back 83

Primary treatment for the patient w/ kidney failure

Types of Renal Replacement Therapy:

♦Intermittent hemodialysis

♦Continuous renal replacement therapy (CRRT)

♦Peritoneal dialysis

Front 84

Principles of hemodialysis & peritoneal Dialysis

Back 84

♦Diffusion (high →low)

♦Osmosis (low → high)

♦Ultra-filtration (movement across a semipermeable membrane as a result of pressure gradient)

Front 85

Temporary Vascular Access

Back 85

Percutaneous venous catheter:

▶Temporary

▶Available immediately

▶Jugular is preferred site

▶inserted in OR or IR

▶Infection risk
▶Air embolism
▶Pneumothorax

Front 86

Permanent Vascular Access (Arteriovenous Fistula)

Back 86

(lower or upper arm placement)

▶surgically created communication btwn artery & vein

▶Matures in 2-3 months

Front 87

Permanent Vascular Access (Arteriovenous Grafts)

Back 87

(synthetic connection)

▶surgically implanted

▶prosthetic graft anastomosed to an artery & vein

▶Matures in 2 - 4 weeks

Front 88

Permanent Vascular Access

Back 88

Front 89

Peritoneal Dialysis

Back 89

The peritoneum acts as the semipermeable membrane to achieve dialysis. Solutes move via osmosis. PD occurs via the transfer of fluid & solute from the bloodstream through the peritoneum into the dialysate solution.

Front 90

Function of Hemodialysis

Back 90

Process of cleansing the blood of accumulated waste products.

➤Removes excess body fluids

Front 91

Complications of HD

Back 91

➤Hypotension

➤Site Infections

➤Bleeding/Clotting

➤Cramps

➤Vascular access issues

➤Dysrhythmias

➤Air Embolism

Front 92

Nursing management: Renal replacement therapy

Back 92

➤Assess site for patency

➤Do not use arm for BP or blood draws

➤Check for thrill & bruit

➤Monitor pulses & neuromuscular status distal to the graft

Front 93

Extracorporeal Shock Wave Lithotripsy (ESWL)

Back 93

Procedure for breaking up stones in kidney or upper ureter so they can be passed spontaneously.

Front 94

Renal Calculi Composition, Contributing Factors, & Treatment

Back 94

Front 95

Urolithiasis & Nephrolithiasis

Back 95

Front 96

Hydronephrosis

Back 96

Expansion of the kidney with urine

Front 97

Ureterostomy

Back 97

Front 98

Nursing Management for Renal Calculi

Back 98

• Painmanagement

-Administer analgesics andantispasmodics as prescribed

-Instruct in methods toreduce discomfort

-Relaxation techniques

• Monitoringand managing potential complications

• Patienteducation

• Psychosocialand emotional support

Front 99

Patienteducation renal calculi

Back 99

•Signs and symptoms to report

•Follow-up care

•Urine pH monitoring

•Measures to prevent recurrent stones•Importance of fluid intake

•Dietary education

•Medication education as needed

Front 100

Types of kidney stones

Back 100

Front 101

Risk Factors for Breast Cancer

Back 101

●Age

●Family Hx

●Early menarche and late menopause

●Previous cancer of the breast, uterus or ovaries

●Nulliparity, late first birth

●Obesity

●High-dose radiation exposure to the chest

Front 102

Early detection of breast cancer

Back 102

Performing breast self exam:

●Perform monthly BSE 7 - 10 days after menses

●Postmenopausal & hysterectomy clients should select a specific day of the month for BSE

Front 103

Nonsurgical Interventions for breast cancer

Back 103

●Chemotherapy

●Radiation therapy

●Hormonal manipulation

Front 104

Surgical Interventions for breast cancer

Back 104

●Lumpectomy

-tumor is excised and removed

●Simple Mastectomy

-breast tissue and the nipple are removed

●Modified Radical Masectomy

-breast tissue, nipple, and lymph nodes are removed

Front 105

Post Interventions for breast cancer

Back 105

●Monitor VS

●Semi-Fowler's position w/ affected arm elevated above the heart to promote drainage & prevent lymphedema

●Encourage coughing & deep breathing

●Use pressure sleeve if edema is severe

●Exercise program

Front 106

Colon Cancer Risk Factors

Back 106

●Age >50, peak at 72 y/o

●Familial polypopsis, family Hx of colon cancer

●Previous polyps, Hx of colon cancer

●Hx of chronic inflammatory bowel disease

●Hx of ovarian or breast cancer

●Sedentary Lifestyle

Front 107

Colon Cancer Primary Prevention

Back 107

●Prevent obesity & weight gain

●Increase physical activity

●Healthy diet

●Avoid Alcohol

Front 108

Colon Cancer Secondary Prevention

Back 108

Screening:

●Digital Rectal Exam

●Sigmoidoscopy

●Barium Enema

●Colonoscopy

●CT Scan

Front 109

Signs/Symptoms for Colon Cancer

Back 109

●Unintended weight loss

●Constipation

●Diarrhea

●Anemia

●Blood in stool

●Abnormal Stools

Front 110

Types of Radiation Therapy

Back 110

1.External beam radiation therapy

2.Internal radiation therapy (brachytherapy)

Front 111

Chemotherapy for Colon Cancer

Back 111

Tyrosine Kinase Inhibitor (Targeted Therapy)

●Bevacizumab (Avastin)

Side Effects:

-hypertension

-bleeding

Front 112

Where does Prostate cancer most commonly metastasize?

Back 112

To the bone