Week 7; Acute Care Kidney Injury & Sexual Dysfunction Flashcards

(103 cards)

1
Q

AKI

A

Rapid reduction in kidney function; failure to maintain fluid and electrolyte balance and acid–base balance with accumulation of nitrogenous waste products in the blood. Evidenced by increased creatinine and BUN. Occurs over a few hours or days, causes systemic effects and complications, can result in death.

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2
Q

Glomerular filtration

A

First step in urine formation. Normal GFR averages 125 mL/min totaling 180 L day – this is included in reabsorption. Otherwise severe dehydration and death. Only about 1-3 L is excreted each day as urine.
GFR is controlled by BP and blood flow.
Kidneys self-regulate their own blood pressure and blood flow which keeps GFR constant
GFR decreases with age.
By age 65 the GFR is about 65mL/min (half of rate of a young adult) which increases risk of fluid overload.
Diabetes, HTN, or heart failure causes an even faster decline
The combination of reduced kidney mass, reduced blood flow, and a greater risk for drug reactions and kidney damage from drugs and contrast media in older adults.

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3
Q

AKI etiology

A

More likely in hospitalized adults with advanced age or pre-existing conditions, burns, third spacing depletes kidney of fluid, reduced cardiac output and fluid loss

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4
Q

3 Categories of Causes of AKI:

A
  1. Prerenal Causes – perfusion reduction, hypovolemia, low cardiac output
  2. Intrarenal Causes - Kidney damage, acute tubular necrosis, injury
  3. Postrenal Causes – Urine Flow Obstruction (Ureteral or Urethral)
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5
Q

Postrenal AKI causes

A

Ureteral obstruction from cancer, calculi, external obstruction, prostate enlargement, calculi, cancer, stricture, blood clot

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6
Q

Nursing priority with AKI

A

Preventing volume depletion and providing early intervention when volume depletion occurs are nursing PRIORITIES
Reduced perfusion is common cause of AKI

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7
Q

Reduced perfusion is a common cause of AKI; assess for:

A

Low urine output – oliguria begins within 1 day after a hypotensive event and can last 1-3 weeks
Decreasing BP
Decreasing pulse pressure
Orthostatic hypotension

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8
Q

Hypovolemic shock review

A

Abnormally decreased volume of circulating fluid causing peripheral circulatory failure
Endangers vital organs
Brain, heart, kidneys are particularly vulnerable
Tachycardia is an early sign of compensation for excessive blood loss
Tachycardia, tachypnea, BP normal initially, decrease or narrowing in pulse pressure (difference between systolic and diastolic)
elevated BP can occur initially until compensatory mechanisms fail
Acidosis with vasodilation and decreased BP, increased bleeding, decreased circulating volume, and subsequent organ death

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9
Q

Health promotion in the patient with AKI

A

Avoid dehydration by drinking 2 to 3 L of water daily, be aware of urine characteristic changes, such as sediment, hematuria (smoky or red color), foul odor, or any other worrisome changes, avoid nephrotoxic substances such as NSAIDS, antibiotics, organic solvents, chemicals like pesticides, heavy metals

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10
Q

Assessment of the patient with AKI

A

Urine characteristic changes or obstructive problems
Recent surgery or trauma
Drug history
Coexisting conditions
Acute illnesses (immunity-mediated AKI)
Anticipate AKI after hypotension or shock

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11
Q

Oliguria output-

A

<400 ml/24 hours

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12
Q

Anuria output-

A

<50 ml/day

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13
Q

Labs in pts with AKI

A

Creatinine, BUN
GFR (normal 90ml/min or higher)
Electrolyte values (K+, phosphorus, sodium)
Renal phosphate increases and calcium binds – so hyperphosphatemia with hypocalcemia
24 hour creatinine clearance

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14
Q

Treatment of AKI

A

Avoid hypotension, maintain fluid balance
Reduce exposure to nephrotoxic agents
Frequently monitor laboratory values
Closely watch I/O
Drug therapy – including diuretics to rid body of retained fluid, waste products (Lasix (furosemide), Mannitol)
Nutrition therapy
Kidney replacement therapy (intermittent versus continuous)

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15
Q

Why is nutrition therapy needed in AKI?

A

Patients with AKI often have high rate of catabolism (protein breakdown). Rate of protein breakdown correlates with the severity of uremia and azotemia (increase presence of nitrogenous wastes in blood). Parenteral nutrition may be indicated because patient is too ill.

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16
Q

Signs of uremia-

A

n/v, anorexia, headache, dizziness, coma, death

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17
Q

Nutrition needs in pts with AKI

A

Several kidney specific supplements that are lower in sodium, potassium and phosphorus but high in calories. Lower protein, carbs increased. Goal is to provide sufficient nutrients to maintain or improve nutrition status, preserve lean body mass, restore or maintain fluid balance and preserve kidney function

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18
Q

Azotemia –

A

build up of nitrogen based wastes

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19
Q

Uremia –

A

azotemia with symptoms

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20
Q

Key features of uremia

A

Metallic taste in mouth
Anorexia
N/V
Muscle cramps
Uremic “frost” on skin
Itching – caused by uremic frost, and excess phosphorus
Fatigue and lethargy
Hiccups
Edema
Dyspnea
Paresthesias

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21
Q

Albumin in the urine is a marker of __ __, whereas GFR reflects __ __.

A

kidney damage, kidney function

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22
Q

Teach patients with mild CKD:

A

carefully managing fluid volume, blood pressure, electrolytes, and other kidney damaging diseases by following prescribed drug and nutrition therapies can slow progression to end-stage kidney disease.

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23
Q

Stage 1 CKD

A

Patient may have normal GFR >90 but have abnormal urine findings, structural abnormalities or genetic traits that point to kidney disease

Patient is at increase risk for kidney damage from infection, pregnancy, dehydration, and hypotension

Careful management of conditions such as diabetes, hypertension, and hear failure can slow onset and progression

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24
Q

Stage 2 CKD

A

GFR reduced ranging between 60-89
Albuminuria may be present
Kidney nephron damage has occurred.
There may be slight elevations in BUN, serum creatinine, uric acid, and phosphorus

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25
Stage 3 CKD
GFR reduction continue and ranges between 30-59 Albuminuria usually present Nephron damage greater and azotemia reflecting poor waste elimination is present
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Stage 4 CKD
Waste elimination poor GFR 15-29 Manage complication Educate about options for renal replacement therapy
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Stage 5 CKD
End stage kidney disease (ESKD) GFR <15 Kidneys cannot maintain homeostasis Waste elimination poor and without kidney replacement therapy death will result
28
Systemic changes associated with CKD: Metabolic changes
Electrolyte changes Early stages hyponatremia, later stages hypernatremia Hyperkalemia – late stage during diuresis - hypokalemia As more nephrons are lost – METABOLIC ACIDOSIS KUSSMAUL respirations – increases with worsening kidney disease Respiratory system tries to adjust or compensate for increased blood hydrogen, acidosis or decreased pH by increasing rate and depth of breathing causing further acidosis, particularly severe in DKA
29
Systemic changes associated with CKD: cardiac changes
Hypertension Hyperlipidemia (increased triglyceride, total cholesterol, and LDL) Heart failure Pericarditis Hematologic/immunity changes GI changes Cognitive and functional changes
30
CKD incidence
African-Americans are nearly 3X as likely to develop kidney diseases than white populations. Kidney disease linked to HTN.
31
Health promotion and maintenance in pts with CKD
Control diseases that lead to CKD, dietary adjustments, weight maintenance, smoking cessation, exercise, limitation of alcohol
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CKD teaching
Teach adults treated for an infection anywhere in the kidney/urinary system to take all antibiotics as prescribed. Urge adults to drink at least 2 L of water daily unless a health problem requires fluid restriction. Caution adults who use NSAIDs to use the lowest dose for the briefest time period because these drugs interfere with blood flow to the kidney. High-dose and long-term NSAID use reduces kidney function.
33
CKD assessment
Weight and height Daily weights, use same scale, same time of day Medical history, especially of kidney or urologic origin Drug use Dietary habits GI and GU problems Energy level
34
Physical assessment/signs and symptoms in CKD
Neurological and sensory changes Fluid overload Tachypnea and hyperpnea Anemia, abnormal bleeding Foul breath, mouth inflammation or ulceration Osteodystrophy Protein, sediment, or blood in urine Skin discoloration or uremic frost
35
CKD assessment
Laboratory assessment Various blood and urine tests GFR estimated from serum creatinine, age, gender, race, and body size Imaging assessment x-ray findings Kidney or CT scan
36
Patients with CKD are at risk for;
fluid overload, decreased cardiac function, and weight loss due to inability to ingest, digest, or absorb food and nutrients as a result of physiologic factors, potential for infection, injury, fatigue, anxiety, depression
37
Erthropoietin
EPO and reduced RBC production decreased. Risk for anemia Patient may be prescribed Erythropoietin-Stimulating Agents such as: Epoetin Alfa (Epogen or Procrit) injection Signals bone marrow to make more RBCs Monitor Hgb levels – do not give if over 13g/dL
38
Common drugs used in CKD
Loop Diuretics – Lasix Vitamins and minerals Combo bicarb, insulin, glucose if K+ rises too high Folic acid, iron supplements Erythropoietin Stimulating Agents – Epogen (anemia), decreases need for blood transfusion
39
Managing acidosis
Sodium bicarb or calcium carbonate to correct mild acidosis Oral phosphorus binding agents to lower serum phosphate levels such as calcium carbonate or calcium acetate) Aluminum hydroxide for acute hyperphosphatemia Vit D supplements to improve calcium absorption
40
Kidney replacement therapy
Used for patients with loss of kidney function and inadequate waste elimination. Indications: uremia, persistent or rapidly rising high potassium levels (greater than 6.5), severe metabolic acidosis (ph less than 7.1), or fluid overload that inhibits tissue perfusion. If AKI occurs with drug or alcohol intoxication, KRT can also remove toxins
41
Hemodialysis
Most commonly done on intermittent basis. Can be done on inpatient, mostly done on outpatient in a dialysis center. Often done 2-3 times per week – takes approx. 4 hours. Most commonly, patient has a fistula for access. A dialysate and blood flow in opposite directions. The dialysate contains a balanced mix of electrolytes and water resembling human serum. Circulating process continues removing wastes. Blood clotting can occur during the procedure and anticoagulation, usually heparin is delivered into the blood circuit via a pump
42
Vascular access for dialysis
Temporary catheter is placed in a central vein, most often internal jugular. Long term dialysis catheter may be placed by interventional radiology Intermittent done at bedside. Most units are portable and a dialysis machine is brought to the unit
43
Continuous Kidney Replacement (hemofiltration)
is an alternative method for removing wastes ad restoring acid-base balance and fluid and electrolyte balance. Continuous Kidney Replacement is done over 12-24 hours. Hospitalized patients are too unstable to tolerate changes and may be in ICU
44
Dialysis disequilibrium syndrome –
headache, N/V. changes in LOC – thought to be caused by rapid reduction in electrolytes
45
Assessment of the pt receiving hemodialysis
Weight, VS, orthostatic hypotension, vascular access device, LOC, headache, N/V, labs, dialysis disequilibrium syndrome, cardiac symptoms, signs of infection
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Peritoneal Dialysis (PD) route
Siliconized rubber catheter placed into abdominal cavity for infusion of dialysate. Types of PD (selection depends on patient’s ability and lifestyle) Continuous ambulatory Multiple-bag continuous ambulatory Automated Intermittent Continuous-cycle
47
Peritoneal Dialysis (PD)
Usually infused by gravity into peritoneal space over a 10-20 minute period according to patient’s tolerance. Fluid stays in the cavity for a specified time prescribed individually for each patient by the nephrologist. Then fluid flows out of the body (drains) by gravity into a drainage bag. Peritoneal dialysis occurs through diffusion and osmosis across the semipermeable peritoneal membrane and capillaries. There are also machines that can perform peritoneal dialysis including at home machines.
48
Automated Peritoneal Dialysis
Permits in-home dialysis during sleep, allowing the patient to be dialysis free during waking hours. The incidence of peritonitis is reduced with APD because fewer connections and disconnections are needed. Also, APD can be used to deliver larger volumes of dialysis solution for patients who need higher clearances.
49
Intermittent peritoneal dialysis (IPD) 
combines osmotic pressure gradients with true dialysis. The patient usually requires exchanges of 2 L of dialysate at 30- to 60-minute intervals, allowing 15 to 20 minutes of drain time. For most patients, 30 to 40 exchanges of 2 L three times weekly are needed. IPD treatments can be automated or manual.
50
PD complications
Peritonitis Pain Tunnel infections Poor dialysate flow Fibrin clot formation Dialysate leakage Other complications
51
Caring for the patient receiving PD
Before treatment: Evaluate baseline vital signs, weight, laboratory tests Continually monitor patient for respiratory distress, pain, discomfort Monitor prescribed dwell time, initiate outflow Observe outflow amount and pattern of fluid
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Kidney transplant
Candidate selection criteria Free of problems that might raise procedural risk Certain conditions preclude kidney transplant Donors Available kidneys matched based on tissue similarity between donor and recipient Organs from LRDs have highest rates of kidney graft survival Physical criteria must be met
53
Kidney transplant pre-op care
Immunologic studies Dialysis 24 hours before surgery
54
Kidney transplant complications
Many complications possible after kidney transplantation. Early detection and intervention improve the chances for graft survival. Rejection is the most serious complication of transplantation and is the leading cause of graft loss. A reaction occurs between the tissues of the transplanted kidney and the antibodies and cytotoxic T-cells in the recipient's blood. These substances treat the new kidney as a foreign invader and cause tissue destruction, thrombosis, and eventual kidney necrosis. Lifetime anti-rejection medication.
55
Post op care of kidney transplant
Urologic management Assessment of hourly urine output × 48 hours Complications Rejection Thrombosis Renal artery stenosis Other complications Immunosuppressive drug therapy
56
Goals for pt with CKD
Achieve and maintain appropriate fluid and electrolyte balance Maintain an adequate nutrition status Avoid infection at the vascular access site Use effective coping strategies Prevent or slow systemic complications of CKD, including osteodystrophy Report an absence of physical signs of anxiety or depression
57
Urolithiasis
Is the presence of calculi or stones in the urinary tract. Stones often do not cause symptoms until they pass into the lower urinary tract causing severe pain. Stones are particles in the urine that occur in amounts too high to stay dissolved in the urine. Particles precipitate and form calculi
58
Nephrolithiasis
is formation of stones in the kidney
59
Ureterolithiasis
Is formation of stones in the ureter.
60
Stones can cause:
Pain associated with ureteral spasm is excruciating and may cause the patient to go into shock form stimulating nearby nerves Hematuria may result from damage to the urothelial lining If obstruction in not removed, urinary stasis can lead to infection and impair kidney function to side of the blockage As blockage persist, hydronephrosis can result
61
hydronephrosis
Enlargement of kidney and possibly permanent damage
62
Stone formation r/t
Dehydration Obesity Diabetes Gout Calcium, vitamin D and high dose Vitamin C
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Prevention of stone formation:
high intake of fluids, fruit vegetables, low consumption of protein and a balanced intake of fats and carbs
64
Renal Colic –
Severe pain related to stones. Sometimes sudden, unbearable pain, causes N/V, pallor, diaphoresis. A large stationary stone may not cause pain because it is not moving, when stone reaches bladder, frequency and dysuria can occur
65
Urinary tract obstruction
is an emergency and must be treated immediately to preserve kidney function
66
Assessment of pt with calculi
Check for bladder distention Assess pain – onset, location, description, intensity, Pale, ashen, diaphoretic UA – low pH is associated with uric acid and cysteine stones, high pH is associated with calcium phosphate and struvite stones 24 hour urine collection – determine whether supersaturation of common stone particles is present Hematuria WBC and bacteria may be present as a result of urine stasis Serum WBC elevated Current standard for confirmation – CT can
67
Assessment of pt with calculi
Check for bladder distention Assess pain – onset, location, description, intensity, Pale, ashen, diaphoretic UA – low pH is associated with uric acid and cysteine stones, high pH is associated with calcium phosphate and struvite stones 24 hour urine collection – determine whether supersaturation of common stone particles is present Hematuria WBC and bacteria may be present as a result of urine stasis Serum WBC elevated Current standard for confirmation – CT can
68
Managing pt with calculi
Acute nursing interventions focus on promoting comfort and prevent infection and urinary obstruction Most patient expel the stone without invasive procedures The larger the stone and higher up in the urinary tract, the less likely to pass When passed, should be capture if possible for lab analysis
69
Pain management for the pt with renal calculi
Opioids to control severe pain NSAIDS such as ketorolac (Toradol) in acute phase may be effective NSAIDS interfere with renal autoregulation and the risk for impairment is greater in patients with pre-existing kidney disease Also NSAIDS increase risk for bleeding
70
Drug combo for stones
thiazide diuretic and allopurinol combined with high fluid intake. These increase urine volume and decree pH and help increase the excretion of the stones
71
Other interventions for stones
Lithotripsy – extracorporeal shock wave lithotripsy; use of sound, laser, or dry shock waves to break up the stone Surgical management – using a stent to keep ureter open enlarging passage Surgical removal
72
Preventing obstruction –
high intake of fluids and accurate I&O
73
Treat underlying cause –
lower calcium levels with thiazide diuretics or treat gout
74
Education for the pt being treated with calculi
Finish entire prescription of antibiotics Resume usual activities Balance regular exercise with work and rest Return to work 2 days to 6 weeks after surgery depending on type of intervention, personal tolerance, and primary provider’s directives Depending on type of stone – take medications Drink at leas 3L of fluids per day to dilute potential stone-forming crystals, prevent dehydration and promote urine flow
75
Additional education for the pt with renal calculi
Monitor urine pH as directed, expect bruising after lithotripsy, urine may be bloody after surgery for several days, pain in the kidney or bladder region may signal beginning of an infection or formation of another stone. Report pain, fever, chills or difficulty with urination to pcp, keep follow up appointments as directed by primary care provider
76
Normal menses involves minor discomfort, such as:
Breast tenderness, cramping, low back pain, mood swings
77
Dysmenorrhea
Pain associated with menses, one of most common menstrual dysfunctions
78
Dysfunctional uterine bleeding (DUB)
Heavy uterine bleeding that is irregular, painless
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Primary Dysmenorrhea
Hormonal, common in young women with normal menstrual function
80
Primary dysmenorrhea s/s
Pelvic pain that radiates to the groin Low backache lasting 12–48 hours Pain radiating to lower back, thighs Diarrhea Headache Nausea, vomiting Anorexia Breast tenderness Pain begins on first day of menses or 3–5 days before Typically peaks 24 hours after menses begins, decreases in 2–3 days
81
Secondary dysmenorrhea
Related to pathology or diseases of uterus, pelvic area. More likely in women ages 30–50. Pain may occur at any time in menstrual cycle, can be severe. Dull lower abdominal pain radiating to back, down thighs. May begin early in menstrual cycle, last longer than primary dysmenorrhea pain
82
Endometriosis
Most common cause of secondary dysmenorrhea Cells from endometrial tissue implant and grow outside uterus, responding to estrogen and progesterone. Mature, open, bleed each month, causing pain, fibrosis, adhesions. May occur anywhere in body, usually on organs in lower pelvis
83
Dysfunctional uterine bleeding (DUB)
Involves little or no pain. Profuse painless bleeding preceded by long stretches of amenorrhea. Most often associated with anovulatory cycles. Cycles produce thickened endometrial lining that begins irregular sloughing, prolonged heavy bleeding.
84
Primary dysmenorrhea etiology
Caused by release of prostaglandins → uterine contractions to expel menstrual fluid, tissue Other inflammatory mediators may prolong contractions, decrease blood flow. Pain from passage of menstrual tissue, lack of exercise, anxiety about menses Pain may be associated with shape, position of reproductive organs
85
Secondary dysmenorrhea etiology
Caused by abnormalities or disease in the pelvic area, congenital malformations such as tumors, cysts, pelvic adhesions, pelvic inflammatory disease (PID), infections, cervical stenosis, uterine leiomyomas, adenomyosis, endometriosis.
86
Endometriosis etiology
Thought to have genetic component or related to immune dysfunction
87
DUB etiology
Hormonal, similar to abnormal uterine bleeding caused by uterine tumors, endometrial or cervical cancer, polyps, ovarian cysts, bleeding disorders, complications of pregnancy. Causes of abnormal uterine bleeding must be ruled out before diagnosis of DUB can be made
88
Dysmenorrhea risk factors
Early age at menarche Long or heavy menstrual periods Smoking Family history of dysmenorrhea
89
Endometriosis risk factors
Menarche before age 11 Cycle length <27 days Heavy or prolonged menses Sedentary lifestyle Increased dietary fat First-degree relative with endometriosis
90
DUB risk factors
Age Teens, early 20s Approaching menopause Stress Extreme weight changes Obesity Thyroid disease Metabolic disorders Use of hormone replacement therapy (HRT) or some types of hormonal contraceptives Use of intrauterine contraception (IUC) device
91
Prevention
Lifestyle changes may benefit patients at risk for them: Balanced diet, avoiding sugary and salty foods Avoiding caffeine, alcohol, cigarettes Regular exercise and stress-relieving activities Healthy, gradual weight loss for overweight patients Once diagnosis has been made, prevention of future episodes depends on Long-term maintenance of prescribed treatment regimen Even in absence of symptoms
92
Focuses of care
Identify underlying cause Reestablish functional capacity Manage pain
93
Focus of care of woman with DUB
Identify, treat underlying disease, hormonal disorder Patient to keep diary of menstrual patterns to help diagnose cause
94
Pharmacologic therapy for dysmenorrhea
Combined oral contraceptives (COCs), Depo-Provera, danazol, or gonadotropin-releasing hormone (GnRH) agonists to suppress ovulation COCs and progesterone injections to relieve cramping Nonsteroidal anti-inflammatory drugs (NSAIDs) to relieve cramping Selective serotonin reuptake inhibitors (SSRIs) to manage mood, help patient cope with chronic pain Diuretics to relieve bloating
95
To correct menstrual irregularities
COCs for anovulatory DUB Depo-Provera to regulate uterine bleeding Hormonal IUCs to control irregular bleeding Conjugated estrogens and medroxyprogesterone for heavy bleeding Oral iron supplements to replace iron lost through bleeding
96
ED s/s
– Inability of male to attain or maintain erection sufficient for sexual intercourse – May involve total or inconsistent inability to achieve erection or ability to sustain erection only briefly – Penis may become semi-erect but lack sufficient rigidity for intercourse
97
ED characteristics
– Characterized as disorder of arousal – May or may not be associated with loss of libido – Occurs in men of all ages – Can be chronic, intermittent, or episodic
98
ED dx:
Medical diagnosis: dysfunction present ≥3 months Psychiatric diagnosis: dysfunction present ≥6 months
99
ED risks
Older men affected at higher rates – Rates for chronic or complete ED lower than those for occasional ED
100
ED causes:
Vascular, neurologic, urologic, endocrine, respiratory, iatrogenic, lifestyle related, psychologic, aging process
101
Aging process r/t ED
Less elastic collagen in penis interferes with veno-occlusive mechanism Declining ability of skin to sense vibrotactile stimulation Hypogonadism → decreased testosterone Likelihood of chronic conditions that are linked to ED
102
Prevention of ED
▪ Regular exercise ▪ Balanced diet ▪ Healthy body weight ▪ Abstaining from tobacco, alcohol – Mitigation of risk factors specific to particular patients ▪ Men with diabetes: maintain appropriate blood glucose levels ▪ Men with depression: seek counseling – Many medications used to treat problems related to ED can themselves produce erectile problems as side effect
103
Medications for ED
–Oral, injection into penis, or insertion into urethra –Oral medications: sildenafil citrate (Viagra), vardenafil hydrochloride (Levitra), tadalafil (Cialis), avanafil (Stendra) ▪ Injectable medications for ED –Alprostodil –Difficult to administer, used for patients who cannot take oral drugs