Transcript Case study: Neck Pain

CASE STUDY: SILENT DISEASE
Fran Connolly FNP- S
PATIENT & ENCOUNTER
B.H. is a 57 year old white female who presents in her gynecology
office (Capital Region OB/GYN) for her annual exam.
Her initial visit occurred on 2/10/2015.
She had no complaints.
The only significant finding on her ROS was her 24 hour dietary review
which consisted of eating ½ gallon of ice cream nightly and 3 nights a
week it was her dinner.
HISTORY OF PRESENT ILLNESS
Initial visit to her Primary Care Physician was on 1/6/15
At that visit she had routine lab work done which consisted
of a CBC with diff, CMP, thyroid panel, cholesterol, and
HgA1c.
With results of her labs, her PCP ordered an U/S which was
completed on 2/2/15.
She had no complaints at her PCP visit as well.
INITIAL PLAN
Lifestyle Modification to include:
Dietary changes
Exercise
MEDICAL HISTORY
General: Good health, last physical 12/2014.
Hypertension, hyperlipidemia (Pt. denies this). Bladder polyp removal
9/2011
Denies all other history including HTN, hyperlipidemia, stroke, migraines,
lung disease, asthma, liver, kidney or gallbladder disease, cancer,
diabetes, hepatitis, TB or psychiatric disorders.
Denies history of accidents or injuries.
Unsure of childhood vaccines. Influenza 10/2014, Tdap 8/2009.
Allergies: Sulfa (rash), PCN (rash). Denies any allergies to food, latex or
environment.
No medications. Pt refuses to take any medications. Has been
recommended to start anti-hypertensives.
MEDICAL HISTORY
SOCIAL HISTORY
Married
No living children. Stillborn 1986
Retired from NYS as
administrative assistant.
Denies smoking, illicit drug use
and any alcohol use.
Caffeine: 1-2 cups coffee and 35 cans of Pepsi daily.
Very sedentary. Denies any
exercise. Enjoys watching T.V. and
reading.
Calcium: milk, yogurt, cheese
daily. Ice cream ½ gallon daily.
Sleeps 7-8 hours night.
FAMILY HISTORY
Mother: deceased at 65 from
breast cancer
Father: deceased at 87 “old age”
Sister: hypertension,
hyperlipidemia
Grandparents: unknown
Denies any family history of
bleeding/clotting disorders,
seizures and neurological
disorders. Denies any family
history of pulmonary disease.
Denies psychiatric, liver or kidney
disease, hepatitis, endocrine,
infectious diseases, or polio.
REVIEW OF SYSTEMS
General: States she is in good health. Denies any fever, chills, malaise,
night sweats, or appetite or weight change. .
Skin: Denies any rashes, changes in moles, tick bites, pigmentation or
texture changes, or excessive sweating.
Head: Denies any headache, dizziness, syncope, or head injuries.
Neck: Denies any lumps, swollen glands, pain or stiffness, trauma, or
change in range of motion.
Respiratory: Denies any pain, dyspnea, wheezing, or shortness of
breath.
Heart: Denies any chest pain, murmurs, palpitations, or edema.
Gastrointestinal: Denies any change in appetite. No intolerance to food,
dysphasia, heartburn, nausea, or vomiting. Bowels regular; denies any
constipation, diarrhea, hemorrhoids, or jaundice.
REVIEW OF SYSTEMS
Genitourinary: Denies any difficulty urinating, burning, discharge,
nocturia, polyuria.
Female Genitourinary: Denies any pain, unusual bleeding, discharge.
Ammenorrhea. Menopause 4 years ago. Last Pap smear 2013. Not
sexually active. Denies libido.
Breast: Denies any lumps, pain, masses or tenderness. The patient
reports that she does perform self-breast exams, but she is not
consistent. .
Hematological: Denies any past diagnosis of disease, anemia, easy
bleeding or bruising.
Endocrine: + hot flashes occasionally. Denies any heat or cold
intolerances, excessive thirst or hunger, or polyuria.
Psychiatric: Denies any depression, anxiety, or mood changes. Denies
any suicidal or homicidal ideations.
PHYSICAL FINDINGS
Constitutional: BP180/95, repeat 162/92 after exam, HR 85, RR 18,
T98.1, denies pain.
Ht: 5’4” Wt: 163 lbs BMI: 26
General: Well nourished, well developed, well hydrated, slightly overweight. Alert & oriented x 3. Not in acute distress. Appropriate mood
and affect. Skin: Pink, warm & dry. No rashes or lesions.
Skin: Pink, warm, and dry. No rashes, moles or lesions.
Head: Normocephalic, symmetric, no lesions. Hair grey & course, even
distribution.
Neck/Lymph: Supple with full range of motion. Trachea midline. No
carotid bruits. No lymphadenopathy. Thyroid not palpable.
Thorax/Lungs: Pt sitting upright, Resp resting 18/min, regular and even;
Chest expansion symmetric. Lungs clear with auscultation
anteriorly/posteriorly in all lobes. No rales, rhonchi, or wheezing.
PHYSICAL FINDINGS
CV/PV: S1 S2 present in APETM with bell and diaphragm. Regular
apical rate. No heaves or thrills. No murmurs, rubs, gallops, or clicks.
RRR. Extremities pink, warm to touch without edema.
Abdomen: Rounded, no lesions, bulges, scars/striae, masses or rashes.
Smooth, pink, even color, hair with even distribution. Movement only with
respirations. Umbilicus inverted, midline. No hernia visible. BS x 4
quadrants. No bruits. Percussion yields tympany in all 4 quadrants. Abd
soft, no tenderness, no guarding, no masses, organomegaly or
herniations. No CVA tenderness. No rebound tenderness.
Breasts: Pendulous, symmetrical with no visible lesions, dimpling or lumps.
Breast exam performed sitting and supine with hands overhead. No
lumps or masses palpated. No lymphadenopathy present on breast, tail
or axilla, no tenderness with palpation. Nipples present, equal, no
discharge.
Female: Pubic hair grey, distribution scattered. Vaginal wall pink, moist,
and well rugated without lesions. Introitus pale pink, dry. Cervix
visualized, pink, without lesions, and negative for cervical motion
tenderness on palpation. No blood or discharge present.
DIFFERENTIAL DIAGNOSIS
Viral Hepatitis (070.9)
Alcohol Hepatitis (571.1)
Hemochromatosis (275.03)
Wilson Disease (275.1)
Cirrhosis (571.5)
Autoimmune Hepatitis (571.42)
Celiac Disease (579.0)
Hypertension (401.9)
Hyperlipidemia (272.4)
DIAGNOSTIC/LAB TESTS
Labs: CBC with differential, CMP, cholesterol panel, thyroid panel,
HgA1c, PT/INR, iron panel, hepatitis panel
- AST 111 (mild to moderate increase)
- ALT 134 (mild to moderate increase)
- ALT/AST Ratio: 1.2 (usually >1 in NASH <2)
- Alkaline Phosphate 96
- total bilirubin 0.7
- triglycerides 170
- HDL 40
- LDL 122
- total cholesterol 268
Abdominal U/S of RUQ: patterns of fatty liver infiltrates in the right
lobe of liver
Doppler studies to evaluate patency of the venous system
CT scan and MRI of abdomen
Biopsy if indicated
(Albeldawi, 2014 & Dunphy, Winland-Brown, Porter & Thomas, 2011)
DIAGNOSIS
Nonalcoholic Steatohepatitis (NASH) (571.9)
A.K.A. Nonalcoholic Fatty Liver Disease (NAFLD)
Hypertension (401.9)
Hyperlipidemia (272.4)
Menopausal Status (V49.81)
NONALCOHOLIC STEATOHEPATITIS (NASH)
The term for nonalcoholic fatty liver disease (NAFLD) which can lead to
cirrhosis and end-stage liver disease.
NASH can range from fatty infiltrates of the liver to steatosis with
inflammation and hepatocyte necrosis.
Clinical diagnosis requires:
- hepatic steatosis by imaging/histology
- no significant alcohol consumption
- no competing etiologies
- no coexisting causes for chronic liver disease
NASH is the most severe form of NAFLD.
Coexistent conditions that are associated with NASH are obesity, DM2,
metabolic syndrome and hyperlipidemia.
(Albeldawi, 2014 & Porth, 2011)
ETIOLOGY
The cause is unknown, but linked to obesity, insulin resistance and
metabolic syndrome.
Insulin resistance is the most important trigger of fatty liver disease and
NASH.
These conditions can remain stable for years and therefore progression
may come when another comorbidity appears.
Triggers can include cytokine-mediated inflammation, lipid peroxidation
and apoptosis.
(Albeldawi, 2014)
INCIDENCE
There is a worldwide distribution and is the most common form of
chronic liver disease in the Western world.
NAFLD affects 6.3-33% and NASH 3-17% of people in the US.
9-20% of NASH patients develop cirrhosis.
22-33% of cirrhotics die of complications of liver failure or
require liver transplant.
The increase in prevalence is on track with the epidemic in
obesity and DM.
Predominant age group 50-60’s
The presence of metabolic syndromes can increase the future
development of NASH by 4-11 fold.
(Albeldawi, 2014)
RISK FACTORS
Obesity
- associated in 25-93% of patients with NASH
Diabetes
- present in 30-50% of patients with NASH
Hyperlipidemia
- found in up to 92% of patients with NASH
Less common risk factors: hypothyroidism, hypopituitarism,
sleep apnea, and polycystic ovarian syndrome.
(Albeldawi, 2014 & Porth, 2011)
PATHOPHYSIOLOGY
NASH is a lipid accumulation within hepatocytes and formation of free
radicals.
The primary metabolic abnormalities that lead to this accumulation is yet
to be fully discovered, but thought to include shifts in the pathways for
uptake, synthesis, degradation, or secretion of hepatic lipids resulting from
insulin resistance.
When insulin resistance develops, free fatty acids are inappropriately
shifted to non adipose tissue including the liver. The insulin resistance also
decreases the inhibition of lipolysis and increase lipogenesis.
Obesity increases the synthesis and reduces oxidation of free fatty acids.
When the capacity of the liver to export triglyceride is exceeded, excess
fatty acids are deposited within the liver, hence the development of
steatosis.
(Albeldawi, 2014 & Porth, 2011)
SIGNS & SYMPTOMS
Usually asymptomatic and an incidental finding on annual exam which can
include an enlarged liver on exam and increased liver enzymes on labs.
-Fatigue/Malaise
-Discomfort RUQ of abdomen
-Hepatomegaly is present in 75% of patients with NASH
Once advanced: Can include weakness, nausea, anorexia, weight loss, fatigue,
malnutrition, puritis, jaundice, edema, menstrual abnormalities, loss of libido,
impotence, sterility, gynomastia, enlarged firm liver edge palpable below the
right costal margin.
- Ascites
- Varices
- Encephalopathy
(Albeldawi, 2014 & Dunphy, Winland-Brown, Porter & Thomas, 2011)
INTERVENTIONS
The aim of treatment is to slow progression of the disease and prevent
liver related illness.
Treat associated comorbidities such as cholesterol, DM, & obesity.
Medications should be restricted to patients at risk for developing
advanced liver disease.
There is no evidenced-based medications proven to treat NASH.
Vitamin E 800 IU daily improves liver histology (1st Line therapy)
OTC Medications: MVI, Vitamin B12, folate, thiamine, magnesium, milk
thistle and zinc
Liver biopsy for definitive diagnosis and staging
Bariatric surgery for weight loss (which can also cause NASH)
Liver transplant. Although NASH can redevelop after transplantation
(Albeldawi, 2014 & Porth, 2011)
EDUCATION
Dietary education
- Protein intake should be increased to 1-1.5 grams per kg daily
- Restrict calories, carbohydrates
- Avoid alcohol
Exercise education
With progression:
- daily weights to monitor for fluid retention and ascites
- medications to avoid Tylenol, Vitamin A, Tetracycline, Dilantin
(Albeldawi, 2014, Dunphy, Winland-Brown, Porter & Thomas, 2011 & Porth, 2011)
FOLLOW-UP
Should be regular monitoring to detect progression through
physical exam, labs, symptoms and diagnostics.
Referral to registered dietitian or nutritionist
Consult Hepatologist
Consult Gastroenterologist
(Albeldawi, 2014 & Porth, 2011)
REFERENCES
Albeldawi, M. (2014). The 5-minute clinical consult 2014 (22nd ed.).
Lippincott, Williams & Wilkins, Philadelphia, PA.
Dunphy, L.M., Winland-Brown, J.E., Porter, B.O. & Thomas, D.J. (2011).
Primary care: The art and science of advanced practice nursing (3rd ed.).
Philadelphia, PA: F. A. Davis Company.
Porth, C.M. (2011). Essentials of Pathophysiology (3rd ed.). Philadelphia,
PA: Lippincott Williams & Wilkins