NR 508 Week 2 TD and Quiz
PART 1: (Ch 17, 18, 21, 24, 52, 53)
Cynthia is a 65-year-old African American female who presents to the
clinic for a check-up. Her last examination was ~5 years ago. She has no
specific, significant, or urgent complaint. She explains that her only
issues are thirst, fatigue, and leg numbness and tingling, which is
beginning to occur more often. You decide to do a physical exam, as
well as draw labs and receive the following results:
Social history: no smoking or alcohol consumption.
Physical examination:
GEN: well nourished, slightly obese female
VS: BP 180/103 HR 73 RR 13 T 98.4 Weight 90 kg,
Height 5’6”
HEENT: PERRLA
COR: RRR (regular rate & rhythm), NMRG (No
murmur (valve), rub (friction/fluid around
pericardium), gallop (valve))
CHEST: CTA
NEURO: monofilament test shows decreased
peripheral sensation
EXT: normal
Laboratory (fasting):
Na 139 mEq/L N (135-145)
K 3.8 mEq/L N (3.5-5)
ALT 34 U/L N (0-40)
Ca 9.1 mg/dL N (8.6-10)
CL 102 mmol/L N (95-105)
HCO3 22 mEq/L N (22-28)
AST 39 U/L N (0-40)
TP 6 g/dL T. Pro?? N (5.6-8.4)
BUN 33 mg/dL H (8-21)
SCr 2.0 mg/dL H (0.5-1.5)
Alb 4.1 g/dL N (3.2-4.8)
Cholesterol 254 mg/dL H (<200)
BG 300 mg/dL H
, TSH 0.12 mU/mL L (0.4-4.8)
UA: SG 1.013 mg/24h (N), pH 6.5 (N), +++ protein
(from DM and hyperthyroidism)
UR SG 1.002 – 1.030, pH 4.6-7.9
What are the major problems in this patient, and what diagnoses do
these values indicate? HTN, DM, Hyperlipidemia, Diabetic peripheral
neuropathy, Hyperthyroidism, proteinuria?
Additionally, what is your assessment and pharmacological plan for
each of these problems including the medication, dose, and mechanism
of action?
Cynthia, a 55-year-old African American female, presents to the office with
complaints of polydipsia, fatigue, and frequent leg numbness and tingling.
Upon examination, Cynthia is found to have a BMI of 32, elevated blood
pressure, and decreased peripheral sensation. Based on her physical exam,
blood and urine lab work are ordered. Cynthia’s lab work and the physical
exam reveal a number of issues including chronic kidney disease (CKD),
hypertension (HTN) secondary to CKD, hyperthyroidism, diabetes mellitus
type 2 (DM2) that is uncontrolled, diabetic peripheral neuropathy,
hyperlipidemia, proteinuria, fatigue, polydipsia, and obesity. Cynthia’s major
problems along with the pharmacological plan will be addressed below.
Chronic kidney disease, stage 3B (calculated GFR of 30mL/min/1.73 m2,
Calculated creatinine clearance (CrCl) = 26-32 mL/min): Angiotensin-
converting enzyme (ACE) inhibitors aid renal functions in hypertensive
patients by way of angiotensin II and autoregulation of the glomerular
filtration rate (GFR) (Mann & Hilgers, 2017). Angiotensin II causes
constriction at the afferent and efferent arterioles and causes a beneficial
increase in the efferent resistance (Mann & Hilgers, 2017). This is beneficial
because it causes an increase or stabilization in intraglomerular pressure,
which helps maintain or increase the GFR (Mann & Hilgers, 2017). Using an
ACE inhibitor to lower hypertension in patients with renal disease will also
reduce or regulate intraglomerular pressure (Mann & Hilgers, 2017).
An ACE inhibitor will be ordered to aid in renal function as well as for her
HTN.
, HTN, secondary to CKD: Weight loss via diet and exercise are a must.
Approximately 80 to 85 percent of CKD patients also have HTN (Mann,
2016). Using an ACE inhibitor to lower hypertension in patients with renal
disease will also reduce or regulate intraglomerular pressure (Mann & Hilgers,
2017). We must also consider the patient has DM2 when prescribing HTN
medications. An ACE or an angiotensin II receptor blocker (ARB) is the
preferred HTN medications for patients with comorbidities of DM, with the
ACE being the preferred method. Thiazide diuretics can have an adverse effect
on the metabolism of glucose, therefore they are not the preferred choice of
treatment for patients with HTN and DM (Bakris, 2017). Some patients may
need more help controlling their BP; in this case, a combination of an ACE (or
ARB) along with a dihydropyridine calcium channel blocker (CCB) such as
amlodipine has proven effective (Bakris, 2017).
Considering this patient has HTN, DM2, and CKD, an ACE inhibitor would be
the treatment of choice. I would prescribe Lisinopril 40mg daily for Cynthia’s
HTN and CKD. I would have Cynthia keep a BP log and return in 1 week for a
follow up and evaluation of BP.
Hyperthyroidism: This is a serious discussion that must be had with the
patient, with the best options of treatment explained. After thorough
explanation I would let the patient decide the treatment option. The two best
options are Methimazole or Radioactive Iodine (RAI).
Methimazole, a thioamides, inhibits iodine from binding and coupling to
tyrosine, which inhibits the synthesis of thyroid hormone. Methimazole does
not destroy the thyroid and therefore has little risk of causing permanent
hypothyroidism. The major downfall is that it does not provide a cure, only
symptom management with the hope of remission (Schneider et al., 2014). If
the patient chooses this option, standard dosing is Methimazole 30-40mg daily
for 4-8 weeks where the dose is decreased by 1/3 every month until
maintenance dose is achieved. The maintenance dose is 5-10mg daily.
Radioactive Iodine (RAI) is considered to be a permanent, cost-effective
option because it either destroys or removes all tissue portions of the thyroid
that are hyperactive (Schneider et al., 2014). RAI is given orally in the form of
sodium iodine (131-I) in either a capsule or a solution (Ross, 2017). The RAI
is quickly integrated into the thyroid, which results in considerable tissue
damage from the beta emissions (Ross, 2017). Ultimately, it causes erosion of
PART 1: (Ch 17, 18, 21, 24, 52, 53)
Cynthia is a 65-year-old African American female who presents to the
clinic for a check-up. Her last examination was ~5 years ago. She has no
specific, significant, or urgent complaint. She explains that her only
issues are thirst, fatigue, and leg numbness and tingling, which is
beginning to occur more often. You decide to do a physical exam, as
well as draw labs and receive the following results:
Social history: no smoking or alcohol consumption.
Physical examination:
GEN: well nourished, slightly obese female
VS: BP 180/103 HR 73 RR 13 T 98.4 Weight 90 kg,
Height 5’6”
HEENT: PERRLA
COR: RRR (regular rate & rhythm), NMRG (No
murmur (valve), rub (friction/fluid around
pericardium), gallop (valve))
CHEST: CTA
NEURO: monofilament test shows decreased
peripheral sensation
EXT: normal
Laboratory (fasting):
Na 139 mEq/L N (135-145)
K 3.8 mEq/L N (3.5-5)
ALT 34 U/L N (0-40)
Ca 9.1 mg/dL N (8.6-10)
CL 102 mmol/L N (95-105)
HCO3 22 mEq/L N (22-28)
AST 39 U/L N (0-40)
TP 6 g/dL T. Pro?? N (5.6-8.4)
BUN 33 mg/dL H (8-21)
SCr 2.0 mg/dL H (0.5-1.5)
Alb 4.1 g/dL N (3.2-4.8)
Cholesterol 254 mg/dL H (<200)
BG 300 mg/dL H
, TSH 0.12 mU/mL L (0.4-4.8)
UA: SG 1.013 mg/24h (N), pH 6.5 (N), +++ protein
(from DM and hyperthyroidism)
UR SG 1.002 – 1.030, pH 4.6-7.9
What are the major problems in this patient, and what diagnoses do
these values indicate? HTN, DM, Hyperlipidemia, Diabetic peripheral
neuropathy, Hyperthyroidism, proteinuria?
Additionally, what is your assessment and pharmacological plan for
each of these problems including the medication, dose, and mechanism
of action?
Cynthia, a 55-year-old African American female, presents to the office with
complaints of polydipsia, fatigue, and frequent leg numbness and tingling.
Upon examination, Cynthia is found to have a BMI of 32, elevated blood
pressure, and decreased peripheral sensation. Based on her physical exam,
blood and urine lab work are ordered. Cynthia’s lab work and the physical
exam reveal a number of issues including chronic kidney disease (CKD),
hypertension (HTN) secondary to CKD, hyperthyroidism, diabetes mellitus
type 2 (DM2) that is uncontrolled, diabetic peripheral neuropathy,
hyperlipidemia, proteinuria, fatigue, polydipsia, and obesity. Cynthia’s major
problems along with the pharmacological plan will be addressed below.
Chronic kidney disease, stage 3B (calculated GFR of 30mL/min/1.73 m2,
Calculated creatinine clearance (CrCl) = 26-32 mL/min): Angiotensin-
converting enzyme (ACE) inhibitors aid renal functions in hypertensive
patients by way of angiotensin II and autoregulation of the glomerular
filtration rate (GFR) (Mann & Hilgers, 2017). Angiotensin II causes
constriction at the afferent and efferent arterioles and causes a beneficial
increase in the efferent resistance (Mann & Hilgers, 2017). This is beneficial
because it causes an increase or stabilization in intraglomerular pressure,
which helps maintain or increase the GFR (Mann & Hilgers, 2017). Using an
ACE inhibitor to lower hypertension in patients with renal disease will also
reduce or regulate intraglomerular pressure (Mann & Hilgers, 2017).
An ACE inhibitor will be ordered to aid in renal function as well as for her
HTN.
, HTN, secondary to CKD: Weight loss via diet and exercise are a must.
Approximately 80 to 85 percent of CKD patients also have HTN (Mann,
2016). Using an ACE inhibitor to lower hypertension in patients with renal
disease will also reduce or regulate intraglomerular pressure (Mann & Hilgers,
2017). We must also consider the patient has DM2 when prescribing HTN
medications. An ACE or an angiotensin II receptor blocker (ARB) is the
preferred HTN medications for patients with comorbidities of DM, with the
ACE being the preferred method. Thiazide diuretics can have an adverse effect
on the metabolism of glucose, therefore they are not the preferred choice of
treatment for patients with HTN and DM (Bakris, 2017). Some patients may
need more help controlling their BP; in this case, a combination of an ACE (or
ARB) along with a dihydropyridine calcium channel blocker (CCB) such as
amlodipine has proven effective (Bakris, 2017).
Considering this patient has HTN, DM2, and CKD, an ACE inhibitor would be
the treatment of choice. I would prescribe Lisinopril 40mg daily for Cynthia’s
HTN and CKD. I would have Cynthia keep a BP log and return in 1 week for a
follow up and evaluation of BP.
Hyperthyroidism: This is a serious discussion that must be had with the
patient, with the best options of treatment explained. After thorough
explanation I would let the patient decide the treatment option. The two best
options are Methimazole or Radioactive Iodine (RAI).
Methimazole, a thioamides, inhibits iodine from binding and coupling to
tyrosine, which inhibits the synthesis of thyroid hormone. Methimazole does
not destroy the thyroid and therefore has little risk of causing permanent
hypothyroidism. The major downfall is that it does not provide a cure, only
symptom management with the hope of remission (Schneider et al., 2014). If
the patient chooses this option, standard dosing is Methimazole 30-40mg daily
for 4-8 weeks where the dose is decreased by 1/3 every month until
maintenance dose is achieved. The maintenance dose is 5-10mg daily.
Radioactive Iodine (RAI) is considered to be a permanent, cost-effective
option because it either destroys or removes all tissue portions of the thyroid
that are hyperactive (Schneider et al., 2014). RAI is given orally in the form of
sodium iodine (131-I) in either a capsule or a solution (Ross, 2017). The RAI
is quickly integrated into the thyroid, which results in considerable tissue
damage from the beta emissions (Ross, 2017). Ultimately, it causes erosion of
