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Hypothyroidism: A Clinical Case Review
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A 53-year-old woman presents to her primary care provider with complaints of fatigue, weight gain, and constipation. She states that her weight has gradually increased over the last year despite no change in her activity level or eating habits. She works roughly 8 hours a day as a nutrition assistant, but she falls asleep as soon as she gets home in the afternoon.
She lacks motivation to do anything during the weekend, and notes that she does not feel like herself. Upon questioning, the patient reports the following changes: thinning of her scalp hair, brittle nails, dry skin, and cold intolerance. Physical examination confirms dry skin, brittle nails, coarse and dry hair, and abdominal distension. The only medication she takes is a multivitamin daily. She has a positive family history for autoimmune disorders and stroke.
Normal Thyroid Anatomy and Physiology
The thyroid gland is a small, butterfly-shaped gland located in the neck, under the trachea. 1 The thyroid functions as an endocrine gland and produces thyroid hormones and calcitonin, which are responsible for controlling metabolism, growth, and serum electrolyte concentrations. 1
Similar to other endocrine glands, the thyroid has a regulatory feedback system that starts in the hypothalamus, where thyrotropin-releasing hormone is released into the hypothalamic-hypophyseal portal system and transported to the anterior pituitary gland. 2 Thyrotropin-releasing hormone then stimulates the pituitary gland to release thyroid-stimulating hormone (TSH). 2 TSH travels to the thyroid and binds to receptors located on the follicular cells of the thyroid gland, where it activates a cascade of events inside the follicular cells that ultimately cause the release of thyroxine (T4) and triiodothyronine (T3), the thyroid hormones. 2,3 It is important to note that although the thyroid does produce and release both T4 and T3, most of T3 is made in the periphery via the deiodination of T4. 3
This cascade of hormones is regulated by a negative feedback system: when the levels of T4 and T3 increase in the bloodstream, they travel back to the hypothalamus and pituitary to signal them to stop releasing their respective hormones. 2 When the levels of T4 and T3 decrease, the hypothalamus and pituitary return to secreting thyrotropin-releasing hormone and TSH, respectively. 2
Epidemiology of Hypothyroidism
Hypothyroidism, the condition in which the thyroid gland does not produce enough hormone, occurs in approximately 4.6% of the population in the United States. 4 The vast majority of cases involve women (85%). 1,3 Thyroid deficiency compromises almost all body functions, and if left undiagnosed or untreated, it can lead to infertility, Hashimoto encephalopathy, and myxedema coma. 3,5-7
Autoimmune dysfunction is one of the major causes of thyroid disease. 8 In the case of hypothyroidism, Hashimoto thyroiditis is the most common autoimmune presentation. It is characterized by infiltration of the thyroid by T and B lymphocytes. 8 This leads to thyroiditis, an inflammatory reaction of the thyroid gland that leads to the production of antibodies to thyroid antigens, thyroid peroxidase, and thyroglobulin. Ultimately, the follicular cells of the thyroid are destroyed, thereby interfering with thyroid hormone synthesis. 8
Risk factors for developing Hashimoto thyroiditis include iodine consumption, smoking, radiation exposure, female sex, aging, and genetics. 8 Those with autoimmune thyroid disease are more likely to have other autoimmune disorders (polyautoimmunity). Polyautoimmunity is so common that guidelines now recommend searching for other autoimmune disorders in patients with autoimmune thyroid disease, as well as poor treatment outcomes, before initiating combination therapy for hypothyroidism. 8
Signs and Symptoms
The manifestation of hypothyroidism can vary markedly from patient to patient. At this time, no clear guidelines exist for screening for hypothyroidism. The US Preventive Services Task Force does not recommend screening patients for thyroid dysfunction. 9 Other associations, including the American Academy of Family Physicians and the American College of Physicians, suggest screening for thyroid dysfunction only in women older than 60 years. 10 Some clinicians may find it reasonable to screen all patients at risk for hypothyroidism. 10 Those at risk include patients with other autoimmune disorders, history of radiation exposure, or family history of thyroid disease; women; and those 60 years of age or older. 3
Symptoms of hypothyroidism are nonspecific and reflect the generalized slowing of the metabolic processes and include fatigue, lethargy, cold intolerance, and weakness. 3 Signs and symptoms secondary to matrix glycosaminoglycan accumulation include coarse and dry hair, puffy eyelids and face, enlargement of the tongue, and hoarseness (Table 1). 3,11,12 Of note, older patients often present with symptoms that could be attributed to other conditions, whereas younger patients usually display signs and symptoms more typical of hypothyroidism. 12 Physical signs include an enlarged thyroid, bradycardia, hypertension, and slow relaxation phase of deep tendon reflexes. 3 Thinning of the outer halves of the eyebrows, also known as Queen Anne sign, and galactorrhea are rare additional findings. 3
Clinicians must exclude a multitude of other disorders that mimic hypothyroidism, especially in older patients. The differential diagnosis includes anemia, other autoimmune disorders, chronic fatigue syndrome, constipation, depression, early menopause, adrenal dysfunction, normal aging processes, and pituitary dysfunction. 9,13
Our patient presented early in the course of her condition and had many of the typical symptoms of hypothyroidism. Her family history of other autoimmune disorders was an additional clue. Her presentation led her provider to order a series of tests to help in diagnosis.
From the January/February 2020 Issue of Clinical Advisor
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Case Study: 60-Year-Old Female Presenting With Shortness of Breath
Case presentation.
The patient is a 60-year-old white female presenting to the emergency department with acute onset shortness of breath. Symptoms began approximately 2 days before and had progressively worsened with no associated, aggravating, or relieving factors noted. She had similar symptoms approximately 1 year ago with an acute, chronic obstructive pulmonary disease (COPD) exacerbation requiring hospitalization. She uses BiPAP ventilatory support at night when sleeping and has requested to use this in the emergency department due to shortness of breath and wanting to sleep.
She denies fever, chills, cough, wheezing, sputum production, chest pain, palpitations, pressure, abdominal pain, abdominal distension, nausea, vomiting, and diarrhea.
She reports difficulty breathing at rest, forgetfulness, mild fatigue, feeling chilled, requiring blankets, increased urinary frequency, incontinence, and swelling in her bilateral lower extremities that are new-onset and worsening. Subsequently, she has not ambulated from bed for several days except to use the restroom due to feeling weak, fatigued, and short of breath.
There are no known ill contacts at home. Her family history includes significant heart disease and prostate malignancy in her father. Social history is positive for smoking tobacco use at 30 pack years. She quit smoking 2 years ago due to increasing shortness of breath. She denies all alcohol and illegal drug use. There are no known foods, drugs, or environmental allergies.
Past medical history is significant for coronary artery disease, myocardial infarction, COPD, hypertension, hyperlipidemia, hypothyroidism, diabetes mellitus, peripheral vascular disease, tobacco usage, and obesity. Past surgical history is significant for an appendectomy, cardiac catheterization with stent placement, hysterectomy, and nephrectomy.
Her current medications include fluticasone-vilanterol 100-25 mcg inhaled daily, hydralazine 50 mg by mouth, 3 times per day, hydrochlorothiazide 25 mg by mouth daily, albuterol-ipratropium inhaled every 4 hours PRN, levothyroxine 175 mcg by mouth daily, metformin 500 mg by mouth twice per day, nebivolol 5 mg by mouth daily, aspirin 81 mg by mouth daily, vitamin D3 1000 units by mouth daily, clopidogrel 75 mg by mouth daily, isosorbide mononitrate 60 mg by mouth daily, and rosuvastatin 40 mg by mouth daily.
Physical Exam
Initial physical exam reveals temperature 97.3 F, heart rate 74 bpm, respiratory rate 24, BP 104/54, HT 160 cm, WT 100 kg, BMI 39.1, and O2 saturation 90% on room air.
Constitutional: Extremely obese, acutely ill-appearing female. Well-developed and well-nourished with BiPAP in place. Lying on a hospital stretcher under 3 blankets.
HEENT:
- Head: Normocephalic and atraumatic
- Mouth: Moist mucous membranes
- Macroglossia
- Eyes: Conjunctiva and EOM are normal. Pupils are equal, round, and reactive to light. No scleral icterus. Bilateral periorbital edema present.
- Neck: Neck supple. No JVD present. No masses or surgical scarring.
- Throat: Patent and moist
Cardiovascular: Normal rate, regular rhythm, and normal heart sound with no murmur. 2+ pitting edema bilateral lower extremities and strong pulses in all four extremities.
Pulmonary/Chest: No respiratory status distress at this time, tachypnea present, (+) wheezing noted, bilateral rhonchi, decreased air movement bilaterally. The patient was barely able to finish a full sentence due to shortness of breath.
Abdominal: Soft. Obese. Bowel sounds are normal. No distension and no tenderness
Skin: Skin is very dry
Neurologic: Alert, awake, able to protect her airway. Moving all extremities. No sensation losses
Initial Evaluation
Initial evaluation to elucidate the source of dyspnea was performed and included CBC to establish if an infectious or anemic source was present, CMP to review electrolyte balance and review renal function, and arterial blood gas to determine the PO2 for hypoxia and any major acid-base derangement, creatinine kinase and troponin I to evaluate the presence of myocardial infarct or rhabdomyolysis, brain natriuretic peptide, ECG, and chest x-ray. Considering that it is winter and influenza is endemic in the community, a rapid influenza assay was obtained as well.
Largely unremarkable and non-contributory to establish a diagnosis.
Showed creatinine elevation above baseline from 1.08 base to 1.81, indicating possible acute injury. EGFR at 28 is consistent with chronic renal disease. Calcium was elevated to 10.2. However, when corrected for albumin, this corrected to 9.8 mg/dL. Mild transaminitis is present as seen in alkaline phosphatase, AST, and ALT measurements which could be due to liver congestion from volume overload.
Initial arterial blood gas with pH 7.491, PCO2 27.6, PO2 53.6, HCO3 20.6, and oxygen saturation 90% on room air, indicating respiratory alkalosis with hypoxic respiratory features.
Creatinine kinase was elevated along with serial elevated troponin I studies. In the setting of her known chronic renal failure and acute injury indicated by the above creatinine value, a differential of rhabdomyolysis is determined.
Influenza A and B: Negative
Normal sinus rhythm with non-specific ST changes in inferior leads. Decreased voltage in leads I, III, aVR, aVL, aVF.
Chest X-ray
Findings: Bibasilar airspace disease that may represent alveolar edema. Cardiomegaly noted. Prominent interstitial markings were noted. Small bilateral pleural effusions
Radiologist Impression: Radiographic changes of congestive failure with bilateral pleural effusions greater on the left compared to the right
Differential Diagnosis
- Acute on chronic COPD exacerbation
- Acute on chronic renal failure
- Bacterial pneumonia
- Congestive heart failure
- Pericardial effusion
- Hypothyroidism
- Influenza pneumonia
- Pulmonary edema
- Pulmonary embolism
Confirmatory Evaluation
On the second day of the admission patient’s shortness of breath was not improved, and she was more confused with difficulty arousing on conversation and examination. To further elucidate the etiology of her shortness of breath and confusion, the patient's husband provided further history. He revealed that she is poorly compliant with taking her medications. He reports that she “doesn’t see the need to take so many pills.”
Testing was performed to include TSH, free T4, BNP, repeated arterial blood gas, CT scan of the chest, and echocardiogram. TSH and free T4 evaluate hypothyroidism. BNP evaluates fluid load status and possible congestive heart failure. CT scan of the chest will look for anatomical abnormalities. An echocardiogram is used to evaluate left ventricular ejection fraction, right ventricular function, pulmonary artery pressure, valvular function, pericardial effusion, and any hypokinetic area.
- TSH: 112.717 (H)
- Free T4: 0.56 (L)
- TSH and Free T4 values indicate severe primary hypothyroidism.
BNP can be falsely low in obese patients due to the increased surface area. Additionally, adipose tissue has BNP receptors which augment the true BNP value. Also, African American patients with more excretion may have falsely low values secondary to greater excretion of BNP. This test is not that helpful in renal failure due to the chronic nature of fluid overload. This allows for desensitization of the cardiac tissues with a subsequent decrease in BNP release.
Repeat arterial blood gas on BiPAP ventilation shows pH 7.397, PCO2 35.3, PO2 72.4, HCO3 21.2, and oxygen saturation 90% on 2 L supplemental oxygen.
CT chest without contrast was primarily obtained to evaluate the left hemithorax, especially the retrocardiac area.
Radiologist Impression: Tiny bilateral pleural effusions. Pericardial effusion. Coronary artery calcification. Some left lung base atelectasis with minimal airspace disease.
Echocardiogram
The left ventricular systolic function is normal. The left ventricular cavity is borderline dilated.
The pericardial fluid is collected primarily posteriorly, laterally but not apically. There appeared to be a subtle, early hemodynamic effect of the pericardial fluid on the right-sided chambers by way of an early diastolic collapse of the RA/RV and delayed RV expansion until late diastole. A dedicated tamponade study was not performed.
The estimated ejection fraction appears to be in the range of 66% to 70%. The left ventricular cavity is borderline dilated.
The aortic valve is abnormal in structure and exhibits sclerosis.
The mitral valve is abnormal in structure. Mild mitral annular calcification is present. There is bilateral thickening present. Trace mitral valve regurgitation is present.
- Myxedema coma or severe hypothyroidism
- Pericardial effusion secondary to myxedema coma
- COPD exacerbation
- Acute on chronic hypoxic respiratory failure
- Acute respiratory alkalosis
- Bilateral community-acquired pneumonia
- Small bilateral pleural effusions
- Acute mild rhabdomyolysis
- Acute chronic, stage IV, renal failure
- Elevated troponin I levels, likely secondary to Renal failure
- Diabetes mellitus type 2, non-insulin-dependent
- Extreme obesity
- Hepatic dysfunction
The patient was extremely ill and rapidly decompensating with multisystem organ failure, including respiratory failure, altered mental status, acute on chronic renal failure, and cardiac dysfunction. The primary concerns for the stability of the patient revolved around respiratory failure coupled with altered mental status. In the intensive care unit (ICU), she rapidly began to fail BiPAP therapy. Subsequently, the patient was emergently intubated in the ICU. A systemic review of therapies and hospital course is as follows:
Considering the primary diagnosis of myxedema coma, early supplementation with thyroid hormone is essential. Healthcare providers followed the American Thyroid Association recommendations, which recommend giving combined T3 and T4 supplementation; however, T4 alone may also be used. T3 therapy is given as a bolus of 5 to 20 micrograms intravenously and continued at 2.5 to 10 micrograms every 8 hours. An intravenous loading dose of 300 to 600 micrograms of T4 is followed by a daily intravenous dose of 50 to 100 micrograms. Repeated monitoring of TSH and T4 should be performed every 1 to 2 days to evaluate the effect and to titrate the dose of medication. The goal is to improve mental function. Until coexistent adrenal insufficiency is ruled out using a random serum cortisol measurement, 50 to 100 mg every 8 hours of hydrocortisone should be administered. In this case, clinicians used hydrocortisone 100 mg IV every 8 hours. Dexamethasone 2 to 4 mg every 12 hours is an alternative therapy.
The patient’s mental status rapidly worsened despite therapy. In the setting of her hypothyroidism history, this may be myxedema coma or due to the involvement of another organ system. The thyroid supplementation medications and hydrocortisone were continued. A CT head without contrast was normal.
Respiratory
For worsening metabolic acidosis and airway protection, the patient was emergently intubated. Her airway was deemed high risk due to having a large tongue, short neck, and extreme obesity. As the patient’s heart was preload dependent secondary to pericardial effusion, a 1-liter normal saline bolus was started. Norepinephrine was started at a low dose for vasopressor support, and ketamine with low dose Propofol was used for sedation. Ketamine is a sympathomimetic medication and usually does not cause hypotension as all other sedatives do. The patient was ventilated with AC mode of ventilation, tidal volume of 6 ml/kg ideal body weight, flow 70, initial fio2 100 %, rate 26 per minute (to compensate for metabolic acidosis), PEEP of 8.
Cardiovascular
She was determined to be hemodynamically stable with a pericardial effusion. This patient’s cardiac dysfunction was diastolic in nature, as suggested by an ejection fraction of 66% to 70%. The finding of posterior pericardial effusion further supported this conclusion. The posterior nature of this effusion was not amenable to pericardiocentesis. As such, this patient was preload dependent and showed signs of hypotension. The need for crystalloid fluid resuscitation was balanced against the impact increased intravascular volume would have on congestive heart failure and fluid overload status. Thyroid hormone replacement as above should improve hypotension. However, vasopressor agents may be used to maintain vital organ perfusion targeting a mean arterial pressure of greater than 65 mm Hg as needed. BP improved after fluid bolus, and eventually, the norepinephrine was stopped. Serial echocardiograms were obtained to ensure that the patient did not develop tamponade physiology. Total CK was elevated, which was likely due to Hypothyroidism compounded with chronic renal disease.
Infectious Disease
Blood cultures, urine analysis, and sputum cultures were obtained. The patient's white blood cell count was normal. This is likely secondary to her being immunocompromised due to hypothyroidism and diabetes. In part, the pulmonary findings of diffuse edema and bilateral pleural effusions can be explained by cardiac dysfunction. Thoracentesis of pleural fluid was attempted, and the fluid was analyzed for cytology and gram staining to rule out infectious or malignant causes as both a therapeutic and diagnostic measure. Until these results return, broad-spectrum antibiotics are indicated and may be discontinued once the infection is ruled out completely.
Gastrointestinal
Nasogastric tube feedings were started on the patient after intubation. She tolerated feedings well. AST and ALT were mildly elevated, which was thought to be due to hypothyroidism, and as the TSH and free T4 improved, her AST and ALT improved. Eventually, these values became normal once her TSH level was close to 50.
Her baseline creatinine was found to be close to 1.08 in prior medical records. She presented with a creatinine of 1.8 in the emergency department. Since hypothyroidism causes fluid retention in part because thyroid hormone encourages excretion of free water and partly due to decreased lymphatic function in returning fluid to vascular circulation. Aggressive diuresis was attempted. As a result, her creatinine increased initially but improved on repeated evaluation, and the patient had a new baseline creatinine of 1.6. Overall she had a net change in the fluid status of 10 liters negative by her ten days of admission in the ICU.
Mildly anemic otherwise, WBC and platelet counts were normal. Electrolyte balance should be monitored closely, paying attention to sodium, potassium, chloride, and calcium specifically as these are worsened in both renal failure and myxedema.
Daily sedation vacations were enacted, and the patient's mental status improved and was much better when TSH was around 20. The bilateral pleural effusions improved with aggressive diuresis. Breathing trials were initiated when the patient's fio2 requirements decreased to 60% and a PEEP of 8. She was eventually extubated onto BiPAP and then high-flow nasal cannula while off of BiPAP. Pericardial fluid remained stable, and no cardiac tamponade pathology developed. As a result, it was determined that a pericardial window was unnecessary. Furthermore, she was not a candidate for pericardiocentesis as the pericardial effusion was located posterior to the heart. Her renal failure improved with improved cardiac function, diuretics, and thyroid hormone replacement.
After extubation patient had speech and swallow evaluations and was able to resume an oral diet. The patient was eventually transferred out of the ICU to the general medical floor and eventually to a rehabilitation unit.
Despite the name myxedema coma, most patients will not present in a coma status. This illness is at its core a severe hypothyroidism crisis that leads to systemic multiorgan failure. Thyroid hormones T3, and to a lesser extent, T4 act directly on a cellular level to upregulate all metabolic processes in the body. Therefore, deficiency of this hormone is characterized by systemic decreased metabolism and decreased glucose utilization along with increased production and storage of osmotically active mucopolysaccharide protein complexes into peripheral tissues resulting in diffuse edema and swelling of tissue. [1]
Myxedema coma is an illness that occurs primarily in females at a rate of 4:1 compared to men. It typically impacts the elderly at the age of greater than 60 years old, and approximately 90% of cases occur during the winter months. Myxedema coma is the product of longstanding unidentified or undertreated hypothyroidism of any etiology. Thyroid hormone is necessary throughout the body and acts as a regulatory hormone that affects many organ systems. [2] In cardiac tissues, myxedema coma manifests as decreased contractility with subsequent reduction in stroke volume and overall cardiac output. Bradycardia and hypotension are typically present also. Pericardial effusions occur due to the accumulation of mucopolysaccharides in the pericardial sac, which leads to worsened cardiac function and congestive heart failure from diastolic dysfunction. Capillary permeability is also increased throughout the body leading to worsened edema. Electrocardiogram findings may include bradycardia and low-voltage, non-specific ST waveform changes with possible inverted T waves.
Neurologic tissues are impacted in myxedema coma leading to the pathognomonic altered mental status resulting from hypoxia and decreased cerebral blood flow secondary to cardiac dysfunction as above. Additionally, hypothyroidism leads to decreased glucose uptake and utilization in neurological tissue, thus worsening cognitive function.
The pulmonary system typically manifests this disease process through hypoventilation secondary to the central nervous system (CNS) depression of the respiratory drive with blunting of the response to hypoxia and hypercapnia. Additionally, metabolic dysfunction in the muscles of respiration leads to respiratory fatigue and failure, macroglossia from mucopolysaccharide driven edema of the tongue leads to mechanical obstruction of the airway, and obesity hypoventilation syndrome with the decreased respiratory drive as most hypothyroid patients suffer from obesity.
Renal manifestations include decreased glomerular filtration rate from the reduced cardiac output and increased systemic vascular resistance coupled with acute rhabdomyolysis lead to acute kidney injury. In the case of our patient above who has a pre-existing renal disease status post-nephrectomy, this is further worsened. The net effect is worsened fluid overload status compounding the cardiac dysfunction and edema. [3]
The gastrointestinal tract is marked by mucopolysaccharide-driven edema as well leading to malabsorption of nutrients, gastric ileus, and decreased peristalsis. Ascites is common because of increased capillary permeability in the intestines coupled with coexistent congestive heart failure and congestive hepatic failure. Coagulopathies are common to occur as a result of this hepatic dysfunction.
Evaluation: The diagnosis of myxedema coma, as with all other diseases, is heavily reliant on the history and physical exam. A past medical history including hypothyroidism is highly significant whenever decreased mental status or coma is identified. In the absence of identified hypothyroidism, myxedema coma is a diagnosis of exclusion when all other sources of coma have been ruled out. If myxedema coma is suspected, evaluation of thyroid-stimulating hormone (TSH), free thyroxine (T4), and serum cortisol is warranted. T4 will be extremely low. TSH is variable depending on the etiology of hypothyroidism, with a high TSH indicating primary hypothyroidism and a low or normal TSH indicating secondary etiologies. Cortisol may be low indicating adrenal insufficiency because of hypothyroidism. [4]
Prognosis: Myxedema coma is a medical emergency. With proper and rapid diagnosis and initiation of therapy, the mortality rate is still as high as 25% to 50%. The most common cause of death is due to respiratory failure. The factors which suggest a poorer prognosis include increased age, persistent hypothermia, bradycardia, low score Glasgow Coma Scale, or multi-organ impairment indicated by high APACHE (Acute Physiology and Chronic Health Evaluation) II score. For these reasons, placement in an intensive care unit with a low threshold for intubation and mechanical ventilation can improve mortality outcomes. [3] [5]
Pearls of Wisdom
- Not every case of shortness of breath is COPD or congestive heart failure (CHF). While less likely, a history of hypothyroidism should raise suspicion of myxedema coma in a patient with any cognitive changes.
- Myxedema is the great imitator illness that impacts all organ systems. It can easily be mistaken for congestive heart failure, COPD exacerbation, pneumonia, renal injury or failure, or neurological insult.
- Initial steps in therapy include aggressive airway management, thyroid hormone replacement, glucocorticoid therapy, and supportive measures.
- These patients should be monitored in an intensive care environment with continuous telemetry. [6]
Enhancing Healthcare Team Outcomes
This case demonstrates how all interprofessional healthcare team members need to be involved in arriving at a correct diagnosis, particularly in more challenging cases such as this one. Clinicians, specialists, nurses, pharmacists, laboratory technicians all bear responsibility for carrying out the duties pertaining to their particular discipline and sharing any findings with all team members. An incorrect diagnosis will almost inevitably lead to incorrect treatment, so coordinated activity, open communication, and empowerment to voice concerns are all part of the dynamic that needs to drive such cases so patients will attain the best possible outcomes.
Article Details
Article Author
Article Editor:
Wankanit S,Mahachoklertwattana P,Anantasit N,Katanyuwong P,Poomthavorn P, Myxoedema coma in a 2-year-old girl with untreated congenital hypothyroidism: Case report and literature review. Journal of paediatrics and child health. 2018 Dec 12; [PubMed PMID: 30548708]
Yafit D,Carmel-Neiderman NN,Levy N,Abergel A,Niv A,Yanko-Arzi R,Zaretski A,Wengier A,Fliss DM,Horowitz G, Postoperative myxedema coma in patients undergoing major surgery: Case series. Auris, nasus, larynx. 2018 Nov 16; [PubMed PMID: 30454972]
Heksch RA,Henry RK, Myxedema Coma due to Hashimoto Thyroiditis: A Rare but Real Presentation of Failure to Thrive in Infancy. Hormone research in paediatrics. 2018 May 4; [PubMed PMID: 29730659]
Hawatmeh A,Thawabi M,Abuarqoub A,Shamoon F, Amiodarone induced myxedema coma: Two case reports and literature review. Heart & lung : the journal of critical care. 2018 Jul - Aug [PubMed PMID: 29793782]
Tran M,Vincent L,Ho G,Kelly K,Bouvet M,Meier A, Critical Consideration of Myxedema Coma in the Postoperative Setting: A Case Report. A [PubMed PMID: 30169383]
Munir A, Myxedema Coma. Journal of Ayub Medical College, Abbottabad : JAMC. 2018 Jan-Mar; [PubMed PMID: 29504346]
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Hypothyroidism and nursing care
Learn to recognize the symptoms of this commonly overlooked condition.
By Dorothy Moore, DNP, FNP-C, CCRN
Sandra Reynolds, a 64-year-old homeless woman, is admitted to your unit for rehabilitation after being injured by a hit-and-run driver. She sustained a compound pelvic fracture and several contusions and abrasions. Ms. Reynolds has not had regular medical care for several years. She’s 5’3″, weighs 185 pounds, and has thinning gray-brown hair. Her skin is dry and rough, and she says she frequently feels cold. Ms. Reynolds looks much older than her stated age and has little interest in anything except sleeping. When she talks to you, her voice is hoarse and her speech is slow. She is constipated. Ms. Reynolds’ vital signs are: heart rate 56 beats/minute, blood pressure 143/82 mm Hg, temperature 97.4° F (36.3° C), and respiratory rate 14 breaths per minute.
As an inpatient rehab nurse working with Ms. Reynolds, you observe her lack of energy, mental state, and aged appearance. All of these findings are attributable, you reason, to her recent trauma and the effects of homelessness. But after reading this article, you should also think about hypothyroidism as a potential source of her signs and symptoms.
Hypothyroidism, also known as myxedema, is second to diabetes mellitus as the most common endocrine disorder in the United States. It’s six times more likely to occur in women than men and is more common in older people. About 10% of women over age 60 have subclinical hypothyroidism. Because it affects all of the body’s systems, mimicking many other disease processes, hypothyroidism can be overlooked as an explanation for a patient’s clinical presentation. This article reviews the pathophysiology of hypothyroidism, as well as its causes, symptoms, diagnosis, treatment, and nursing care.
About the thyroid
The thyroid’s main job is as master regulator of metabolism. It’s located in the front of the neck, below the larynx and in front of the trachea. It has two lobes, giving it a butterfly shape. The thyroid produces two hormones, thyroxine (T4) and triiodothyronine (T3), by extracting iodine from the blood. Thyroid cells are the only cells in the body that absorb and use iodine. Every cell in the human body relies on T3 and T4 to manage its metabolism.
To regulate T3 and T4 production, the thyroid works in a feedback loop with the hypothalamus and the anterior pituitary gland, which is called the hypothalamic-pituitary-thyroid (HPT) axis. (See Understanding the HPT axis .)
Primary hypothyroidism occurs when the thyroid is damaged and can’t produce T3 and T4. Secondary hypothyroidism is caused by pituitary gland dysfunction, and tertiary hypothyroidism results from problems with the hypothalamus. This article focuses on the most common thyroid problem—primary hypothyroidism.
Causes of primary hypothyroidism
The most common cause of hypothyroidism is autoimmune thyroiditis, or Hashimoto’s thyroiditis; damage to the thyroid through surgery, ablation, or radiation treatment are less common causes. Other autoimmune diseases, such as scleroderma or amyloidosis, can cause hypothyroidism.
A rare outcome of hypothyroidism is myxedema coma, which is severe physiologic decompensation that can lead to death. Myxedema coma is a true medical emergency with a high mortality rate, but with iodized salt and improved medical surveillance, the annual incidence is only 0.22 per million population.
Symptoms of hypothyroidism
Ms. Reynolds’ skin is pale and cool, which is common in patients with hypothyroidism. Because the turnover of new cells is delayed with slowed metabolism, her skin has a characteristic dry, rough quality. Ms. Reynolds’ face is puffy, and her voice is hoarse because of tongue enlargement. She has coarse, thinning hair, brittle fingernails, and periorbital edema. These are all findings associated with hypothyroidism.
People with hypothyroidism experience a slowing of metabolic processes, which can result in fatigue, slow speech, constipation, cold intolerance, weight gain, bradycardia, and decreased deep tendon reflexes. One study showed the most common symptoms are tiredness, dry skin, and shortness of breath. The signs of hypothyroidism are numerous, often subtle, and not specific to hypothyroidism. (See Recognizing hypothyroid symptoms .)
Hypothyroidism can masquerade as vitamin B12 or D deficiency, iron deficiency, chronic kidney disease, obstructive sleep apnea, or viral infections, such as mononucleosis. Because symptoms overlap with so many other conditions, diagnosing hypothyroidism based on clinical presentation alone is not possible; laboratory testing is required.
Fortunately, we can measure thyroid hormone levels in the blood and pinpoint a diagnosis. As a nurse, you can expect orders for lab draws of serum thyroid-stimulating hormone (TSH) and possibly free T4. (Free T4 is not bound to protein, so it can be used by the body.) You’ll want to be able to understand and explain the purpose of these lab tests to your patients.
- Hypothyroidism is diagnosed when a person has an elevated serum TSH level and a low serum free T4 level.
- If a patient’s TSH level is elevated, but the serum free T4 is low, then the likely diagnosis is subclinical hypothyroidism .
- A low serum-free T4 level with a normal TSH may indicate a secondary cause of hypothyroidism, and further testing will be done to look at hypothalamic-pituitary gland insufficiency. (See Diagnosing hypothyroidism .)
Hypothyroidism is treated with synthetic T4 (levothyroxine), which is available in tablet, soft gel, and liquid form, although tablet is the most common. Studies show no benefit to taking both T4 and T3, since T4 is converted to T3 in the peripheral tissues. Generic and proprietary formulations of T4 are equally effective, but switching back and forth isn’t recommended. Patients remain on thyroid monitoring and supplementation for life.
Nursing considerations
Teach patients about the many drug interactions with levothyroxine and about the importance of establishing a daily routine to help maintain even hormone levels. Levothyroxine should be taken on an empty stomach with water, at least 1 hour before eating. Even coffee has been shown to interfere with the absorption of T4. And levothyroxine is incompatible with many other medications, so it should be taken alone. Medications that bind with levothyroxine and reduce its bioavailability include bile acid sequestrants (such as sevelamer), calcium supplements (including calcium acetate, carbonate, and citrate), aluminum, magnesium, lanthanum, and simethicone.
Taking levothyroxine with anticoagulants can increase the effect of anticoagulants. With some medications, such as antacids, advise patients to allow 4 to 6 hours to pass between taking each medication.
Although patients are traditionally instructed to take levothyroxine first thing in the morning on an empty stomach, a randomized double-blind study showed that taking it at bedtime results in better absorption. This schedule change may be particularly helpful for patients who take many medications in the morning that are incompatible with levothyroxine.
After beginning levothyroxine, symptom improvement can take up to 6 weeks, and dosing may need to be titrated, which is usually done at 3- to 6-week intervals. Patients should begin to feel a restored sense of energy, improved cognitive function, thickening of hair, and other symptom improvements.
You suggest to Ms. Reynolds’ provider that perhaps she has hypothyroidism. TSH and T4 levels are ordered, and your suspicions are confirmed—her TSH is 7.5 mlU/L and her T4 level is 3.9 mcg/dL. Levothyroxine is ordered. Over the course of the next 2 weeks of her rehab, Ms. Reynolds begins to feel more energetic and involved in her care, she’s more alert, and she’s willing to talk with a caseworker about transitional housing. Your astute call enabled her to get the treatment she needed to improve her quality of life.
Dorothy Moore is a staff nurse at Kaiser Permanente Emergency Department, in Oakland, California, and an adjunct lecturer at California State University in Hayward.
Selected references
American Thyroid Association. Thyroid function tests .
Drugs.com. Levothyroxine drug interactions
Dunn D, Turner C. Hypothyroidism in women. Nurs Womens Health . 2016;20(1):93-8.
Gaitonde DY, Rowley KD, Sweeney LB. Hypothyroidism: An update. Am Fam Physician . 2012;86(3)244-51.
LeFevre ML; US Preventive Services Task Force. Screening for thyroid dysfunction: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med . 2015;162(9):641-50.
Nygaard B. Primary hypothyroidism. Am Fam Physician . 2015;91(6):359-60.
Rugge JB, Bougatsos C, Chou R. Screening and treatment of thyroid dysfunction: An evidence review for the US Preventive Services Task Force. Ann Intern Med . 2015;162(1):35-45.
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Hypothyroidism Nursing Diagnosis and Nursing Care Plans
Hypothyroidism nursing care plans diagnosis and interventions.
Hypothyroidism NCLEX Review and Nursing Care Plans
Hypothyroidism is a disorder in which the thyroid produces and releases insufficient thyroid hormone into the bloodstream, also known as underactive thyroid, which causes fatigue, weight gain, and an inability to tolerate cold temperatures.
Thyroid insufficiency affects all physiological processes and can range from minor to severe. As a result, the metabolism will slow down. Patients who have had past hypothyroidism treated with radioiodine, antithyroid drugs, or thyroidectomy are more likely to develop hypothyroidism. Hormone replacement therapy is the most common treatment for hypothyroidism.
Types of Hypothyroidism
The types of hypothyroidism are categorized based on their causes:
- Central hypothyroidism. The pituitary gland, the hypothalamus, or both are unable to stimulate thyroid hormone production.
- Secondary or pituitary hypothyroidism. The cause is solely a problem in the pituitary gland itself.
- Tertiary or hypothalamic hypothyroidism. This refers to a hypothalamic condition that causes insufficient TSH secretion as a result of diminished TRH stimulation.
- Cretinism. The thyroid disease that is present from birth.
- Myxedema or severely advanced hypothyroidism. Myxedema occurs when the thyroid levels are exceedingly low. Myxedema can cause a variety of symptoms, including:
- Low body temperature
- Heart failure
Signs and Symptoms of Hypothyroidism
The severity of the hormone deficiency affects the signs and symptoms of hypothyroidism. Problems usually emerge gradually, over a period of years.
At first, hypothyroidism symptoms such as fatigue and weight gain may go unnoticed or may simply be attributed to becoming older. However, as the metabolism slows, the patient may experience more evident problems.
The symptoms of hypothyroidism commonly develop slowly over time. This can include:
- Numbness and tingling in the hands
Constipation
- Weight Gain
- Muscle Weakness
- High blood cholesterol levels
- Cold Intolerance
- Dry, coarse skin and hair
- Decreased libido
- Frequent and heavy menstrual period
- Physical changes in the face including drooping eyelids, puffiness in the eyes and face
- Hoarseness of voice
Causes of Hypothyroidism
Several diseases and factors could cause hypothyroidism, the following are included:
- Inflammation of the thyroid gland which damages the gland’s cells.
- Autoimmune diseases. Autoimmune thyroiditis or Hashimoto’s disease is the most common cause of hypothyroidism in adults.
- Atrophy of the thyroid gland. When aging, the thyroid gland shrinks in size.
- Therapy for hyperthyroidism, such as radioactive iodine and thyroidectomy.
- Medications- TSH production can be reduced by certain drugs, iodine compounds, and antithyroid medicines.
- Iodine deficiency or excess. The thyroid gland is affected by an imbalance in iodine levels in the body.
- Autoimmune or Hashimoto’s thyroiditis. This happens when the immune system attacks the thyroid gland.
- After pregnancy. This is often referred to as postpartum thyroiditis.
Risk Factors for Hypothyroidism
Hypothyroidism can affect people of all ages, genders and ethnicities, it is a common condition particularly among the following:
- Women above the age of 50
- Men who have had radiation therapy for head and neck cancer
- Patients who have primary or thyroidal hypothyroidism
- Family history of thyroid disease
- Family history of autoimmune disease
- Patients with autoimmune disease
- Caucasian or Asian ethnicity
- Women experiencing hormonal changes due to pregnancy, childbirth, or menopause
- People with chromosomal abnormalities like Down syndrome or Turner’s syndrome
Diagnosis of Hypothyroidism
- Physical assessment – the thyroid gland is inspected and palpated on a regular basis in all patients.
- Thyroid-stimulating blood tests- Because of its high sensitivity, measuring serum TSH concentration is the single best screening test for thyroid function.
- Serum T3 and T4 tests – The quantities of protein-bound and free hormones that occur in response to TSH secretion are included in total T3 or T4 measurements.
- Thyroid antibody test – Antithyroid antibodies can be detected using immunoassay techniques in patients with Hashimoto’s thyroiditis.
Treatment for Hypothyroidism
Hypothyroidism is a treatable condition. However, it is needed to continuously take the medication on a regular basis in order to balance the level of hormones in the body. The patient may live a normal and healthy life with careful management and follow-up check up with the healthcare practitioner to ensure that the treatment is working properly.
Hypothyroidism is typically treated by supplementing the hormone that the thyroid no longer produces. This is usually done with the help of a medicine in which when taken orally, raises the amount of thyroid hormone the body produces, balancing its levels.
- Medical Management.The main goal of hypothyroidism treatment is to replace the missing hormone and restore a normal metabolic state.
- Pharmacological Treatment. The preferred preparation for treating hypothyroidism and suppressing nontoxic goiters.
- Prevention of Cardiac Dysfunction. A decline in blood supply is tolerated without overt signs of coronary artery disease as long as metabolism is normal and the tissues require very little oxygen.
- Supportive Therapy. The patient’s oxygen saturation should be monitored, fluids should be administered with caution, external heat should be avoided, and oral thyroid hormone therapy should be continued.
Prevention of Hypothyroidism
Hypothyroidism can be prevented by doing the following:
- Increased consumption of iodine. In hypothyroidism, iodine intake is the most important preventive method.
- Early detection. Thyroid tests after thyroid surgery or therapy may help to diagnose hypothyroidism early and treat it effectively.
Nursing Considerations for patients with Hypothyroidism
- Encourage rest. Rest and exercise as tolerated through space activities.
- Protect against cold. Provide the patient with an extra blanket or layer of clothing.
- Avoid excessive heat exposure. Instruct the patient to avoid use of an external heat source.
- Monitor the temperature. Keep an eye on the patient’s body temperature.
- Increase oral fluid intake Encourage the patient to increase fluid consumption while adhering to the fluid restriction guidelines.
- Provide fiber-rich foods to the patient.
- Take care of respiratory symptoms. Observe the patient’s breathing depth, rate, pattern, pulse oximetry, and ABG.
- Encourage pulmonary exercises. Encourage the patient to perform deep breathing, coughing, and the use of spirometry incentives.
- Always orient the patient about the current environment. Educate the patient about the time, place, date, and events that are taking place.
Nursing Diagnosis for Hypothyroidism
Hypothyroidism nursing care plan 1.
Imbalanced Nutrition: More Than Body Requirements
Nursing Diagnosis: Imbalanced Nutrition: More Than Body Requirements related to increased metabolic needs intake secondary to hypothyroidism, as evidenced by decreased appetite, sedentary level of activity, and weight gain.
Desired Outcome: The patient will be able to maintain a stable weight and take in necessary nutrients by adhering to the nutrition plan.
Hypothyroidism Nursing Care Plan 2
Deficient Knowledge
Nursing Diagnosis: Deficient Knowledge related to exposure to the disease, new disease process and unawareness of available information resources secondary to hypothyroidism, as evidenced by asking a few and limited questions about the disease and thyroid hormone replacement and inability to handle the disease process.
Desired Outcomes:
- The patient will verbalize understanding of the disease by stating factual information.
- The patient will adhere to the medication regimen.
Hypothyroidism Nursing Care Plan 3
Nursing Diagnosis: Fatigue related to impaired metabolic state secondary to hypothyroidism, as evidenced by lethargy, impaired concentration, increased rest periods, inability to perform daily tasks and lack of energy.
- The patient will be able to determine the source of fatigue as well as the specific areas of control.
- The patient will be able to express a reduction of fatigue and an increased ability to finish desired daily activities.
Hypothyroidism Nursing Care Plan 4
Activity Intolerance
Nursing Diagnosis: Activity Intolerance related to fatigue and reduced cognitive function secondary to hypothyroidism, as evidenced by inability to perform daily activities, muscle weakness and inability to sleep.
- The patient will be able to participate in physical activities.
- The patient will achieve an increased conditioned physical state.
- The patient will have unremarkable vital signs.
- The patient will verbalize an increased tolerance to perform daily activities.
- The patient will demonstrate effective energy management techniques.
Hypothyroidism Nursing Care Plan 5
Nursing Diagnosis: Constipation related to reduced gastrointestinal function secondary to hypothyroidism, as evidenced by infrequent passage of stool, anorexia and distended abdomen.
- The patient will be able to pass soft, formed stool at a frequency that the patient considers “normal.”
- The patient will verbalize relief from constipation.
- The patient will be able to choose how to prevent or cure constipation.
- The patient will verbalize constipation prevention techniques
Nursing References
Ackley, B. J., Ladwig, G. B., Makic, M. B., Martinez-Kratz, M. R., & Zanotti, M. (2020). Nursing diagnoses handbook: An evidence-based guide to planning care . St. Louis, MO: Elsevier. Buy on Amazon
Gulanick, M., & Myers, J. L. (2022). Nursing care plans: Diagnoses, interventions, & outcomes . St. Louis, MO: Elsevier. Buy on Amazon
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Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2018). Medical-surgical nursing: Concepts for interprofessional collaborative care . St. Louis, MO: Elsevier. Buy on Amazon
Silvestri, L. A. (2020). Saunders comprehensive review for the NCLEX-RN examination . St. Louis, MO: Elsevier. Buy on Amazon
Disclaimer:
Please follow your facilities guidelines, policies, and procedures.
The medical information on this site is provided as an information resource only and is not to be used or relied on for any diagnostic or treatment purposes.
This information is intended to be nursing education and should not be used as a substitute for professional diagnosis and treatment.
Anna Curran. RN, BSN, PHN Clinical Nurse Instructor
Emergency Room Registered Nurse Critical Care Transport Nurse Clinical Nurse Instructor for LVN and BSN students
Anna began writing extra materials to help her BSN and LVN students with their studies and writing nursing care plans. She takes the topics that the students are learning and expands on them to try to help with their understanding of the nursing process and help nursing students pass the NCLEX exams.
Her experience spans almost 30 years in nursing, starting as an LVN in 1993. She received her RN license in 1997. She has worked in Medical-Surgical, Telemetry, ICU and the ER. She found a passion in the ER and has stayed in this department for 30 years.
She is a clinical instructor for LVN and BSN students and a Emergency Room RN / Critical Care Transport Nurse.
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Endocrine Case Studies
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Show Answers
Shirley, a 34 year old woman comes to the physician’s office complaining of feeling jittery all the time and suffering from intolerance to heat. The physician rules out menopause because Shirley is young. He suspects hyperthyroid disease.
What other symptoms will the physician look for in Shirley to suggest a diagnosis of hyperthyroid disease?
What tests are performed to confirm the diagnosis?
The physician decides to treat conservatively using medications. List the drugs and explain the action of medication given to treat hyperthyroidism.
How will blood tests be used to follow and evaluate the effect of medication?
Medication alone is not sufficient and so Shirley is scheduled for surgery. What are the surgical options for Shirley? Explain assessment observations for possible postoperative complications from a thyroidectomy.
What post-operative teaching about head control will Shirley need?
What teaching topics are necessary to prepare Shirley for life adjustment after thyroidectomy?
Explain the symptoms and treatment for thyroid storm.
List symptoms the nurse will observe if the parathyroid gland is injured or removed during surgery.
Case Study: Hypo Thyroid Disease – Myxedema
Jeanine has been dieting and exercise and trying unsuccessfully to lose weight. Her nutrition counselor suggests that Jeanine to her physician.
Whenever a person is over weight they may ask the physician the question, “Do I have low thyroid function?” (I hope) because it is much easier to take a pill to lose weight and regain energy than it is to tackle the alternative of diet and exercise.
List the symptoms of low thyroid function.
What tests will confirm the diagnosis?
List the drugs and explain the action of medication given to treat hypothyroid disease.
How will blood tests be used to follow and evaluate the effect of medication? Jeanine for life adjustment with hypothyroid disease?
What will precipitate a Myxedema coma?
Case Study Continued: Hypo Parathyroid Disease
During a postoperative checkup Shirley demonstrates a positive Chvosteck’s sign. The physician next tests for Trousseau’s sign, and then orders a bone scan.
How did Shirley develop hypoparathyroid disease?
Explain Chvosteck and Trusseau’s signs.
Why did the physician order a bone scan?
The physician may require Shirley to wear a Holter Monitor because….?
What is the function of parathyroid hormone? How is this related to calcium?
List blood studies the physician will use to follow parathyroid function.
What is the purpose of Shirley taking Vitamin D and Phosphate-binding drugs?
Describe patient teaching needed when taking Phosphate-binding drugs.
Case Study: Hyper Pituitary Secretion
Fred complains of joint pain. He has had to buy new shoes every month because the old ones feel too small. His wife says, “Fred looks different.” The physican’s diagnosis is Acromegaly caused by a pituitary tumor.
List the symptoms of Acromegaly.
Explain transsphenoidal pituitary surgery.
What are the complication for transsphenoidal surgery?
Is there cause for concern if Fred has a post nasal drip after surgery?
Why are the following medications prescribed for Fred? Vasopressin, Levothyroxine, somatrotropin, glucocorticoids?
Case Study: Diabetes Insipidus
After a stroke Samuel develops Diabetes Insipidus.
What are the symptoms of Diabetes Insipidus?
How is this connected with the kidney?
Describe the action and administration of DDAVP (Vasopressin).
Case Study: Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Anthony says, “This is crazy. I have lung cancer, how did I get a disease of the Pituitary gland?”
List the symptoms of SIADH.
What is the connection between lung cancer and the pituitary gland?
Explain teaching for recording daily observation and restrictions Anthony will need to follow for managing SIADH?
Case Study: Diabetes Mellitus
I. Explain the physiology that creates the three symptoms of diabetes.
II. What is the function of each of these pancreas cells?
III. A client is admitted to the hospital with diabetic ketoacidosis. The nurse understands that the elevated ketones present in this disease is caused by the incomplete oxidation of ______________
IV. List five symptoms of hypoglycemia AND five symptoms of hyperglycermia.
V. Fill in the insulin times on this chart.
VI. What is an appropriate nursing action when patient’s blood sugar test is 50?
VII. Contrast DKA and HHNS. Compare means how are they different.
VIII. What is the triad of treatment for Diabetes Mellitus?
IX. Describe Dawn phenomenon and Somogi phenomenon.
Case Study: Hyper Secretion of Adrenal Gland – Cushing Disease
The adrenal gland is easy!
John is receiving large doses of prednisone for a chronic disease. The side effects of steroid medications like prednisone and decadron are the same as Cushing’s Syndrome which is over production and hyper secretion of corticosteroid hormone.
List the symptoms of Cushing’s Syndrome. Compare this list with a list of the side effects of steroid medications. See how they are the same.
The treatment is…….?
Look up a list of steroid mediation and review the differences in their use? Why are so many different steroid medications available in oral and parenteral form?
What is the difference between Cushing Disease and Cushing Syndrome?
If a person has an exacerbation of a chronic disease and prednisone is prescribed, what is the rationale for giving an initial large dose and then tapering doses?
Case Study: Hypo Secretion of the Adrenal Gland – Addison’s Disease
People are complementing John on his beautiful tan. The problem is John has not been out in the sun or to a tanning salon. In addition he has been losing weight.
List the symptoms of Addison’s Disease
Explain the physiology responsible for the symptoms of Addison’s Disease
What is the treatment for Addison’s Disease?
List medications used to treat Addison’s Disease.
Describe the immediate intervention for a person in Addisonian Crisis.
Case Study: Tumor of the Adrenal Gland
What is pheochromocytoma?
Describe collection procedure for 24 hour urine for VMA.
List symptoms when monitoring patient for hypertensive crisis.
What medications will be prescribed to treat hypertensive crisis?
How is life altered after an adrenalectomy?
Nicole Whitworth is the founder of Your Nursing Tutor. She has a BSN and an MA in Clinical Psychology, and has been a professional nursing tutor for over 12+ years. Nicole specializes in getting nursing students through school confidently and calmly so that everything finally “clicks”. She is also the creator of the Silver Bullet Study System, an easy-to-follow study method that automatically trains your brain to become a nurse at the same time that you study for your normal nursing classes.
3 thoughts on “Endocrine Case Studies”
I am a new professor teaching pharmacology to undergraduate BSN students. I am attempting to locate an excellent resource for case studies
Hello, I noticed that there is a typo the word liver is missing the r. I noticed you used the word on when talking about calcium in the bone is it on it or in it? I have a test on endocrine in a few days and I will do all you recommend. I greatly appreciate you, explaining this like you do.
Thank you, Bev
The calcium isn’t really “on” it OR “in” it…it’s just PART of it. I know that might sound kind of confusing, but if you think of bone at the molecular level it is really just a grouping of a bunch of molecules that stick together and create the properties you see in bone. So calcium (and several other things) are all one of many components that are a part of bone. Good question!
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Hypothyroidism.
Nikita Patil ; Anis Rehman ; Ishwarlal Jialal .
Affiliations
Last Update: August 8, 2022 .
- Continuing Education Activity
Hypothyroidism results from low levels of thyroid hormone with varied etiology and manifestations. The drug of choice for the treatment of hypothyroidism is thyroid hormone replacement. Untreated hypothyroidism increases morbidity and mortality. This activity reviews etiology, clinical presentation, diagnosis, and management of hypothyroidism.
- Review the causes of hypothyroidism.
- Describe the laboratory parameters of hypothyroidism.
- Summarize the treatment for hypothyroidism.
- Explain strategies to optimize care coordination among interprofessional team members to improve outcomes for patients affected by hypothyroidism.
- Introduction
Hypothyroidism results from low levels of thyroid hormone with varied etiology and manifestations. Untreated hypothyroidism increases morbidity and mortality. In the United States, autoimmune thyroid disease (Hashimoto thyroiditis) is the most common cause of hypothyroidism, but globally lack of iodine in the diet is the most common cause. The patient presentation can vary from asymptomatic disease to myxedema coma. Today, the diagnosis of hypothyroidism is easily made with simple blood tests and can be treated with exogenous thyroid hormone.
Hypothyroidism is majorly divided into two categories, primary and secondary (central) hypothyroidism. Hypothyroidism is termed primary when the thyroid gland itself is not able to produce adequate amounts of thyroid hormone. The less common, secondary, or central hypothyroidism is labeled when the thyroid gland itself is normal, and the pathology is related to the pituitary gland or hypothalamus.
The most prevalent etiology of primary hypothyroidism is an iodine deficiency in iodine-deficient geographic areas worldwide. Autoimmune thyroid diseases are the leading causes of hypothyroidism in the United States and the iodine-sufficient regions. Hashimoto thyroiditis is the most common etiology in the United States, and it has a strong association with lymphoma. Etiology can be influenced locally by iodine fortification and the emergence of new iodine-deficient areas. [1]
Other common causes of hypothyroidism include:
- Drugs such as amiodarone, thalidomide, oral tyrosine kinase inhibitors (sunitinib, imatinib) stavudine, interferon, bexarotene, perchlorate, rifampin, ethionamide, phenobarbital, phenytoin, carbamazepine, interleukin-2, and lithium, [1]
- Thyroid radioactive iodine therapy
- Thyroid surgery
- Radiotherapy to head or neck area
- Central hypothyroidism from neoplastic, infiltrative, inflammatory, genetic, or iatrogenic disorders of the pituitary or hypothalamus. [2]
- A new class of cancer medications such as anti- CTLA - 4 and anti- PD - L1 / PD - 1 therapy has been associated with both primary and/or secondary hypothyroidism.
Postpartum thyroiditis affects nearly 10% of women and often presents 8-20 weeks after the delivery of the infant. Only a few women require treatment with thyroid hormone. However, some women are at high risk for permanent hypothyroidism or recurrent postpartum thyroiditis in future pregnancies.
The use of radioactive iodine to manage Grave disease usually results in permanent hypothyroidism in about 80-90% of the patients within 8-20 weeks after treatment. Radiation treatment to the head and neck area can also result in hypothyroidism.
A relatively uncommon cause of primary hypothyroidism is subacute granulomatous thyroiditis, also known as de Quervain disease. It commonly occurs in middle-aged women and is usually a self-limiting disease.
Autoimmune polyendocrinopathy type-1 results from a mutation in the AIRE gene and is a constellation of Addison disease, hypoparathyroidism, and mucocutaneous candidiasis.
Secondary and tertiary hypothyroidism, also known as central hypothyroidism is caused by a defect in the hypothalamic-pituitary axis. Its causes include the following:
- Pituitary tumors
- Tumors compressing hypothalamus
- Sheehan syndrome
- Thyroid releasing hormone (TRH) resistance
- TRH deficiency
- Lymphocytic hypophysitis
- Radiation therapy to the brain
- Drugs such as dopamine, prednisone, or opioids [3]
- Epidemiology
The NHANESIII (National Health and Nutrition Examination Survey) study found the prevalence of overt hypothyroidism among adults in the United States (12 years of age and older) to be 0.3% and subclinical hypothyroidism 4.3%. Female gender and increasing age were associated with higher thyroid-stimulating hormone (TSH) and the prevalence of antithyroid antibodies. [4]
Hypothyroidism is more prevalent in women with small stature at birth and low body mass index in childhood.
- Pathophysiology
The most common cause of hypothyroidism is the inability of the thyroid gland to produce a sufficient amount of thyroid hormone; however, less commonly pituitary and hypothalamus may also result in thyroid dysfunction. The hypothalamus secretes thyrotropin-releasing hormone (TRH) that stimulates the pituitary gland to produce thyroid-stimulating hormone (TSH). Thyroid-stimulating hormone stimulates the thyroid gland to produce and secrete mainly T4 (approximately 100-125 nmol daily) and smaller quantities of T3. The half-life of T4 is 7-10 days, and eventually, T4 is converted to T3 peripherally by 5'-deiodination. Levels of T3 majorly and T4, to some extent, in turn, exert negative feedback on the production of TRH and TSH. Alteration in the structure and function of any of these organs or pathways can result in hypothyroidism.
The decline in the production of T4 results in an increase in the secretion of TSH by the pituitary gland, causing hypertrophy and hyperplasia of the thyroid parenchyma, thereby leading to increased T3 production.
- Histopathology
Autoimmune thyroiditis causes an increase in the turnover of iodine and impaired organification. Chronic inflammation of the parenchyma leads to predominant T-cell lymphocytic infiltration. [2] If this persists, the initial lymphocytic hyperplasia and vacuoles are replaced by dense fibrosis and atrophic thyroid follicles. Co-existing or associated malignancy, such as papillary thyroid cancer, can also be seen. [5]
- History and Physical
It is important to maintain a high index of suspicion for hypothyroidism since the signs and symptoms can be mild and nonspecific and different symptoms may be present in different patients. Typical features such as cold intolerance, puffiness, decreased sweating and skin changes may not be present always.
Inquire about dry skin, voice changes, hair loss, constipation, fatigue, muscle cramps, cold intolerance, sleep disturbances, menstrual cycle abnormalities, weight gain, and galactorrhea. [2] Also obtain a complete medical, surgical, medication, and family history.
History of adverse pregnancy and neonatal outcomes should also be sought. [6]
Symptoms of depression, anxiety, psychosis, cognitive impairments such as memory loss can be present. [7] Rarely patients can present with ascites, [8] rhabdomyolysis, and pericardial effusion. [9]
Patients can also present with carpal tunnel syndrome, sleep apnea, hyponatremia, hypercholesterolemia, congestive heart failure, and prolonged QT interval. [2]
Hashimoto disease is difficult to differentiate clinically; however, some features are specific for this condition such as:
- Fullness of throat
- Painless thyroid enlargement
- Episodic neck pains and/or sore throat
A careful physical examination may reveal some clues since the signs of hypothyroidism are very subtle. Physical examination may be significant for the following:
- Enlarged thyroid gland
- Weight gain
- The slowness of speech and movements
- Coarse and brittle hair
- Pallor and jaundice
- Dull facial expressions
- Macroglossia
- Bradycardia
- Pericardial effusion
- Prolonged ankle reflex relaxation time [2]
However, most of the patients have normal thyroid examinations.
Serum TSH level is used to screen for primary hypothyroidism in most patients. In overt hypothyroidism, TSH levels are elevated, and free T4 levels are low. In subclinical hypothyroidism, TSH levels are elevated, and free T4 levels are normal. [2]
Central hypothyroidism is of pituitary or hypothalamic origin. TSH produced can be biologically inactive and can affect the levels of bioactive TSH, hence the diagnosis of central hypothyroidism should be based on free T4 rather than TSH. [2]
Labs should include evaluation for autoimmune thyroid diseases with levels of anti-thyroid antibodies such as the thyroid peroxidase antibodies. [2]
Patients with subclinical hypothyroidism and thyroid peroxidase antibody positivity have a greater risk of developing overt hypothyroidism [2] . The studies have shown that 50% of the patients will develop primary hypothyroidism in the course of 20 years. The decision to follow up periodically with clinical evaluation as well as lab tests is based on clinical judgment as there are no clear-cut guidelines in this regard.
Hospitalized patients should undergo TSH testing only when thyroid dysfunction is suspected. [2] Slight abnormalities of TSH in sick patients during their hospital stay should hint towards euthyroid sickness. However, if the values of TSH are very high, it does suggest hypothyroidism. "Reverse T3" will be elevated when the patient has euthyroid sickness; however, it is not routinely checked in clinical practice.
Laboratory workup may reveal hyperlipidemia, elevated serum CK, elevated hepatic enzymes, and anemia. [2] BUN, creatinine, and uric acid levels can also be elevated. [10]
Imaging studies (ultrasound) of the neck are not routinely recommended for hypothyroidism.
Screening for Hypothyroidism
While there are no universal guidelines on screening the public for thyroid disease, the American Thyroid Association recommends that screening should commence at the age of 35 and should continue every five years. Individuals at high risk for hypothyroidism include the following:
- Women over the age of 60
- Patients with a prior history of head and neck irradiation
- Patients with autoimmune disorders and/or type 1 diabetes
- Positive thyroid peroxidase antibodies
- Family history
- Treatment / Management
Hypothyroidism is mainly treated with levothyroxine monotherapy. [11]
Thyroid replacement treatment can exacerbate co-existing adrenal insufficiency. Patients with known or suspected adrenal insufficiency should be tested and treated for adrenal insufficiency while awaiting results. [2] Adrenal insufficiency can also be associated with subclinical hypothyroidism that is reversible with the treatment of adrenal insufficiency. [12] In patients who have confirmed adrenal insufficiency consider a reassessment of thyroid tests following an adequate treatment of adrenal insufficiency. It is important to rule out or treat adrenal insufficiency when a patient has severe hypothyroidism as in myxedema coma.
Replacement levothyroxine dose is 1.6 mcg/kg per day; however, in elderly and atrial fibrillation patients, it is important to reduce the dose [11] . In order to help the absorption, levothyroxine should be taken 30-45 minutes before breakfast and at least 3 hours post-meal at bedtime which are the convenient times for most patients. Moreover, elemental supplements such as calcium, magnesium, to name a few, do affect the absorption of levothyroxine. Commonly used medications such as proton pump inhibitors also have a negative impact on levothyroxine absorption. Maintaining a consistent formulation or brand of levothyroxine is essential. [11] There can be slight variations in the dose of the generic formulations, which can have a clinical impact in a small sub-set of very sensitive hypothyroid patients.
Switching to the intravenous (IV) form in the hospitals is indicated when a patient is unable to take thyroid replacement orally, or there is suspected myxedema coma. The dose of levothyroxine is reduced to generally 50% of the oral dose. The conversion is somewhat controversial in terms of the exact dose as different experts use different conversion percentages.
Gel formulations of thyroid hormone replacements, such as Triocent, are being used in malabsorption syndromes. Medications such as sucralfate, calcium preparations, and bile acid sequestrants can interfere with the absorption of levothyroxine. [2] However, the levothyroxine absorption test is done to prove that a patient can not absorb levothyroxine.
Based on the 2012 Clinical Practice Guidelines for Hypothyroidism in Adults by the American Association of Clinical Endocrinologists and the American Thyroid Association, therapy should be monitored and titrated based on TSH measurements. Serum-free T4 can also be used. Labs should be drawn every 4 to 8 weeks until target levels are achieved after starting the treatment, after any dose changes, changes in formulation or brand of levothyroxine, [2] after starting or stopping of any medications that may affect levels. If stable, then the monitoring interval can be extended to 6 months, and afterward if still, it is stable then, further monitoring can be extended to 12 months or can be done at shorter intervals on a case-to-case basis along with clinical evaluation. [2] Central hypothyroidism should be monitored based on free T4 rather than TSH. [2]
Patients with cardiac disease should be monitored for the development of any symptoms of angina and atrial fibrillation. [2] If a patient is overly treated with thyroid replacement for an extended period of time, screening for osteoporosis is warranted. [11]
Effective treatment helps to achieve a clinical improvement of signs and symptoms, along with an improved sense of patient well-being and normal TSH (or free T4 levels as applicable). [13] However, since the symptoms of hypothyroidism are non-specific, if a patient's labs are normalized while on thyroid replacement treatment, it signifies that symptoms are not from hypothyroidism. This is a difficult situation that providers need to deal with and strong counseling skills are of great help.
A comprehensive workup for other differentials is recommended for unresolved symptoms in the presence of biochemical euthyroidism. There is a lack of strong evidence supporting the routine inclusion of triiodothyronine (T3) preparations with levothyroxine in the treatment of hypothyroidism. [14] FDA has approved treatment options such as armor or nature thyroid; however, it is important to understand that these formulations increase risks of cardiac arrhythmias. Moreover, these formulations are not approved for pregnant patients due to the T3 component as well as in thyroid cancer patients, where strict TSH goals are required.
If symptoms persist despite normalization of TSH/free T4 levels, then non-endocrine etiologies should be considered.
- Differential Diagnosis
Owing to the subtle signs and symptoms of hypothyroidism, the list of differential diagnoses is extensive. Differential diagnosis is based on signs and symptoms; for instance, fatigue can point to iron deficiency anemia, sleep apnea, depression, and rheumatological diseases. [14] The following disorders may have to be considered in the differentials:
- Euthyroid sick syndrome
- Myxedema coma
- Riedel thyroiditis
- Subacute thyroiditis
- Thyroid lymphoma
- Iodine deficiency
- Addison disease
- Chronic fatigue syndrome
- Dysmenorrhea
- Erectile dysfunction
- Familial hypercholesterolemia
- Infertility
Without treatment, hypothyroidism may have a risk of high morbidity and mortality. It can eventually lead to coma or even death. In children, failure to treat hypothyroidism can result in severe mental retardation. A leading cause of death in adults is heart failure. With treatment, most patients have a good prognosis, and the symptoms usually reverse in a few weeks or months.
- Complications
Severe hypothyroidism may present as myxedema coma and is an endocrine emergency. Prompt recognition and early treatment in the intensive care unit (ICU) are essential, and even then, mortality reaches 25% to 60%. [15]
Myxedema crisis should be suspected in cases where there is encephalopathy, hypothermia, seizures, hyponatremia, hypoglycemia, arrhythmias, cardiogenic shock, respiratory failure, and fluid retention. [15]
Factors leading to an increased risk of myxedema crisis include inadequate doses of thyroid hormone, interruption in treatment, undiagnosed hypothyroidism, or presence of acute illness such as sepsis [15] , perhaps due to increased metabolic demands.
Supportive treatment should be provided in the intensive care unit with fluid and electrolyte management, ventilator support, vasopressors, treatment of coexisting acute illness, and hypothermia. [15]
Thyroid replacement treatment is with intravenous hydrocortisone at stress doses followed by intravenous levothyroxine then switched to oral levothyroxine after clinical improvement. The reason to give steroids is that these patients may have adrenal insufficiency, which can lead to an Addisonian crisis if the thyroid deficiency is replaced without addressing adrenal insufficiency. It is recommended to check for Adrenal insufficiency but wait for the results and start treatment with steroids.
If the treatment is effective, this should result in cardiopulmonary and cognitive improvement. [11] There should also be an associated improvement in laboratory derangements, including an up-trending of free T4, which should be measured every 1 to 2 days during the initial treatment period. Low-dose intravenous liothyronine (T3) can be considered until initial improvement. [11] TSH may not reflect changes in such cases as it can take up to 4 weeks to normalize, hence it may not be helpful.
Endocrinology consultation should be considered.
- Enhancing Healthcare Team Outcomes
Hypothyroidism affects multiple organ systems across all age groups and affects patient well-being and ability to function on a daily basis. This disorder is best managed by the primary care physician or endocrinologist. Treatment is with levothyroxine monotherapy (Grade A, Best Evidence Level 1). [2]
Effective treatment calls for a team-based and patient-centered approach. When patient symptoms are not adequately controlled despite normalization of thyroid labs, it is important to rule out nonendocrine pathologies for the nonspecific symptoms.
Endocrinology consultation is also recommended in complex scenarios such as preconception, pregnancy, congenital and pediatric hypothyroidism, failure of treatment, thyroid replacement absorption issues, co-existing cardiac or other endocrine disorders, difficulty in interpretation of thyroid test results, drug-induced hypothyroidism. [2] Other specialists that may be needed are psychiatrists, obstetrician-gynecologist, pediatricians, cardiologists, and intensivists.
It is helpful to work closely with a pharmacist to determine medication and food interactions, the effect of changes in levothyroxine formulations, and to investigate the causes for the requirement of unusually high doses of levothyroxine or fluctuating TSH levels. Prompt notification of unusually high levels of TSH by laboratory personnel, and close monitoring of vital signs, and mental status by nurses can facilitate early treatment and better outcomes, especially in the inpatient setting such as in myxedema coma. Rapid response teams can be effectively utilized when severe long-term hypothyroidism causes hemodynamic instability from myxedema coma. Close interprofessional communication with all the involved teams is essential to improve patient outcomes. [Level 5]
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Tablets or scalpel: Pituitary hyperplasia due to primary hypothyroidism. Contributed from Ahmed Imran Siddiqi MBBS, MRCP Stephanie E. Baldeweg MD, FRCP, FRCP Et al Radiology Case Reports ,Volume 10, Issue 2, 2015, 1099
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- Myxedema Coma due to Hashimoto Thyroiditis: A Rare but Real Presentation of Failure to Thrive in Infancy. [Horm Res Paediatr. 2018] Myxedema Coma due to Hashimoto Thyroiditis: A Rare but Real Presentation of Failure to Thrive in Infancy. Heksch RA, Henry RK. Horm Res Paediatr. 2018; 90(5):332-336. Epub 2018 May 4.
- Review The Myxedema coma in children and adolescents: A rare endocrine emergency - Personal experience and review of literature. [Acta Biomed. 2021] Review The Myxedema coma in children and adolescents: A rare endocrine emergency - Personal experience and review of literature. De Sanctis V, Soliman A, Daar S, Di Maio S, Alhumaidi N, Alali M, Sabt A, Kattamis C. Acta Biomed. 2021 Nov 3; 92(5):e2021481. Epub 2021 Nov 3.
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it was a case study on hypothyroidism in pediatric patient pharmaceutical care plan ,Diagnostic Technics ,treatment and patient counseling was given to the patient representative.
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- 1. CASE STUDY ON HYPOTHYROIDISM Presented by Shazia Afreen 336112820104 To The pharmacy practice dept SSRCP
- 2. Name: xyz Gender: Female Weight: 19 Kgs Consultant: Dr.N.S.Rao IP no: 443466 Age: 7yrs Department: Pediatric Unit: II DOA: 23-02-2015 DOD: 25-02-2015 Chief Complaints: C/O: Swelling over neck since 6 months progressive in nature. H/O: Cold and weight gain. Past Medical History: No data found. Past Medication History: No data found Social History: Diet-Mixed Family History: Nothing significant Patient Demographic Details
- 3. Parameters Reported value Normal value Day 1 Day 2 Day 3 Pulse rate 93 110 100 70-90/min Respiratory rate 28 30 30 18–30/min Diagnosis: Hypothyroidism. Physical Examination Complete Biologicaland Pathological details: Co Parameters Reported value Normal value T3 0.62 ng/ml 0.92-2.4 ng/ml T4 0.3 ng/dL 0.8 - 1.8 ng/dL TSH >100 mIU/L. 0.3 - 3.04 mIU/L.
- 4. Drug Chart S. No Brand Name Generic Name Category Dose Route Fre q Days of treatment 1 2 3 01 Tab.Thyroxine Levo- Thyroxine Thyroxine hormone 75 mg PO OD + + + 02 Syp.Zincovit VitA,B,D Minerals:zn,ki Vitamin &Mineral supplement 5 ml PO TID + + + Syp.Zincovit:vitamin A 1250 IU, vitamin D3 100 IU, vitamin E 2.5 IU, vitamin B12 0.5 mcg, vitamin B1 0.75 mg, vitamin B2 0.75 mg, vitamin B6 0.5 mg, D-panthenol 1.25 mg, nicotinamide 7.5 mg, copper 25 mcg, zinc 5 mg, L-lysine monohydrochloride 5 mg, potassium iodide
- 5. Discharge medication S. No Brand Name Generic Name Category Dose Route Freq 01 Tab.Thyroxine Levo-Thyroxine Thyroxine hormone 75 mg PO OD 02 Syp.Zincovit VitA,B,D Minerals:zn,ki Vitamin &Mineral supplement 5 ml PO TID
- 6. PHARMACEUTICAL CAREPLAN: [SOAP ANALYSIS] Subjective: C/O: Swelling over neck since 6 months progressive in nature. H/O: Cold and weight gain. Objective evidence: Pulse rate ,TSH levels are increased. T3and T4 levels decreased. Assessment: Hypothyroidism: Hypothyroidism, or underactive thyroid, develops when the thyroid gland f ails to produce or secrete as much thyroxine (T4)as the body needs. Becaus e T4 regulates such essential functions as heart rate, digestion, physical gro wth, and mentaldevelopment, an insufficient supply of this hormone can slo w lifesustaining processes, damage organs and tissues inevery part of the b ody, and lead to life-threatening complications. Signs and symptoms: Goiter,Retarded growth
- 7. • Slow heart rate • Tiredness,Inability to tolerate cold • Dry, flaky skin • Puffiness in the face, especially around the eyes • Impaired memory and difficulty in thinking (which may appear as a new learning disability),Emotional depression • Drowsiness, even after sleeping through the night • Constipation Diagnosis: • Serum TSH:It is the most sensitive screening test for hypothyroidism and for diagnosing primary hypothyroidism. • Serum Free T4:It is a useful test for diagnosing primary hypothyroidism. • Serum Free T3:This test is not required for the diagnosis of hypothyroidism. However, serum T3 levels are decreased in euthyroid sick syndrome. • Serum antithyroid :Radioisotope thyroid imaging:This test is useful for measuring iodine uptake or to screen for ectopic thyroid tissue.
- 8. Hypothyroidism: Planning Monitoring parameters: Therapeutic parameters: Thyroid function rests: Serum TSH, Serum Free T4,Serum Free T3,Radioisotope thyroid imaging. Toxicity parameters: Levothyroxine sodium: Hair loss during the first few months of treatment. headache, sleep problems (insomnia), nervousness, irritability, fever, hot flashes, sweating, pounding heartbeats or fluttering in your chest, changes in your menstrual periods, or appetite or weight changes. Drugs: •Levothyroxine sodium Category: Synthetic thyroid hormone Mechanism: Levothyroxine is a synthetic form of thyroxine(T4), an endogenous hormone secreted by the thyroid gland, which is converted to its active metabolite, L-triiodothyronine (T3).T4 and T3 bind to thyroid receptor proteins in the cell nucleus and cause metabolic effects through the control of DNA transcription and protein synthesis. Pharmacist intervention: Not needed.
- 9. DRUG INTERACTIONS List of drug interactions Drug-Drug interactions: Not Found Drug-Food interactions: Levothyroxine sodium + Food Effect: T4 absorption is increased by fasting and decreased by foods such as soybean flour (e.g., infant formula), cotton seed meal, walnuts, dietary fiber, calcium, and calcium fortified juices. Summary: Reduced absorption of Levothyroxine sodium in the presence of food. Severity: Moderate Onset of action: Rapid Management: Levothyroxine sodium should be administered one hour before or two hours after meals. Mechanism: Pharmacokinetic; Absorption Literature reports: Not Found Reference: Drugs.com, medscape.com, ehealthme.com
- 10. PATIENT COUNSELLING • Eat nutritious and balanced diet. • Some vegetables and beans might have a potential to fight against this illness. They are broccoli, c--cabbage, sprouts, cauliflower, soybeans, turnips and mustard green. • Do not consume excessive dairy products for at least 3-4 months until the disease is cured. • Do not take foods high in iodine because iodine will increase the activity of thyroid gland. • Consume more vitamin B 12, vitamin C and vitamin E in diets is essential as they have antioxidant properties that are beneficial in deactivating the harmful effects of free radicals causing hyperthyroidism. • Avoid taking nicotine, caffeine, alcohols, carbonated liquids and processed foods. • Bracing, which restricts motion and supports the joint, can reduce pain during walking and help prevent further deformity. • Immobilization. Protecting the foot from movement by wearing a cast or removable cast-boot may be necessary to allow the inflammation to resolve. • Physical therapy- Exercises to strengthen the muscles, especially when the osteoarthritis occurs in the ankle, this may give greater stability and help avoid injury that might worsen the condition.
- 11. Thank you
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Endocrinology
- Thyroid storm: A case from the endocrine teaching clinics
June 12, 2018
A 33-year-old woman presented to an outside facility with increasing shortness of breath, orthopnea, paroxysmal nocturnal dyspnea and increasing lower limb edema — findings suggestive of biventricular heart failure. Further questioning revealed a two- to three-month history of unintentional weight loss, heat intolerance, diarrhea, abdominal pain and palpitations.
The symptoms started about six months after her most recent delivery of a healthy child. Her past medical history was significant for obesity, mild asthma requiring occasional albuterol use and third trimester gestational hypertension during her recent pregnancy (managed without pharmacotherapy).
On presentation, the patient showed signs of tachycardia (118 beats per minute) and tachypnea (22 breaths per minute) and had lower extremity pitting edema. Laboratory testing was significant for hyperthyroidism:
- Thyroid-stimulating hormone (TSH) < 0.1 mIU/L (normal, 0.49 to 4.67 mIU/L)
- Free thyroxine (FT4) 2.6 ng/dL (normal, 0.7 to 1.8 ng/dL)
The serum brain natriuretic peptide was markedly increased at 2,819 pg/mL (normal < 100 pg/mL). Chest X-ray demonstrated cardiomegaly. The patient was diuresed and started on beta-adrenergic blockade and 10 mg of methimazole three times a day. An echocardiogram demonstrated a severely dilated left ventricle and an ejection fraction of 10 to 15 percent.
Cardiovascular surgery operating room at Mayo Clinic
This image from a cardiovascular surgery operating room is representative of the significant amount of equipment and coordinated care required during insertion, adjustment or both of ECMO or to support patients with ECMO who require an operation.
Despite treatment, shortness of breath and hypotension necessitated intra-aortic balloon pump placement and intubation, and she was transferred to Mayo Clinic in Rochester, Minnesota. On arrival, she was sedated, intubated and hypotensive on inotropic support. A repeat echocardiogram revealed an ejection fraction of 9 percent. Due to severe cardiogenic shock, venoarterial extracorporeal membrane oxygenation (VA ECMO) cannulation was initiated.
Endocrinology was consulted. Mild exophthalmos was noted without dermopathy or acropachy. The patient's presentation with decompensated heart failure, preceding gastrointestinal complaints, and tachycardia was highly suggestive of thyroid storm (Burch and Wartofsky Point Scale 40).
Aggressive therapy was started with 200 mg of propylthiouracil administered every four hours, 100 mg of hydrocortisone administered every eight hours and a saturated solution of potassium iodine administered two hours after propylthiouracil. Repeat biochemical testing revealed a TSH of < 0.01 mIU/L (normal, 0.4 to 4.0 mIU/L), FT4 of 3.4 ng/dL (normal, 0.9 to 1.7 ng/dL) and a total tri-iodothyronine of 308 ng/dL (normal, 80 to 200 ng/dL).
Right midthyroid lobe demonstrating increasing vascularity
Doppler ultrasound of right midthyroid lobe demonstrating increasing vascularity.
While thyroid receptor antibodies were pending, a bedside ultrasound revealed a hypervascular thyroid gland. The patient's clinical picture was most consistent with cardiogenic shock in the setting of thyroid storm of autoimmune origin, and possible postpartum cardiomyopathy.
Despite treatment, five days later the patient was still clinically and biochemically hyperthyroid with serum TSH of 0.02 mIU/L and FT4 of 5.4 ng/dL by equilibrium dialysis (employed because of her significantly altered protein status). Given the critical nature of the patient's condition and the need for rapid normalization of her thyroid status, total thyroidectomy was recommended.
Microscopic magnification of thyroid tissue
Low (A) and high (B) microscopic magnification of thyroid tissue demonstrating epithelial hypertrophy and invagination forming papillary projections and scalloping of colloid (red arrows) consistent with Graves' disease.
Plasmapheresis was initiated to optimize preoperative thyroid levels. Endocrine and cardiovascular surgeons collaborated to perform a total thyroidectomy during which anticoagulation, necessary for ECMO, was held. Pathology revealed diffuse follicular hyperplasia consistent with Graves' disease. As expected, the patient also had an elevated thyroid receptor antibody concentration of 20 IU/L (normal, 0 to 1.75 IU/L).
Postoperatively, anticoagulation was restarted without complication.
Following total thyroidectomy, the patient improved and was able to be weaned off vasopressor support and she was extubated. Thyroid replacement therapy was initiated. Unfortunately, her cardiac function remained suboptimal (ejection fraction of 15 percent), and therefore a left ventricular assist device was placed to bridge to cardiac transplantation.
As highlighted in an article in the journal Thyroid in 2012, thyroid storm is a life-threatening condition and early recognition is essential — mortality remains high (11 percent) despite improvements in management. The diagnosis should be considered in an individual with severe symptoms of multiorgan dysfunction and biochemical thyrotoxicosis. Several scoring systems have been devised to assist recognition and early implementation of aggressive treatment. The authors note that a high level of suspicion is important.
In this case, despite aggressive nonsurgical management of hyperthyroidism, additional cardiovascular support was required. ECMO can be used in such cases, and a growing body of literature supports its use in thyroid storm-induced cardiogenic shock refractory to usual treatment — as highlighted in an article in the journal Thyroid in 2011.
Total thyroidectomy for thyroid storm on ECMO, however, has not been reported, but occurred without complication in this case. Close collaboration between endocrinology, endocrine surgery and cardiovascular surgery is vital. Reports suggest that rapid cardiac function recovery with the normalization of thyroid hormone occur following thyroidectomy. In the current case, cardiac function improved, but left ventricular assist device (LVAD) therapy was eventually required to bridge to cardiac transplantation, suggesting an additional underlying cardiomyopathy. The patient was able to be discharged home with an LVAD, awaiting heart transplantation.
- Early recognition and appropriate treatment of thyroid storm — which may include thyroidectomy — is essential to improve outcome.
- Thyroidectomy should be pursued when medical therapy fails to control the thyrotoxicosis.
- ECMO should be considered as a means of cardiac support in patients who are unresponsive to conventional therapy until thyroid hormone normalization can be achieved.
For more information
Akamizu T, et al. Diagnostic criteria, clinical features, and incidence of thyroid storm based on nationwide surveys. Thyroid. 2012;22:661.
Hsu LM, et al. Extracorporeal membrane oxygenation rescues thyrotoxicosis-related circulatory collapse. Thyroid. 2011;21:439.
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Hyperthyroidism Case Study
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Hyperthyroidism is a disorder that falls under the category of endocrine disorders. The thyroid gland is overactive and produces more thyroid hormones than the body needs. As a result, there is a myriad of symptoms that the patient will encounter. The symptoms can begin to affect a person’s life if not treated.
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It will include three hypothyroidism nursing care plans with NANDA nursing diagnoses , nursing assessment, expected outcome, and nursing interventions with rationales .
Hypothyroidism Case Scenario
A 47-year-old woman presents to her primary care physician with complaints of fatigue and unexplained weight gain. The patient complains of feeling mildly unwell for the last 6 months and has experienced a variety of miscellaneous symptoms.
She has noticed her skin is more dry than usual and she has been experiencing frequent constipation. Thinking she was dehydrated, she tried to increase her water intake but noticed no improvement.
She also has been unable to participate in her daily walking club due to fatigue. Over the last 6 months, she has gained 12 kg and states “I expected some weight gain because I wasn’t walking as much, but this seems excessive!”
Upon assessment, the patient is alert and oriented. Her temperature is 37.5 ˚C, heart rate is 56 BPM, blood pressure is 124/82 mmHg, respirations 20 breaths per minute, and oxygen saturation is 99% on room air.
Aside from some dry skin and mild ankle swelling, her assessment is within normal limits.
The patient’s blood work reveals an elevated TSH level of 5.2 IU/mL and a decreased T4 level of 0.8 ng/dL.
The patient is diagnosed with Hypothyroidism.
#1 Sample Nursing Care Plan for Hypothyroidism – Fatigue
Nursing assessment.
Subjective Data:
- The patient is unable to complete her regular exercise routine due to fatigue.
Objective Data:
- The patient is slightly bradycardic.
- She has gained 12 kg in 6 months.
- TSH level of 5.2 IU/mL and T4 level of 0.8 ng/dL.
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Fatigue related to hormone deficiency as evidenced by weight gain, bradycardia, and inability to complete her regular exercise routine.
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Short-term goal: The patient will be able to list a few strategies for managing fatigue in the short term.
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#2 sample nursing care plan for hypothyroidism – risk for overweight.
- The patient reports decreased activity and gaining 12 kg in 6 months.
Hypothyroidism Nursing Diagnosis
Risk for overweight related to decreased metabolic process as evidenced by weight gain of 12 kg in 6 months.
Goal/Desired Outcome
Short-term goal: By the end of the shift the patient will state the relationship between excess weight and hypothyroidism.
Long-term goal: The patient will lose excess weight and maintain a normal BMI.
Hypothyroidism Nursing Interventions with Rationales – Risk for overweight
#3 sample nursing care plan for hypothyroidism – deficient knowledge, advertisements if(typeof ez_ad_units = 'undefined'){ez_ad_units.push([[300,250],'nurseship_com-mobile-leaderboard-1','ezslot_15',664,'0','0'])};__ez_fad_position('div-gpt-ad-nurseship_com-mobile-leaderboard-1-0'); nursing assessment.
- The patient initially thought her symptoms were due to dehydration.
Deficient knowledge related to new diagnosis as evidenced by confusion about symptoms of hypothyroidism.
Short-term goal: By the end of the shift the patient will state the importance of hormone replacement therapy and taking the medication in the morning, at the same time every day, and on an empty stomach.
Long-term goal: The patient will take Synthroid regularly and her TSH and T4 levels will return to normal.
Hypothyroidism Nursing Interventions with Rationales – Deficient knowledge
Related hypothyroidism nursing diagnosis (nanda).
Additional hypothyroidism nursing diagnoses are listed below.
- Constipation related to decreased physical activity; decreased gastric motility.
- Decreased activity tolerance may be related to the stiffness of the muscles; dyspnea on exertion.
- Impaired physical mobility may be related to excessive fatigue and weakness; muscular pain; alteration in reflexes.
- Impaired skin integrity may be related to dry or scaly skin; swelling.
- Impaired gas exchange may be related to respiratory depression.
To conclude, here we have formulated a scenario-based sample nursing care plan for Hypothyroidism. Prioritized nursing diagnosis includes fatigue, risk for overweight, and deficient knowledge .
Additionally, these sample hypothyroidism nursing care plans comprise nursing assessment, NANDA nursing diagnosis, goal, and interventions with rationales.
Recommended Readings & References
Ackley, B., Ladwig, G., Makic, M., Martinez-Kratz, M., & Zanotti, M. (2020). Nursing Diagnoses Handbook: An Evidence-based Guide to Planning Care (12th ed.). Elsevier.
Comer, S. and Sagel, B. (1998). CRITICAL CARE NURSING CARE PLANS. Skidmore-Roth Publications.
Doenges, M., Moorhouse, M., & Murr, A. (2013). Nurse’s Pocket Guide: Diagnoses, Prioritized Interventions, and Rationales (13th ed.). F. A. Davis Company.
Herdman, T., Kamitsuru, S. & Lopes, C. (2021). NURSING DIAGNOSES: Definitions and Classifications 2021-2023 (12th ed.). Thieme.
Swearingen, P. (2016). ALL-IN-ONE CARE PLANNING RESOURCE (4th ed.). Elsevier/Mosby.
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Thyroid Papillary Carcinoma and Hyperthyroidism: A Case Study
1.Department of Medicine, Section of Endocrinology, Aga Khan University Hospital, Karachi, Pakistan 2.Medical Student, Aga Khan Medical College, Karachi, Pakistan 3.Consultant Diabetologist & Endocrinologist, Bolan Medical University Hospital, Quetta, Pakistan 4.Department of Medicine and Section of Endocrinology, Aga Khan University Hospital Karachi, Pakistan *Correspondence to [email protected]
The authors have declared no conflicts of interest.
Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License .
Background: Concurrent thyroid cancer and hyperthyroidism is a rare finding. The frequency of this association is very variable. A rare case of papillary thyroid cancer associated with hyperthyroidism is described here.
Case: A 49-year-old male presented to the authors’ outpatient clinic with complaints of a painless left-sided anterior neck swelling that had persisted for the past 8 months. He also reported weight loss for the same duration. The anterolateral swelling was non-tender, asymmetrical, mobile, and rubbery.
Investigations: Biochemical analysis confirmed hyperthyroidism. Ultrasound examination of the neck showed a well-defined, solid, and cystic lesion in the left lobe and isthmus of thyroid gland. The solid portion had few specks of calcification. A radioactive thyroid scan showed increased tracer uptake in the left lobe. Papillary carcinoma of thyroid origin was discovered after fine-needle aspiration of the left anterior cervical lymph node. After preparation, a total thyroidectomy was done. Examination of histopathology confirmed papillary thyroid carcinoma.
Treatment: Following radioactive thyroid ablation, the patient was started on suppressive doses of thyroxine daily.
Conclusion: Although thyroid cancer with hyperthyroidism is a rare finding, it should not be disregarded. To avoid missing this unusual yet uncommon discovery, a detailed history and physical examination should be performed, as well as all required investigations.
Thyroid cancer is the most common malignant endocrine tumour in the world, but it only accounts for 1% of all cancers. 1 The most common form of thyroid cancer is papillary thyroid cancer (PTC). 2 High-dose external radiation exposure is the most significant risk factor of PTC. Radiation causes genetic lesions that lead to neoplastic transformation. 3 The majority of radiation-induced PTC cases have RET /PTC fusions, which are established genetic rearrangements. 4
Thyroid hormone development is excessive in patients with hyperthyroidism. Graves’ disease, toxic multinodular goitre, thyroiditis, and exogenous thyroid intake are all common causes of hyperthyroidism.
The coexistence of thyroid cancer and hyperthyroidism is uncommon. A review of literature reports the weighted average of prevalence of malignancy to be 3.1% amongst solitary hyperfunctioning nodules. 5 Furthermore, thyroid carcinoma and hyperthyroidism are thought to be related conditions, and, therefore, pose significant diagnostic, therapeutic, and prognostic challenges. 5
Unfortunately, due to a lack of population-based data, determining the incidence of thyroid carcinoma in Pakistan is difficult. 6
A rare case of PTC and concurrent hyperthyroidism is reported here.
A 49-year-old male with a swelling on the left side of his neck presented to the authors’ outpatient clinic. The swelling was painless and had been gradually increasing in size over 8 months. The patient also reported a significant weight loss of 5–6 kg over the same duration. There were no associated complaints of dyspnoea, dysphagia, hoarseness, heat or cold intolerance, palpitations, changes in urinary or bowel habits, or a past medical history of similar complaints. He was a non-smoker, who denied ever having been exposed to radiation in the head and neck area during his childhood or adolescence. The patient also denied having any family history of thyroid dysfunction or cancer.
The physical examination showed a middle-aged man who was afebrile, had a resting pulse rate of 96 beats per minute, a respiratory rate of 28 breaths per minute, and a blood pressure of 128/70 mmHg. On ophthalmological examination, there was no exophthalmos or lid lag on eye movement. There were no fine tremors and no voice hoarseness.
No thyroid nodule was palpable on neck examination. However, there was a palpable left anterolateral cervical lymph node. This node was asymmetrical, rubbery, mobile, non-tender, and not attached to any overlying or underlying tissue.
Complete blood count was normal. Thyroid function test revealed a thyroid-stimulating hormone (TSH) of 0.010 mIU/L (normal range: 0.4–4.0 mIU/L) and a free T4 of 2.6 ng/dL (normal range: 0.7–1.8 ng/dL). Ultrasound examination of the neck showed a well-defined, cystic, and solid lesion in the left lobe and isthmus of the thyroid gland, measuring 21x11x16 mm. The solid portion measured 9×6 mm, with few specks of calcifications. Sub-centimetre lymph nodes were noted in Levels I, II, IV, and V of the neck bilaterally. The largest lymph node was seen on the left side, which measured 9 mm.
An ultrasound examination of the neck showed a well-defined cystic and solid lesion in the left lobe and isthmus of the thyroid gland ( Figure 1 ).
Figure 1: Ultrasound of thyroid.
A radioactive scan was requested to determine thyroid functioning because the thyroid function tests were consistent with hyperthyroidism. These findings were consistent with the presence of a functional nodule. Increased tracer uptake was seen in the left lobe during the scan. The patient was subsequently started on carbimazole and propranolol. The hot nodule was not biopsied because of the very low risk of malignancy. Fine-needle aspiration of the left anterior cervical lymph node was performed to evaluate for sinister pathologies like tuberculosis, lymphoma, or metastasis. The histopathological report revealed metastatic papillary carcinoma of thyroid origin.
Complete thyroidectomy with radical neck dissection was planned. Propranolol 40 mg three times daily and carbimazole 30 mg/day were instituted to prevent a potential thyroid storm during surgery. The patient underwent the surgery without any complications. The presence of multicentric oval nuclei with grooving on histopathological examination confirmed PTC. The specimen sent included the thyroid gland (right lobe, left lobe, and isthmus); Level II, III, and IV lymph nodes on the right; Level II, III, IV, and V on the left; and Level VI of the neck. Bifocal PTC was identified with tumour size of 2.0×1.7×1.0 cm in isthmus and 0.5×0.4×0.3 cm in the left lobe. All lymph nodes were identified as being negative for the disease, except one lymph node in the left Level III measuring 0.1 cm, with no extra nodal extension. Pathological tumour-node-metastases was reported as pT1b N1b.
A haematoxylin and eosin stain of thyroid tissue showed classical PTC, with the cuboidal epithelium exhibiting nuclear clearing, crowding, and intranuclear groove ( Figure 2 ). Calcification is seen at the lower-left corner.
Figure 2: Haematoxylin and eosin stain of thyroid tissue.
One lymph node in left cervical Level III was involved by the tumour. The size of the nodal metastasis was 0.1 cm with no extra nodal extension. All of the other lymph nodes were negative for metastasis.
Post-operative thyroid function test revealed a TSH of 29.4 mIU/mL, thyroglobulin of 0.04 ng/mL (normal range: 20–25 ng/mL), and anti-thyroglobulin antibody of 0.26 IU/ml (normal range: less than 20 IU/mL). The patient received a post-operative dose of radioactive iodine (RAI) 150 mCi. Post-ablative thyroid scan findings were suggestive of functioning residual thyroid tissue in the neck with bilateral cervical lymphadenopathy. To hold TSH below 0.1 mIU/mL, the patient was started on a suppressive dose of thyroxine.
In certain cases, a hyperfunctioning thyroid nodule is thought to rule out thyroid cancer. 7 Thyroid cancer and hyperthyroidism may occur as a result of a fortuitous malignancy in the thyroid gland of a patient with clinical hyperthyroidism, or as a rare case of thyroid cancer presenting with hyperthyroidism. 8
In patients with hyperthyroidism, the possibility of thyroid malignancy is rare, but should not be disregarded. 9 Several studies have reported cases where thyroid malignancy and hyperthyroidism occur together. 10-12 Diagnosis relies on histopathological and clinical correlation.
The exact cause of thyroid cancer with coexistent hyperthyroidism is unclear. Thyroid carcinoma can cause hyperthyroidism due to somatic mutations in TSH receptor genes. These mutations increase thyroid levels by activating the cyclic adenosine monophosphate cascade, which causes hormone secretion. 9 The combination of mutated TSH receptors and TSH stimulating further growth have been linked to the development of malignancy, but this has not yet been confirmed. 13,14
Thyroid cancer caused by an autonomous thyroid nodule needs careful consideration and evaluation. Some factors, however, can aid in determining whether hyperthyroidism is caused by primary hyperfunctioning thyroid carcinoma. These include if there is no improvement in thyrotoxicosis after RAI treatment; if ultrasound findings show hypoechoic stable nodules with microcalcifications; or if there is rapid tumour growth. 15 In the authors’ case, the patient did not receive RAI for thyrotoxicosis to monitor any positive or negative treatment outcomes. However, the ultrasonographic findings of a solid lesion with few specks of calcifications were suggestive of underlying thyroid malignancy. Family history of thyroid cancer, a prior history of head and neck irradiation, nodules having microcalcifications, irregular margins and taller-than-wide shape, genetic mutations, tumour size greater than 4 cm, fixation to adjacent structures, and signs of tumour invasion have all been identified as additional risk factors for malignancy. 16
Studies point out an increased incidence of follicular thyroid carcinoma (FTC) with concomitant hyperthyroidism. Mirfakhraee et al. 5 reported that out of 77 patients, 28 had thyroid carcinoma in a solitary hyperfunctioning nodule. The FTC subtype accounted for the majority of hyperfunctioning thyroid carcinomas.Similarly, Qiu et al. 17 found that the FTC subtype was prevalent in 60.5% of functional metastatic thyroid carcinomas, with five cases being hyperfunctioning. Patients with metastatic hyperfunctioning FTC have a poor prognosis compared with patients with PTC. As a result, patients with hyperfunctioning thyroid carcinoma tend to have a high prevalence of FTC, with an especially high prevalence among patients with metastatic disease. However, in this study, the hyperfunctioning thyroid carcinoma is of a papillary subtype with a mild clinical picture of hyperthyroidism.
Two studies, however, reported PTC with hyperthyroidism and extensive disease metastasis. The authors attributed the high level of free thyroid hormones to bone metastasis. 18 This explains a relatively innocuous clinical presentation (cervical lymph node involvement with no widespread metastasis) in this case, as the concentration of free thyroxine was within the higher range of the normal level.
The mainstay treatment of thyroid carcinoma with concomitant hyperthyroidism is surgery. This method not only confirms the condition after a pathological examination, but it also removes the cancer and resolves the use of anti-thyroid drugs as a hyperthyroidism treatment, as these are often implemented to prevent a potential thyroid storm. Other options for treatment include RAI fractionation or minimally invasive local ablation. 19 In patients with primary hyperfunctioning thyroid carcinoma, RAI is primarily used as a treatment alternative after surgery. 20
Thyroid carcinoma and hyperthyroidism coexisting is an uncommon occurrence. Each thyroid nodule should be assessed with a high index of suspicion for malignancy. To prevent ignoring this unusual but important association, thorough medical history and physical examinations should be undertaken, as well as all other necessary investigations.
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Hyperthyroidism Case Study Nursing
Added on - 2020-04-15
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Nursing interventions for a patient with hypothyroidism include the following: Promote rest. Space activities to promote rest and exercise as tolerated. Protect against coldness. Provide extra layer of clothing or extra blanket. Avoid external heat exposure. Discourage and avoid the use of external heat source. Mind the temperature.
Symptoms of hypothyroidism are nonspecific and reflect the generalized slowing of the metabolic processes and include fatigue, lethargy, cold intolerance, and weakness. 3 Signs and symptoms...
Case Study: 60-Year-Old Female Presenting With Shortness of Breath Medical Reference Case Study: 60-Year-Old Female Presenting With Shortness of Breath Case Presentation The patient is a 60-year-old white female presenting to the emergency department with acute onset shortness of breath.
People with hypothyroidism experience a slowing of metabolic processes, which can result in fatigue, slow speech, constipation, cold intolerance, weight gain, bradycardia, and decreased deep tendon reflexes. One study showed the most common symptoms are tiredness, dry skin, and shortness of breath.
Hypothyroidism Case Study Hypothyroidism case study questions and answers. Assignment. University Tarrant County College Course Medical-Surgical Nursing I (VNSG-1429) Academic year2023/2024 Helpful? 00 Comments Please sign inor registerto post comments. Students also viewed Endocrine System Disorders
Hypothyroidism - Case study examples - You are working in a community outpatient clinic where you - Studocu Case study examples you are working in community outpatient clinic where you perform the intake assessment on woman who is attending graduate school and is very Skip to document Ask an Expert Sign inRegister Sign inRegister Home
Hypothyroidism Nursing Care Plan 3 Fatigue Nursing Diagnosis: Fatigue related to impaired metabolic state secondary to hypothyroidism, as evidenced by lethargy, impaired concentration, increased rest periods, inability to perform daily tasks and lack of energy. Desired Outcomes:
List symptoms the nurse will observe if the parathyroid gland is injured or removed during surgery. Case Study: Hypo Thyroid Disease - Myxedema Jeanine has been dieting and exercise and trying unsuccessfully to lose weight. Her nutrition counselor suggests that Jeanine to her physician.
Nursing Case Studies 15 Med-Surg Case Studies for Nursing Students NURSNG.com NursingStudentBooks.com Jon Haws RN CCRN Sandra Haws RD CNSC Taz Kai LLC Case Study Hypothyroidism L.R. is a 35 year old female patient who is being seen for a post-op exam following a partial thyroidectomy 1 month ago. The patient had developed a benign nodule on her thyroid that continued to grow and was starting ...
CASE 1 THYROID DISEASE History: A 50 year old housewife complains of progressive weight gain of 20 pounds in 1 year, fatigue, postural dizziness, loss of memory, slow speech, deepening of her voice, dry skin, constipation, and cold intolerance. Physical examination: Vital signs include a temperature 96.8 o F, pulse 58/minute and regular, BP 110/60.
Hypothyroidism results from low levels of thyroid hormone with varied etiology and manifestations. Untreated hypothyroidism increases morbidity and mortality. In the United States, autoimmune thyroid disease (Hashimoto thyroiditis) is the most common cause of hypothyroidism, but globally lack of iodine in the diet is the most common cause.
it was a case study on hypothyroidism in pediatric patient pharmaceutical care plan ,Diagnostic Technics ,treatment and patient counseling was given to the patient representative. Dr. Shazia Afreen Follow Safety process associate at Vigimedsafe Advertisement Advertisement Recommended case study on HYPOTHYROIDISM Venkata subbareddy Bareddy 12k views
In this case, despite aggressive nonsurgical management of hyperthyroidism, additional cardiovascular support was required. ECMO can be used in such cases, and a growing body of literature supports its use in thyroid storm-induced cardiogenic shock refractory to usual treatment — as highlighted in an article in the journal Thyroid in 2011.
Hypothyroidism could be an autoimmune disease. The immune system protects the body from foreign substances and infection. However, in this case the immune system mistakes the thyroid gland cells and enzymes, as foreign objects and attacks them resulting in the low production of thyroid hormone. [5]
Hypothyroidism means you have too little thyroid hormone. Another term is an "underactive thyroid.". Hypothyroidism is the most common thyroid disorder. It occurs more often in women, it increases with age, and it runs in families. Symptoms include: Tiredness. Mental depression. Sluggishness. Feeling cold.
Free Meningitis Case Study Resource Nursing Case Studies is Nurse inspired and is Nurse driven. Nursing Case Studies has been developed to assist professional nurse educators in their everyday responsibilities of teaching, mentoring and maintaining the best in critical thinking, patient care and...
Here we will formulate sample Hypothyroidism nursing care plans based on a hypothetical case scenario.. It will include three hypothyroidism nursing care plans with NANDA nursing diagnoses, nursing assessment, expected outcome, and nursing interventions with rationales.. Hypothyroidism Case Scenario. A 47-year-old woman presents to her primary care physician with complaints of fatigue and ...
Endocrine System Case Study Anatomy. This product is a case study on Graves Disease requiring students to interpret lab results, make a diagnosis, and give a prognosis based on the patient information in the narrative and lab results. There are 10 pages and 34 questions in this product and it includes an answer sheet.
Symptoms of Hyperthyroidism (Mnemonic) Outline Mrs. Black is a 31 year old female who is 2 weeks postpartum. This morning her husband found her difficult to rouse and confused, and called 911. The husband indicates she has been quite anxious since the birth of their first child.
ATA Trainees' Educational Track Case Studies - Thyroid Cancer Case Study #8 Chhaya D. Makhija, MD University of Nebraska Medical Center Omaha, NE 69 y.o. male seen followup of his papillary thyroid carcinoma T4 N1b M1, stage IVc with known pulmonary metastasis and newly diagnosed right choroidal mets, while on Pazopanib systemic therapy.
Hypothyroidism nursing lecture about pathophysiology, medications/pharmacology, and complications such as myxedema coma. Hypothyroid is where the thyroid gla...
A rare case of papillary thyroid cancer associated with hyperthyroidism is described here. Case: A 49-year-old male presented to the authors' outpatient clinic with complaints of a painless left-sided anterior neck swelling that had persisted for the past 8 months. He also reported weight loss for the same duration.
1NURSING CASE STUDY Case Study: Answer 3 Graves disease or hyperthyroidism is a kind of autoimmune disease that results from the over-production of the thyroid hormones in response to auto-antibodies or long acting thyroid stimulating (LATS) antibodies.