4/20/2020- Monday

Difference between primary, secondary and tertiary hyperparathyroidism. What is the name of the imaging test used before surgery? Patho and lab findings.

Primary hyperparathyroidism is due to an issue in the gland. Most common cause of primary hyperparathyroidism is parathyroid adenoma or hyperplasia of the glands, which will lead to overproduction of PTH and therefore increase calcium production leading to hypercalcemia. PTH stimulates activation of Vit D, activated Vit D increases absorption of calcium from intestines.

As we mention in last class, signs and symptoms of hypercalcemia include:

Bones: bone pain/fractures

Stones: Nephrolithiasis (kidney stones)

Abdominal (symptoms) groans: constipation

Psychic moans: depression, anxiety

Weakness: Decreased DTR (deep tendon reflex)

Secondary hyperparathyroidism is also called reactive hyperparathyroidism because the increase of parathyroid hormone is due as a response of hypocalcemia and is not caused by abnormalities of parathyroid gland. Calcium has a negative feedback effect on parathyroid gland. When levels of calcium are elevated, it will send signal to parathyroid gland to stop secretion of PTH hormone and vice versa. Vitamin D deficiency will result in low calcium levels which will then lead to hyperparathyroidism.

Secondary hyperparathyroidism can be due to chronic renal disease, malnutrition, and vitamin D deficiency. Reports estimate that as many as 90% of patients with chronic renal disease will develop secondary hyperparathyroidism by the time hemodialysis is initiated. Abnormalities in the renal tubular absorption will also lead to reduction of phosphate excretion which will lead to elevated serum phosphate and reduced vitamin D leading to hypocalcemia and finally resulting in secondary hyperparathyroidism.

Management: The management of secondary hyperparathyroidism should be started at the beginning of CKD stage III (estimated GFR, <60 mL/min).

Tertiary hyperparathyroidism occurs when elevated parathyroid hormones due to secondary hyperparathyroidism persist for too long, leading to high calcium levels in the blood. If secondary hyperparathyroidism is not treated, it will progress to tertiary hyperparathyroidism.

Most commonly we see this in the setting of renal transplant where patient with secondary hyperparathyroidism continue to have elevated PTH levels even after the transplant. After correction of the primary disorder (chronic kidney disease) by renal transplant, the enlarged parathyroid tissue fails to go back to normal and continues to over-secrete PTH. Tertiary hyperparathyroidism can also occur in those patients with chronic dialysis which can cause long-standing period of hypocalcemia. Tertiary hyperparathyroidism will have normal or elevated serum calcium concentrations in combination with elevated intact PTH levels. Labs in patients with tertiary HPT may also show decreased vitamin D and phosphate levels.

Treatment: Management of patients with secondary HPT is predominantly medical, while treatment of patients with tertiary HPT is surgical. (total vs. subtotal parathyroidectomy).

Supplementation of calcium using oral calcitriol and vitamin D is usually sufficient to manage PTH levels in patients with Chronic renal failure and secondary HPT. Also treat the underlying issue. In tertiary hyperparathyroidism, calcium and vitamin are usually not given because people with tertiary hyperparathyroidism already have elevated calcium.

Indication for surgery in secondary hyperparathyroidism (parathyroidectomy).

Indication for surgery in tertiary hyperparathyroidism:

Severe hypercalcemia (calcium > 11.5 or 12 mg/dL)

Persistent hypercalcemia (calcium > 10.2 mg/dL more than 3 months to one year)

Severe Osteopenia (low bone mineral density)

Symptomatic hyperparathyroidism

Fatigue

Pruritis

Bone pain or pathologic bone fracture

Peptic ulcer disease

Mental status changes

History of renal calculi

BEWARE OF POSTOP HYPOCALCEMIA, especially with total parathyroidectomy. Surgical strategies can be broadly divided into subtotal or total parathyroidectomy with or without autotransplantation

Imaging: Tests such as a high-resolution parathyroid ultrasound or CT scan or a nuclear medicine scan (called a sestamibi scan)à gold standard. Usually done preop or intra-op by identifying the location of the overactive, enlarged gland. Sestamibi is a small protein which is labeled with the technetium-99. It’s a mild and safe radioactive agent that is injected into the veins of a patient with parathyroid disease and is absorbed by the overactive parathyroid gland.

PTH levels during a parathyroidectomy are also obtained to guarantee the successful resection of the abnormal gland.

Source: https://www.jabfm.org/content/22/5/574

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905047/#!po=6.52174

https://www.saintjohnscancer.org/endocrine/diagnosis-and-treatment/parathyroid-imaging/

https://www.parathyroid.com/sestamibi.htm

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Wednesday 4/22/2020

Discuss the management of the patient. Admit the patient to the hospital. NPO, fluids, what needs to be monitored. Imaging standpoint and lab standpoint.

Enteral nutrition (method of feeding that uses the gastrointestinal (GI) tract to deliver part or all of a person’s caloric requirements. It can include a normal oral diet, the use of liquid supplements or delivery of part or all of the daily requirements by use of a tube (tube feeding)

Indication for intensive care:

Those patients with acute pancreatitis and one or more of the following are usually admitted to intensive care.

Pulse <40 or higher than 150 beats/min

BP less 80/60

RR more than 35 breaths/ min.

Sodium levels less than 110 or more than 170 and potassium levels less than 2 or more than 7.

Serum glucose more than 800 or coma state

Elevated hematocrit (more than 44%) and elevated BUN (more than 20)

We first start with supportive treatment

Supportive Care:

High volume IV fluid resuscitation (lactated ringers preferred over normal saline because it decreases systematic inflammatory response better than normal saline). Usually, we give 20mL per kg over 30 mins followed by 3mL/kg/hr for the next 8-12 hrs. This rate of fluid resuscitation is adjusted based on the patient’s BUN, hematocrit levels, mean arterial pressure and vital signs. The goal for mean arterial pressure is 65-80 mmHg, hematocrit to 34% and BUN to 18mg/dL. We should also keep an eye on urine output as low urine output can also indicate acute tubular necrosis in this case.

Pain Control:

Opioids here can be a safe choice. Hydromorphone or fentanyl can be used for pain relief in severe pancreatitis but we have to be careful and monitor respiratory functions as opioids can result in respiratory depression. Meperidine is also favored over morphine due to its shorter half-life. Also, for meperidine, we need to monitor seizures and neuromuscular side effects.

Nutrition:

Patient who present with mild acute pancreatitis should receive a regular diet on admission. However, if patient is unable to tolerate an oral diet due to abdominal pain, N/V or ileus, they need to be placed on NPO.

In patients with severe acute pancreatitis, enteral nutrition (tube feeding, like a NG tube) should be started as soon they are admitted ( at least within 48hrs). Its recommended to keep these patients in high protein and low-fat diet due to reduction of pancreatic digestive enzymes.

Parental feeding should only be considered if patients cannot tolerate enteral feeding.

Prophylactic antibiotics:

Antibiotics are not routinely used in pancreatitis. However, the only time it is used is when there are signs of infected pancreatic necrosis which can be seen using a CT scan or MRI. Before using antibiotics, an image-guided fine needle aspiration should be performed to collect culture and distinguish infected from sterile necrosis. In the case of infected necrosis,  we can use broad spectrum antibiotics. These patients with extensive necrotizing pancreatitis who show no clinical signs of improvement, should be managed with therapeutic endoscopy, or surgery. In patients with sterile necrosis and in stable conditions, surgery and antibiotics are not indicated.

If a patient starts to develop peripancreatic fluid collections but no suspicion of sepsis, image-guided fine needle aspiration is also indicated to avoid further complications. Surgery should be the last approach if all previous attempts have failed.

Some additional things we need to monitor with acute pancreatitis:

Electrolytes should be monitored, especially the first 48-72 hrs when doing aggressive IV fluid resuscitation. Hypomagnesemia and hypocalcemia are the two most common electrolytes abnormalities.

Glucose should also be monitored. Hyperglycemia which may result from nutritional therapy and can increase the risk of secondary pancreatic infection.

Patients in intensive care should be monitored for abdominal compartment syndrome. Although its rare, its still possible with these patients.

Management of patients with acute gallstone pancreatitis

In patients with gallstone pancreatitis that is also associated with cholangitis, ERCP should be performed early. If pancreatitis is due to alcohol then alcohol intervention should be done for those patients.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4814287/#!po=12.5000

UpToDate-Acute Pancreatitis Management

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Friday 4/24/2020

Make your own 5 PANCE like questions:

1) 50- year old male was walking with his son and suddenly loses consciousness and falls to the ground. Son tried to check his pulse, but no pulses were felt. Once in the ER, EKG showed wide complex tachycardia at a rate of 200/min. CK-MB levels are also elevated. BP was 90/50. Which is the most appropriate intervention at this point?

1. a) perform physical exam
2. b) synchronized cardioversion
3. c) administer aspirin
4. d) defibrillation

ANSWER- D (this is pulseless ventricular tachycardia and the patient is unstable. Pulseless ventricular tachycardia is treated the same way as V.fib which is emergency defibrillation).

2) A 23-year-old man with a history of ulcerative colitis comes in complaining of abdominal pain and vomiting. He is febrile with a heart rate of 125 beats per minutes and blood pressure of 90/60. He has diffused abdominal tenderness and distention. Which imaging studies is most appropriate to diagnose toxic megacolon?

1. a) Colonoscopy
2. b) Computed tomography
3. c) Plain radiography
4. d) Ultrasound

ANSWER- C (Via radiography we are able to see dilation of the colon which is more than 6cm in patient with toxic  megacolon). Colonoscopy and CT would not be used here because of high risk of colonic perforation with colonoscopy and CT is not first line for Toxic megacolon.

3) 50 year old man comes in complaining of burning sensation on his chest for 3 weeks and has a cough. He says that this burning sensation is usually associated when he’s having fatty food and laying down to sleep with no pillow. If this patient’s condition is left untreated, which of the following complications is most likely to develop.

1. a) Esophageal adenocarcinoma
2. b) Hepatocellular carcinoma
3. c) Squamous cell carcinoma
4. d) Gastric carcinoma.

ANSWER- A (This patient has GERD and if left intreated it will progress to Barrett’s esophagus and eventually to Esophageal adenocarcinoma).

4) A 48-year-old man presents with a 4 week history of rectal pain associated with minimal rectal bleeding. On examination there is a small tear of the anorectal mucosa at the 8 o’clock position. Which is the most appropriate initial treatment?

1. a) Botulinum toxin
2. b) Nitroglycerin
3. c) Sitz baths, psyllium fiber, and bulking agents
4. d) Sphincterotomy

ANSWER- C (This patient has rectal fissure and for rectal fissures with no complications, the first line therapy is sitz baths in combination with psyllium fibers and bulking agents).

5) A 45 year old patient comes in with complains of painless bright- red blood per rectum after each bowel movement. You perform a physical exam and notice non-strangulated internal hemorrhoids and give him stool softeners. 3 weeks later patient comes back and reports no improvement. At this point which is recommended for treatment for this patient?

1. a) Injection sclerotherapy
2. b) Observation
3. c) Operative hemorrhoidectomy
4. d) Rubber band ligation

ANSWER D- Rubber band ligation (This patient was initially treated with stool softeners which is one of the first line treatments, however he had to return back because he wasn’t getting any better. Most surgeons use non-operative outpatient therapies, such as rubber band ligation, as treatment. If refractory, or if symptoms are severe which in this case is indicated).

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