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A 56-year-old man comes to the office for follow up of hypertension. The patient had undergone kidney transplantation one year ago for focal segmental glomerulosclerosis. He was originally seen in the office 8 weeks ago for hypertension and had a blood pressure of 210/110 mm Hg, initially he was given amlodipine, but the patient continued have hypertension. Two weeks ago, he was also started on lisinopril. In addition, he takes tacrolimus and low-dose prednisone. The patient currently feels well. Today, blood pressure is 160/90 mm Hg, pulse is 78/min, and respirations are 16/min. Examination shows normal jugular venous pressure, vesicular breath sounds, and normal heart sounds. The transplant site is nontender Laboratory studies reveal a serum creatinine level of 2.4 mg/dL (2 weeks ago: 1.5 mg/dL) Serum tacrolimus level is within the normal therapeutic range.

Explanation

This patient with a history of renal transplant has severe, persistent hypertension. In association with the acute kidney injury (AKI) that developed after initiation of lisinopril, this presentation suggests renovascular hypertension due to transplant renal artery stenosis (RAS). Although most cases of RAS occur in elderly men with diffuse atherosclerotic disease, it can also occur in patients with a transplanted kidney and is commonly associated with operative abnormalities (eg, trauma during organ procurement, abnormal suture placement), viral infection (cytomegalovirus, BK virus), and atherosclerosis of the donor artery. Transplant RAS typically occurs in the first 2 years after transplantation.

Similar to RAS due to other causes, transplant RAS typically manifests with resistant hypertension. A decline in renal function after the addition of ACE inhibitors or angiotensin II receptor blockers is highly suggestive of the diagnosis. Other findings that suggest RAS include a lateralizing abdominal bruit and recurrent flash pulmonary edema. The diagnosis is made with renal vascular imaging (eg, renal Doppler ultrasonography). Management of transplant RAS usually includes angioplasty, possibly with stent placement.

(Choice A) Kidney biopsy is indicated to evaluate for AKI due to acute allograft rejection, which is somewhat less likely in the absence of graft tenderness or fever. In addition, biopsy is invasive, and noninvasive methods of assessment (eg, imaging) should be performed prior to biopsy.

(Choice B) Because transplant RAS is the equivalent of bilateral RAS in a non-transplant patient, the initiation of an ACE inhibitor is likely to trigger AKI. Increased lisinopril dosing would likely further worsen this patient's renal function.

(Choices C and E) High-dose prednisone is a common cause of hypertension, however, low doses are not typically associated with marked hypertension. Toxicity to calcineurin inhibitors (eg, tacrolimus) can cause hypertension and AKI; however, such adverse effects are more common with elevated plasma drug levels. In addition, the timing of this patient's AKI following initiation of lisinopril makes RAS more likely than an adverse effect of immunosuppression.


Points To remember On Finger Tips

Renal artery stenosis (RAS) can occur in the renal allograft, typically within 2 years of transplant. Like other forms of RAS, suggestive findings include persistently elevated blood pressure, decline in renal function with the addition of ACE inhibitors, a lateralizing abdominal bruit, and recurrent flash pulmonary edema. The diagnosis is made with renal vascular imaging (eg, renal Doppler

A 22-year-old woman comes to the emergency department due to abdominal pain. The patient has had intermittent abdominal pain for the past 2 days, but today the pain has worsened and become constant. She has had no nausea, vomiting, or change in bowel or bladder patterns. The patient's medical history is significant for sickle cell disease, for which she is prescribed hydrocodone as needed; she began taking multiple hydrocodone tablets today when the pain got worse but had only minimal relief. Her last menstrual period was 4 months ago, and she has multiple sexual partners. Temperature is 37.1 C (98.8 F), blood pressure is 132/88 mm Hg, and pulse is 90/min. The abdomen is diffusely tender to deep palpation, there is no rebound or guarding. On pelvic examination, the uterus is enlarged and nontender and the cervix is closed. The remainder of the examination is unremarkable. Pelvic ultrasound reveals an intrauterine pregnancy at 12 weeks gestation with a fetal heart rate of 160/min. Bilateral adnexa have normal Doppler blood flow.
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This patient at 12 weeks gestation with abdominal pain is likely having an acute pain episode (ie, vasoocclusive pain crisis) due to sickle cell disease (SCD) Acute pain episodes are more common in pregnancy, likely because of increased metabolic demands and a hypercoagulable state Although the incidence typically increases with gestational age, acute pain episodes can occur in the first trimester, especially if there are other precipitating factors (eg, stress, nausea/vorniting, dehydration)

Acute pain episodes can last from hours to days and commonly involve the chest, abdomen (as in this case), or long bones. Pain occurs due to

repetitive red blood cell sickling, which causes microvascular occlusion, decreased perfusion, and tissue ischemia (eg, abdominal tenderness)

Management is with fluid resuscitation and opioid pain control

in addition to an increased risk of acute pain episodes patients with SCD are at increased risk of preeclampsia and its sequelae, including placental abruption, fetal growth restriction, and preterm delivery. Therefore, these patients require more frequent prenatal care, a baseline 24 hour urine protein level, and low-dose aspinn for preeclampsia prophylaxis

(Choice A) Opioid use and pregnancy are risk factors for constipation due to decreased gastrointestinal motility, however, this patient's pain

preceded her hydrocodone use, and no changes in bowel pattern are present. (Choice B) Ovarian torsion classically presents with intermittent abdominal pain that suddenly becomes constant and severe due to decreased

ovarian blood flow (evidenced on ultrasound) This patient has normal Doppler blood flow to the adnexa

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(Choice C) Having multiple sexual partners is a risk factor for pelvic inflammatory disease (PID), which can cause diffuse abdominal tenderness However, PID also typically causes fever and uterine tendemess. In addition, PID is uncommon in pregnancy because the cervical mucus plug usually protects the uterus from ascending bacteria

(Choice D) Round ligament pain, caused by the ligament being stretched by the gravid uterus, typically presents as a sharp pain that radiates to

the vagina, not as diffuse abdominal pain

(Choice F) Patients with SCD are at increased risk for spontaneous abortion, however, this patient has a closed cervix, a normal fetal heart rate, and no vaginal bleeding, making this diagnosis less likely

Points To Remember on Finger Tips

During pregnancy, patients with sickle cell disease have an increased incidence of acute vascocclusive pain episodes (eg, abdominal pa increased metabolic demands and a hypercoagulable state
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A 43-year-old woman comes to the emergency department due to nausea, dizziness, and headache for a day. Her menses began 2 days ago. She has occasionally had fatigue and dizziness during her menstrual periods, but today's symptoms feel different. The patient has a history of von Willebrand disease, causing recurrent, heavy menstrual blood loss, and is scheduled for an endometrial ablation procedure. Her only medication is intranasal desmopressin taken on the first 3 days of her menstrual period. Temperature is 36.9 C (98.4 F), blood pressure is 120/80 mm Hg, pulse is 92/min and regular, and respirations are 18/min. The patient appears restless. Mucous membranes are moist. Deep tendon reflexes are 2+ throughout and Babinski sign is absent. Sensory examination shows no focal deficits. The chest is clear to auscultation. The abdomen is soft and nontender. There is no peripheral edema. The remainder of the examination is unremarkable.

This patient's acute nausea is likely due to hyponatremia induced by recent use of intranasal desmopressin Desmopressin is an analogue of antidiuretic hormone (ADH) commonly used to treat central diabetes insipidus, it also promotes the release of von Willebrand factor, and can treat mild to moderately heavy menstrual bleeding associated with von Willebrand disease. However, since desmopressin induces physiologic effects of ADH (eg, renal water reabsorption, concentration of urine), it can cause hyponatremia and excess ADH stimulation, manifesting as syndrome of inappropriate ADH secretion (SIADH). Therefore, serum electrolytes should be obtained first in this patient to check for hyponatremia and rule in the diagnosis of SIADH.

Expected laboratory findings in patients with SIADH include hypotonic hyponatremia (due to ADH-mediated water retention and reabsorption), high urine osmolality (ie, concentrated urine), and high urine sodium (due to increased secretion of natriuretic peptides). seen in this patient, SIADH is also associated with euvolemia (eg, absence of edema or jugular venous distension) on physical examination. At first, ADH mediated water reabsorption slightly increases extracellular volume, however, increased natriuretic peptide secretion leads to sodium and water excretion, ultimately normalizing extracellular volume.

(Choice A) Although hypoxemia (eg, from pulmonary embolism) may manifest with nausea, elevated heart rate, and dizziness, this patient has no risk factors for pulmonary disease or symptoms of respiratory distress (eg, shortness of breath, chest pain). Therefore, serum electrolytes are a better initial test

(Choice B) Although acute liver failure may cause excessive bleeding and present with nausea and dizziness, this patient lacks associated findings of jaundice and abdominal pain and has no risk factors (eg, infection, excess alcohol intake).

(Choice C) MRI of the brain can be used to assess for CNS pathology (eg, bleeding, acute stroke) that could manifest with headache or dizziness. However, this patient lacks focal neurologic signs, therefore, a metabolic workup with serum electrolytes is a more appropriate initial test.

(Choice D) Plasma desmopressin is not routinely measured. It may be high in this patient, given her recent medication use with the onset of menses, but serum electrolytes are a more rapid initial step for confirming hyponatremia and SIADH.

Things to remember👇👇
The administration of desmopressin, an analogue of antidiuretic hormone (ADH), can induce the syndrome of inappropriate ADH secretion. Urinary water excretion is impaired, leading to hypotonic hyponatremia. Laboratory studies, including serum electrolytes, urine osmolality, and urine sodium, are the first step in establishing the diagnosis.

A 4-year-old girl is brought to the ED due to severe oral pain. The patient's pain began 2 weeks ago with discomfort while chewing, and has progressively worsened to refusing any oral intake. She had a similar episode of oral pain last year. Medical history includes 2 sinus infections and numerous episodes of cellulitis. Skin cultures from her previous infections isolated Staphylococcus aureus and Streptococcus pyogenes. Physical examination shows periodontal inflammation with ulceration and necrosis. Laboratory results are as follows:

CBC - Hemoglobin-11.8 g/dL
Hematocrit-36%
Platelets-240,000/mm³
Leukocytes-55,000/mm³
Neutrophils-90%
Lymphocytes-8%
Monocytes-2%