TL Flashcards
Factors that increase risk of STI
Inconsistent condom use, intercourse with multiple partners, and intercourse with partners belonging to a population with a high prevalence of STIs
Screening for STI
Chlamydia, gonorrhea, syphillis in non-pregnant patients, HIV, intimate partner violence
Exceptions to parent/guardian informed consent for sexual activity related care
Contraception
Emergency care (eg, ruptured ectopic pregnancy)
Pregnancy care
Sexually transmitted infection
Reportable infectious diseases: diseases affecting unvaccinated
Measles
Rubella
Varicella zoster (chickenpox)
Mumps
Poliovirus (poliomyelitis)
Hepatitis A
Hepatitis B
Corynebacterium diphtheria (diphtheria)
Haemophilus influenzae type b (epiglottitis, meningitis)
Neisseria meningitis (meningitis)
Clostridium tetani (tetanus)
Bordetella pertussis (pertussis)
Reportable infectious diseases: foodborne/waterborne diseases
Vibrio cholera (cholera)
Salmonella enterica (typhoid, salmonellosis)
Shigella (shigellosis)
Shiga-toxin-producing Escherichia coli
Clostridium botulinum (botulism)
Listeria monocytogenes (listeriosis)
Legionella pneumophilia (legionellosis)
Giardia lamblia (giardiasis)
Trichinella species (trichnellosis)
Reportable infectious diseases: mosquito-borne diseases
West Nile virus
Reportable infectious diseases: potential biologic weapons
Bacillus anthracis (anthrax)
Yersinia pestis (plague)
Poxviridae (smallpox)
Reportable infectious diseases: sexually transmitted
Treponema pallidum (syphillis)
Neisseria gonorrhoeae (gonorrhea)
Chlamydia trachomatis serotypes D-K
Haemophilius ducreyi (chancroid)
Hepatitis C
Reportable infectious diseases: tick borne diseases
Borrelia burgdorferi (Lyme disease)
Rickettsia rickettsii (Rocky Mountain spotted fever)
Ehrlichia species (ehrlichiosis)
Francisella tularensis (tularemia)
Reportable infectious diseases: zoonotic diseases
Brucella species (brucellosis)
Rhabdoviruses (rabies)
Chlamydophilia psittaci (psittacosis)
Reportable infectious diseases: other
Mycobacterium tuberculosis (tuberculosis)
Mycobacterium leprae (leprosy)
Coccidiodes immitis (coccidiomycosis)
Cryptosporidium parvum (cryptosporidiosis)
Vancomycin-resistant Staphylococcus aureus (VRSA infections)
Who do you contact for reportable infectious disease?
Local health department
They will then notify state and federal organizations as appropriate
When national agencies become involved in an infectious disease outbreak, the CDC plays a major role
Who do you contact for:
Assault wounds?
Child abuse?
Driving restriction?
Elder abuse?
Intent to harm?
Physician impairment?
Physician misconduct?
Reportable infectious diseases?
Assault wounds? Law enforcement
Child abuse? Child protective services
Driving restriction? may be required to report to the licensing authority (eg, department of motor vehicles)
Elder abuse? Adult protective services
Intent to harm? Law enforcement, person(s) at risk (if applicable)
Physician impairment? Physician health program
Physician misconduct? State medical board
Reportable infectious diseases? Local health department
Contraction alkalosis is a common cause of metabolic alkalosis that can be seen with vomiting and dehydration. What’s the most appropriate initial therapy?
0.9% normal saline bolus
Next:
-Antiemetic: odansetron (5-HT serotonin receptor antagonist), promethazine (primary dopamine receptor antagonist), or meclizine (histamine receptor antagonist)
-Potassium repletion: orally or IV depending on nausea level and severity of hypokalemia
-Other supportive therapy: if warranted based on patient condition, therapy to target hemodynamics, ventilation, oxygenation, etc
Primary nocturnal enuresis greatest risk factor
Family history of bed wetting
Most common in males aged 5-8
Primary nocturnal enuresis definition
Nighttime urinary incontinence in a child aged 5 years or older who has not previously had prolonged period of overnight dryness
Primary nocturnal enuresis etiology
Delayed maturation of bladder control
Decreased bladder capacity
Increased nocturnal urine output
Primary nocturnal enuresis evaluation and treatment
Urinalysis and culture to r/o UTI, DM, diabetes insipidus
Voiding diary
Treat any comorbid conditions (eg, constipation)
Restrict evening fluids
Enuresis alarm
Pharmacotherapy (eg, desmopressin)
24 yo F being evaluated in post-partum unit, oliguria for 8 hours. PMH of gestational DM. Had second degree perineal laceration. Unable to void since delivery but has persistent urinary dribbling while lying in bed. Also has mild lower abdominal tenderness. What is the cause?
Pudendal nerve injury
Perineal lacerations can lead to pudendal nerve injury and postpartum urinary retention. Patients will present with dribbling of urine (due to overflow incontinence), bladder dissension, and an elevated post-void residual volume.
PIC
Urethral injury presentation
Strong urge to void, dysuria, increased frequency, slow and/or interrupted stream when urinating
Perineal ecchymoses in a butterfly pattern, external genitalia ecchymoses, scrotal edema, high riding prostate (non palpable prostate), gross hematuria, or blood at the urethral meatus, especially in the setting of a pelvic fracture)
What has a similar MOA to finasteride?
Sawtooth palmetto (5-alpha reductase inhibitor)
PSGN treatment?
Supportive
-Antibiotics if streptococcal infection is still present
-The resolution of edema is usually rapid and serum creatinine returns to baseline in 3-4 weeks
hematuria typically resolves within 3-6 months
-Indications for referral include cases of refractory hypertension, elevated and rising serum creatinine and persistent fluid overload that does not respond to fluid restriction and diuretic therapy
PIC
6 yo M with swelling around his eyes, dark colored urine for past 2 days. He had a sore throat 1 week ago. NSIM?
Urinalysis
This is PSGN
26 yo F with 1 day of fever, back, and flank pain, 2-3 episodes of non bilious nonbloody emesis. Has 1 male partner and doesn’t use condoms. Has a fever of 101.3, right CVA tenderness. Elevated leukocyte count. NSIM?
Urinalysis and urine culture
PIC
59 yo M comes to ED with 1 day history of fever, chills and dysuria. PMH hypothyroidism, HTN, obesity. Vitals show 101.2, 146/79, HR 92, RR 18. PE shows exquisitely tender prostate on DRE. The most appropriate empiric treatment is?
Trimethoprim-sulfamethoxazole or a fluoroquinolone (eg, ciprofloxacin, levofloxacin)
Patient has acute bacterial prostatitis. E. coli is the MC causative organism
Infectious dysuria in males
PIC
62 yo M presents to ED with severe abdominal pain. He developed sharp, severe, right flank pain this afternoon. The pain comes in waves and is so severe he cannot walk. He had nausea and 3 episodes of non bilious, non bloody emesis. PMH HTN, HLD, gout, BPH. He is in moderate distress and unable to get comfortable, moving around on the exam table frequently. Given most likely dx, wha is likely to be seen on workup?
Gross or microscopic hematuria on urinalysis
Patient has nephrolithiasis
Nephrolithiasis diagnosis and management
Abdominal ultrasound or non contrast spiral CT of the abdomen and pelvis
Hydration and pain control
Strain urine (evaluate composition)
-CCB and tamsulosin may help relax the ureter, resulting in less pain and improved passage of the stone
</= 5 mm: most pass spontaneously
< 10 mm: may pass with medical management alone
10-20 mm: lithotripsy or ureteroscopy
>20 mm: percutaneous nephrolithotomy
Nephrolithiasis characteristics
PIC
73 yo M comes to ED for lower abdominal pain. He has been taking diphenhydramine for nasal congestion for the last week. PMH HTN, BPH. PE shows suprapubic tenderness and tenderness without guarding or rigidity. NSIM?
Urinary catheterization
Patient has urinary retention due to recent diphenhydramine use
Risk factors for acute urine retention
Amitriptyline
atropine
Diphenhydramine
Epidural anesthesia
Opioid analgesics
Pelvic surgery (eg, bladder injury)
Teratogenic effect: Aminoglycosides (gentamicin, neomycin, amikacin, tobramycin, streptomycin)
Ototoxicity (CN VIII damage)
Renal agenesis
Teratogenic effect: ACE-i
Renal failure
Teratogenic effect: Anticonvulsant agents
Neural tube defects
Cardiac defects
Teratogenic effect: Alkylating agents
Cleft palate
Renal agenesis
Teratogenic effect: Folic acid antagonist (trimethoprim, triamterene)
Neural tube defects
Teratogenic effect: Isotretinoin
Cleft palate
Microphthalmia
Cardiac defects
Teratogenic effect: Fluconazole
Bone defects
Congenital heart disease
Teratogenic effect: Lithium
Ebstein anomaly
Teratogenic effect: Methimazole
Aplasia cutis congenita
Teratogenic effect: Tetracyclines
Bone/teeth defects
Teratogenic effect: Warfarin
Fetal hemorrhage
Bone defects
Painless, fixed testicular mass that does not transilluminate. MRI findings of a cystic, calcified, 3.5-cm testicular mass. What is the diagnosis?
Testicular cancer
-Germ cell: 95% of testicular cancers and classified as seminomatous or non-seminomatous
Testicular pathologies
PIC
Epididymitis treatment
Fluoroquinolone (eg, ciprofloxacin)
MC cause in patients over 35 yo = E. coli
MC cause in patients less than 35 yo = suspect gonorrhea or chlamydia and treat with ceftriaxone and doxycycline
78 yo F comes to ED in ambulance from her assisted living facility with bilateral flank pain. Started this morning, 9/10 pain, constant. PMH T2D, HTN, HLD, OA, obesity. Meds metformin, glyburide, lisinopril, simvistatin and ibuprofen. She’s been taking a lot of ibuprofen recently for joint pain. T 100, BP 140/90, HR 98, RR 18. PE shows CVA tenderness, 2-3+ pitting edema in UE and LE, abdomen distended. Urine dipstick shows protein 4+ and hemoglobin 1+. Which diagnostic test will likely provide the definitive diagnosis?
Renal biopsy
This patient has acute interstitial nephritis which occurs several days after initiating or increasing use of a new mediation (often an abx or NSAID). Symptoms include a maculopapular rash, fever, malaise, nausea, and polyarthralgia. Most definitive test for confirming dx is renal biopsy demonstrating mononuclear and eosinophilic inflammatory infiltration of the renal parenchyma with sparing of the glomeruli and blood vessels
PIC
Anterior and posterior chapman points for prostate
Anterior: Posterior IT band (outer femur)
Posterior: Lateral sacral base bilaterally
24 yo M comes to office with rash, fatigue, and decreased urination for the past 2 days. He was in the ED 1 week ago for a staph aureus skin infection and he was started on a 10 day course of antibiotics. T 102, BP 156/94, HR 101. PE reveals 1+ pitting edema in lower extremities bilaterally. Urine studies will most likely reveal?
Eosinophils on microscopy
Patient has acute interstitial nephritis
48 yo M with a 3-day history of intermittent left flank pain and generalized weakness. Reports decrease in urine volume with 1 episode of high urine output. He is a kidney donor. What is the dx?
Obstructive uropathy
PIC
64 yo M comes to the office with complaints of hematuria. He’s had increased urinary frequency for several weeks. PMH BPH treated with meds. Patient has a voiding cystourethrogram. The pathology underlying his dx involves which of the following?
PIC
Chronic outlet obstruction
The patient has urinary bladder diverticulum. BPH is a common cause of this
What should be avoided in neutropenic patients (eg, patients on chemotherapy)
DRE
A rectal exam should be avoided in neutropenic patients if the patient is thrombocytopenia because of increased bleeding risk
16 yo M comes in for monitoring of his kidney condition. He has had worsening hearing loss in both ears, swelling over his eyelids and high BP. FH is positive for a maternal grandfather with similar symptoms as a child. Urinalysis is most likely to reveal?
Red blood cell casts or dysmorphic red blood cells (glomerulonephritis) may be seen
Patient has Alport syndrome (X-linked dominant) caused by a defect in type IV collagen, involving the basement membranes of the kidney and also frequently affecting the cochleas and eyes.
Urinary casts and associated pathologies
PIC
23 yo M brought to ED after falling off a ladder. He reports pain in his pelvis and groin. PE shows stable pelvis, scrotal and perineal ecchymoses, and bladder fullness. Pelvic radiograph shows bilateral inferior pubic ramus fractures. NSIM?
Retrograde urethrogram (gold standard for diagnosing urethral injuries)
Avoid Foley catheter placement
Place a suprapubic catheter if the urethrogram is positive for a urethral injury
Anterior urethral injury: urgent repair (<24 hours)
Posterior urethral injury: suprapubic catheter; delayed repair
In order to prevent the spread of STIs, the following steps are recommended:
-Treat the diagnosed STI with appropriate antibiotics
-Provide counseling on safer sex practices
-Screen for HIV
-Provide hepatitis B vaccine if unvaccinated
-Encourage the patient to contact past sexual partners to be evaluated and, if needed, treated
-Notify the public health department of the disease, as required in all states
57 yo M with increased urinary frequency, especially at night during past few months. BMI is 35. PE reveals slight pitting edema of LE bilaterally and hyperpigmentation of the axilla. The most likely finding on urinalysis is?
Proteinuria
Patient likely has diabetic nephropathy (Kimmelstiel-Wilson disease). Treatment includes either hand ACE-I or ARB with aggressive lifestyle modification and glycemic control
73 yo M presents to office with difficulty urinating. He wakes up 4-5 times a night to urinate, occasionally experiences pelvic discomfort when bladder is full. DRE shows contender prostate without nodules or induration. There is an area of tenderness near his lumbosacral junction and a palpable tender nodule at the medial aspect of the sacral base. His PSA is 12 (reference range: < 4). NSIM?
Transrectal ultrasound guided biopsy
Rule out prostate cancer because of his high PSA
TRUS is negative, MRI-guided biopsy may be used for diagnosis where there is an ongoing concern for prostate cancer because of a further increase in PSA or abnormalities on examination
62 yo M comes to Ed with progressive back pain, fatigue , weight loss and intermittent nocturnal fevers onset 2 months ago. PMH: DM, complicated UTI 3 mo ago. Point tenderness over the right CVA and rubbery nodules superolateral to the umbilicus and around the L1 TP. Slight leukocytosis and elevated ESR. Urinalysis shows mild proteinuria without pyuria or casts. The most likely dx is?
Renal abscess
Bladder injury dx?
Suspected based on clinical findings of suprapubic pain and gross hematuria and confirmed intraoperatively or with CT cystogram
8 yo M with brown urine for past day, LE swelling. Two weeks ago was seen in the office for a sore throat and was given abx. He finished the abx and his sx went away. BP 152/92. PE reveals 2+ pitting edema at the level of the knee. The most appropriate management is?
Diuresis
Treatment for mild cases is supportive, including water and salt restriction and gentle diuresis
Doxycycline MOA
A tetracycline that inhibits the 30s ribosomal subunit
A surgeon is most likely to encounter which vessel whose origin is located just superior to the left renal vein before the left renal vein drains into the inferior vena cava?
Superior mesenteric artery
4 day old newborn with opening of urethra located on the ventral surface of his penis, proximal to the base of his scrotum. His penis is curved ventrally. This patients condition is called?
Chordee
This is a severe form of hypospadias where urethra opens at the base of the scrotum and the the chordee pulls penis down
Ventral opening of urethra = hypospadias
Urethral meatus found on the dorsal surface of the penis = epispadias
When to treat acute pyelonephritis inpatient
-Hemodynamic status (hypotension)
-Ability to reliably consume oral medications (nausea, vomiting, etc)
-Certain comorbidities (eg, renal disease, poorly controlled DM)
-Presence or absence of complicated disease (eg, sepsis, organ failure)
Acute pyelonephritis treatment
Outpatient: oral fluoroquinolone (eg, ciprofloxacin)
Inpatient: IV fluoroquinolones or ahminoglycosides +/- ampicillin
Indications for imaging for acute pyelonephritis
-Complicated pyelonephritis (eg, sepsis, renal failure)
-Persistent symptoms despite 48-72 hours of treatment
-History of nephrolithiasis
-Unusual urinary findings (eg, gross hematuria)
Name the testicular tumor:
-Small, slow growing
-White or yellow on gross pathology
-Cords and tubules along with cells with scant cytoplasm
-HcG and AFP are NOT elevated
Sertoli cell tumor (type of sex cord-stomal tumors)
Gram positive filamentous rod with recent IUD placement cause
Actinomyces israelii
Blunt trauma to kidney with mid-back pain, CVA tenderness, microscopic hematuria. NSIM?
CT abdomen and pelvis with contrast
Low serum calcitriol corresponds to
low serum calcium
Sarcoidosis hypercalcemia
Increased calcitriol and urinary calcium, decreased PTH
PTH is decreased because hypercalcemia in sarcoidosis occurs due to extrarenal calcitriol production in the lungs and lymph nodes and is independent of parathyroid hormone
TLS is marked by the release of intracellular tumor contents into the bloodstream, leading to:
Hyperuricemia: purine nucleic acids from lysed tumor cells are metabolized by xanthine oxidase to uric acid. Because uric acid is poorly soluble in urine, patients often develop obstructing uric acid stones in the renal tubules, which causes AKI.
Hyperphosphatemia: tumor cells frequently contain >3 times more intracellular phosphate than healthy cells. Phosphate (renally excreted) binds calcium in the renal tubules and forms obstructing calcium-phosphate stones; this can also cause AKI and leads to systemic hypocalcemia.
Hyperkalemia: intracellular potassium is released into the circulation, which can cause cardiac arrhythmias.
45 yo M comes to ED with fever, rash and generalized body aches. He recently started a new anti-HTN medication. Urinalysis is positive for eosinophils. What will his renal biopsy show?
Lymphocytic infiltration of the interstitium
Patient likely has allergic interstitial nephritis, most likely from a diuretic
Lupus nephritis
Anti ds-DNA
Decreased C3 and C4
Biopsy is gold standard
Urine sediment with WBC, RBC, or casts (granular, WBC, RBC)
Gold standard for initial diagnosis of bladder cancer
Cytoscopy
Obviously you would get urinalysis before that though and it would show >3 RBC
Risk factors for the development of bladder cancer
Cigarette smoking
Opium use
Occupational carcinogen exposure (including arsenic and trihalomethane compounds from chlorination of drinking water)
How to prevent nephrolithiasis
Increase fluid intake
Increased dietary calcium intake (calcium rich foods)
Increased dietary potassium intake
Decreased dietary sodium intake
Avoidance of high-dose vitamin C supplements
Thiazide diuretics
Allopurinol
If you suspect Alport syndrome in a patient (hematuria and hearing loss), what test would you order first
Genetic testing (COL4A3, COL4A4, COL4A5)
Treatment for UTI due to pseudomonas
Ciprofloxacin, ceftazidime, cefepime
What does choriocarcinoma secrete
B-hCG
Histology reveals abundant necrosis and hemorrhage and mixed cytotrophoblasts and syncytiotrophoblasts
Behcet syndrome
PIC
Treatment of hematuria in someone with sickle cell trait (HbS)
Observation
Increase oral fluid intake
Bed rest
Soft, mobile, flesh-colored, cystic masses act the 4 and 8 o’clock positions at the base of the labia major. Asymptomatic. NSIM?
Observation
Incision and drainage is indicated for painful lesions
Patient has a bartholin gland cyst
Indications for hemodialysis
A- Acidosis: severe metabolic acidosis
E- Electrolytes: severe hyperkalemia
I- Ingestion: toxic alcohol, lithium
O- Overload: refractory fluid overload (refractory to medication management)
U- Uremia: uremic pericarditis or encephalopathy
In cases of suspected toxic alcohol ingestion, hemodialysis should be performed in the setting of
Metabolic acidosis, regardless of drug level
Elevated levels of methanol or ethylene glycol (more than 50 mg/dL
Evidence of end organ damage (eg, visual changes, renal failure)
What diuretic to use when a patient has an allergy to sulfonamides
Ethacrynic acid
Alternative antibiotic to give to a patient with a sulfa allergy for upper UTI
Ciprofloxacin
What to order first in a patient you suspect ADPKD (hypertension, hematuria, bilateral flank pain) in with no known family history
Renal ultrasound
CT/MRI would be a better option in a patient that has a FH of ADPKD
If you suspect cauda equina in a patient, first thing to do is
MRI of lumbar spine
If imaging shows nerve root compression then emergency neurosurgical consult
Approach to painless hematuria
Urinalysis with microscopic analysis
THEN
Cystoscopy
CT urogram or MRI urogram
Urine cytology
Central venous catheters are placed using ultrasound guidance. They are most commonly put into the internal jugular or subclavian veins. After placement, it is important to obtain a
Portable chest x-ray to ensure correct position and evaluate for complications
Only exception to this rule is if a CVC is placed in a hemodynamically unstable or actively decompensating patient
What type of tumor secretes androgens that can cause feminization in adult males and precocious puberty in children?
Leydig cell tumors
Reinke crystals are eosinophilic cytoplasmic crystals characteristic of Legged cells and are present in up to 1/3 of Lydia cell tumors
Type 1 (distal) RTA
Impaired H+ secretion by alpha intercalated cells in the distal tubule
Hypokalemia
Urine pH > 5.5
Type 2 (proximal) RTA
Impaired HCO3- reabsorption in the proximal tubule
Hypokalemia
Urine pH is variable and often <5.5
Type 4 RTA
Reduced aldosterone activity
Hyperkalemia
Urine pH <5.5
53 yo M with occasional red urine for the last 3 months, turns red by end of voiding. He has noticed small clots in his urine. PMH chronic back pain. He smokes a pack of cigarettes daily. T 99.5, BP 140/90. Urinalysis only positive for blood. What is the most likely cause?
Bladder disease
Initial hematuria is characterized by blood at the beginning of the voiding cycle and often reflects a urethral source.
Total hematuria is characterized by blood during the entire voiding cycle and can reflect bleeding from anywhere in the urinary tract (eg, bladder, kidneys).
Terminal hematuria is characterized by blood at the end of voiding cycle and often suggests bleeding from the prostate, bladder neck or trigone, or posterior urethra.
BPH induced obstructive uropathy
This patient with lower urinary tract symptoms (eg, urinary frequency, nocturia, impaired flow) consistent with benign prostatic hyperplasia (BPH) has a slowly rising creatinine level; urinalysis does not show evidence of albuminuria, hematuria, or pyuria, making intrinsic kidney disease less likely. This presentation raises suspicion for BPH-induced obstructive uropathy (eg, enlarged prostate, palpable bladder), which may result in permanent kidney damage due to blockage of free flow of urine.
With obstructive uropathy, a renal ultrasound examination (which should be performed in all patients being evaluated for creatinine elevation or chronic kidney disease) typically reveals hydronephrosis; it can also help assess the extent of kidney injury. If irreversible kidney damage (eg, cortical atrophy on sonogram due to increased pressure) has not yet occurred, management of BPH may improve creatinine levels.
Testicular pain, swelling, dysuria, frequency, urgency. Positive prehn sign, normal testicular lie, normal cremasteric reflex
Epididymitis
Normal prehn is relief of pain with testicular elevation
Localized tenderness to the posterior aspect of the testicle
Urinalysis may show pyuria
Dx based on H&P
Get a urinalysis & also get urine culture and testing for gonorrhea and chlamydia
Tx: >35 & low risk for STI = fluoroquinolone
<35 & high risk for STI = one time dose of ceftriaxone and a day 10 course of doxycycline to cover G&C. Don’t wait for cultures and results of STI to initiate treatment
Alport syndrome EM
Thinning and splitting of the glomerular basement membrane (“basket weave appearance”)
If you suspect ovarian torsion, NSIM?
Transvaginal doppler ultrasound
Hypertension, hypokalemic metabolic alkalosis, low aldosterone, sometimes mild hypernatremia
Liddle syndrome
How would you manage a pediatric patient with symptomatic hypovolemic hypernatremia?
Isotonic fluid like 0.9% normal saline until patient is euvolemic
In asymptomatic patients give hypotonic solution
Once patients are euvolemic, hypotonic fluids (eg, 0.45% saline, 5% dextrose) can be given for ongoing hypernatremia
Most appropriate imaging to establish the diagnosis of nephrolithiasis?
CT abdomen and pelvis without contrast
For pregnant patients get US of the kidneys
How will metabolic acidosis superimposed on respiratory acidosis present?
Low pH and greater than compensated PCO2
Overdiuresis from excessive or chronic diuretic use is a common cause of
Metabolic alkalosis, producing a contraction alkalosis
Testicular torsion management
Manual detorsion then surgical intervention and orchipexy to prevent retorsion
Recent placement of IUD and patient is having pain with intercourse, intermittent vaginal spotting and feeling weak. Gram positive, non-acid fast bacteria. Treatment?
Penicillin G
Bacteria is Actinomyces israelii
Pheochromocytoma diagnosis
24 hour urinary fractionated metanephrine and catecholamine testing
Obtain a serum calcium level to assess for hypercalcemia
MEN2A: pheochromocytoma,primary hyperparathyroidism, medullary thyroid cancer
Red urine, had URI 2 weeks ago. What does light microscopy show
Mesangial proliferation
Patient has IgA nephropathy
Sexual assault protocol
Obtain thorough H&P
Obtain a sexual assault forensic exam (even if the patient already showered)
Management:
-Assess and treat and physical injuries
-Psychologic assessment and support
-Pregnancy prevention
-Treatment and prevention of STIs (NAA for G&C, trichomonas)
-Forensic evaluation
ADPKD frequently progresses to
End-stage kidney disease
How do surgeons assess ureteral injuries intraoperatively?
-Intravenous dye that colors the urine such as sodium fluorescein, indigo carmine, methylene blue
-Intravesical contrast (methylene blue)
-Intravesical fluid distension (mannitol)
-Preoperative oral phenazopyridine
-Cytoscopy
-Retrograde pyelography
Uric acid stone formation can be prevented by
Alkalinizing the urine with potassium citrate. Uric acid becomes soluble at an alkaline pH
Painless HSM, pancytopenia, diffuse infiltrative pulmonary disease
Gaucher
Deficiency of the enzyme glucocerebrosidase
Maternal polyhydramnios, premature delivery, polyuria, failure to thrive, severe hypokalemia, hypochloremia, metabolic alkalosis, normal BP
Bartter syndrome
Defective Na and Cl reabsorption in the thick ascending limb of the LoH
When to image for pyelo?
Persistent symptoms despite 48-72 hours of treatment.
The imaging (CT abdomen pelvis) will evaluate for potential complications such as renal abscess, perinephric abscess, and emphysematous pyelonephritis
How to treat type 4 RTA
Loop or thiazide diuretics
Osmotic demyelination syndrome may develop as a result of the rapid overcorrection of serum sodium. Serum sodium should be corrected no more than 6-8 mEq/L in any 24 hour period. Rapid correction of hyponatremia can be prevented by?
Administering desmopressin with initial treatment
If overcorrection is found, coadministration of desmopressin can help lower the serum sodium to reach the target threshold
A patient presenting with acute respiratory acidosis from hypoventilation leading to hypercarbic respiratory failure should be first managed with
Endotracheal intubation and mechanical ventilation to protect the airway and provide ventilatory assistance
Standard confirmatory test for diagnosing nephrotic syndrome is
24 hour urine protein measurement
If a patient had a granulosa cell tumor, which tumor marker would you use to monitor for disease recurrence?
Inhibin
Renal artery stenosis first diagnostic imaging
Renal artery doppler ultrasound
Renal artery angiogram is the gold standard however it is performed only if the initial imaging is inconclusive due to its invasive nature and potential risks, which include contrast-induced nephropathy, bleeding, infection and atheroembolic phenomena
Treatment of a chancroid from Haemophilus ducreyi
Single dose of oral azithromycin
Alternative treatment regimens: -Ceftriaxone single IM dose
-Erythromycin 3 times a day for 7 days
-Ciprofloxacin twice a day for 3 days
Treatment of Type 1 RTA
Sodium bicarbonate
Treatment of symptomatic primary hyperparathyroidism
Parathyroidectomy
In asymptomatic patients any one of the following are indications for parathyroidectomy:
1) renal function- impaired GFR < 60 mL/mi
2) osteoporosis- bone density consistent with osteoporosis (T-score < -2.5) or vertebral compression fracture
3) age- primary hyperparathyroidism in those age < 50 yo
4) calcium level- serum concentration of calcium > 1 mg/dL above the upper limit of normal
Papillary thyroid cancer diagnosis
TSH: normal or high
Ultrasound: hypo echoic thyroid mass, microcalcifications, extracapsular extension
Fine needle aspiration
Primary hyperparathyroidism ddx
Graves
Toxic multi nodular goiter
Subacute thyroiditis
Subclinical hyperthyroidism
Thyrotoxicosis
Graves: orbitopathy, hyperthyroidism, diffuse thyroid enlargement
Toxic multi nodular goiter: discrete thyroid nodules, hyperthyroidism
Subacute thyroiditis: painful thyroid, hyperthyroidism (signs and sx of hyperthyroidism and a very tender thyroid gland, typically occurs after a viral infection, radioactive iodine scan will show reduced uptake)
Subclinical hyperthyroidism: asymptomatic
Thyrotoxicosis: hyperthyroidism, usually normal thyroid examination
What is myxedema coma (or crisis) and how will you treat it?
Severe hypothyroidism leading to decreased mental status and hypothermia.
It also produces other abnormalities like macroglossia, hypothermia, hypotension, bradycardia, hypoventilation, hyponatremia and hypoglycemia.
Will have high TSH, low free T3 and T4
Initial treatment consists of thyroid hormone (levothyroxine and liothyronine) replacement. Glucocorticoids are often administered as well because of the possibility of concomitant adrenal insufficiency
Chronic deficiency of vitamin B1 (thiamine) can lead to
Wet beriberi characterized by dilated high-output cardiomyopathy
Which insulin is long-acting?
Glargine insulin
Onset of 1-4 hours
Duration of approx 24 hours
How to diagnose diabetes
-HbA1c > 6.5%*
-Fasting plasma glucose > 126 mg/dL*
-Two-hour plasma glucose >200 mg/dl following a 75-gram oral glucose tolerance test*
-Random plasma glucose > 200 mg/dL in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis
- = need two tests with values in the diabetic range to dx diabetes
-Use insulin as first-line in patients with A1c > 10%
What is autonomic neuropathy
Common finding in individuals with long-standing and poorly controlled diabetes, resulting in impaired sympathetic nervous system reflexes and orthostatic hypotension resulting in syncope
Which diabetes drugs cause weight gain
Sufonylureas (eg, glyburide) which increase insulin release from pancreatic beta cells by closing potassium channels in the plasma membrane of these cells
Meglitinides (eg, repaglinide) which block ATP-dependent potassium channels promoting insulin release from pancreatic beta cells
C peptide levels with exogenous insulin
Proinsulin and c-peptide levels are low
Plasma insulin will be high
C-peptide levels will be elevated with sulfonylureas
Factitious hypoglycemia can be caused by the surreptitious use of
exogenous insulin or secretagogues (most commonly sulfonylureas)
Exogenous secretion of insulin (eg, insulinoma) labs
Increased plasma insulin, plasma c-peptide and plasma proinsulin
Exogenous administration of insulin labs
Increased plasma insulin
Decreased plasma c-peptide and plasma proinsulin
Exogenous ingestion of oral hypoglycemic agent (insulin secretagogues) labs
Increased plasma insulin, plasma c-peptide, plasma pro-insulin and insulin secretagogue
Patient has painless jaundice, palpable, contender gallbladder. what is the strong risk factor for the most likely diagnosis
Cigarette smoking
Patient most likely has pancreatic cancer
Young patients with newly-diagnosed T1D should monitor their blood glucose at least
3 times daily
Glucose should be monitored before each insulin dose, usually at least 4 times daily (once before each of 3 meals and once before the administration of long-acting insulin0
What is euthyroid hyperthyroxinemia
Condition in which the serum total thyroxine is abnormal without evidence of thyroid disease (normal TSH)
Will have increased TBG and free T4. Normal TSH and total T3
DKA treatment
If potassium level is:
> 5.2 –> IV insulin + isotonic fluids
> 3.3 and < 5.2 –> IV insulin + IV fluids with added K+
< 3.3 –> IV fluids + K+, hold insulin until K+ > 3.3 to prevent fatal cardiac arrhythmia from total body hypokalemia
MEN 1
MEN 1 mutation
Pituitary adenoma
Parathyroid hyperplasia
Pancreatic islet cell tumors (gastrinoma)
Prolactinoma
MEN 2A
RET oncogene
Parathyroid hyperplasia
Pheochromocytoma
Medullary thyroid carcinoma
MEN 2B
RET oncogene
Pheochromocytoma
Medullary thyroid carcinoma
Marfanoid body habitus
Mucosal neuromas
Medullary thyroid carcinoma
The malignancy is characterized by extracellular amyloid composed of calcitonin from thyroid parafollicular cells
55 yo female with a 1 month history of impaired temporal vision bilaterally, increase in headaches, trouble sleeping and awakening at night gasping for air. BP 140/90. PE shows widened gaps between her teeth without evidence of gingivitis. The most appropriate test to order is
Insulin-like growth factor one (IGF-1) to screen for acromegaly
The patient likely has acromegaly with a mass effect from a pituitary tumor
If hypercortisolism is found on labs then order
ACTH to differentiate ACTH-dependent vs independent causes of Cushing syndrome
Abdominal pain, hypotension, hypokalemia
Adrenal crisis
Suspect adrenal crisis due to steroid withdrawal in post-op patients who suddenly develop hypotension, shock and hyperkalemia. Immediate treatment with corticosteroids should be instituted if adrenal crisis is suspected, even if it has not been confirmed
In pregnant patients with thyroid storm, which medication will you give
Propylthiouracil in the first trimester due to potential teratogenicity of methimazole (aplasia cutis)
Methimazole in the second and third trimesters and in non-pregnant patients due to risk of hepatotoxicity with PTU
15 yo with high BP on 2 separate visits, taking topic acne medication, tanner stage 1 female, minimal body hair. What’s the treatment given the most likely diagnosis
Start spironolactone
Patient has 17-alpha-hydroxylase deficiency which can present with hypertension and delayed puberty (primary amenorrhea, minimal body hair, absence of secondary sexual characteristics) in females
Labs: low cortisol and androgens, elevated ACTH and 11-deoxycortisone
Management involves spironolactone to block the effects of excessive aldosterone production and a glucocorticoid to treat inadequate cortisol production
Insulin adjustments
Basal insulin is adjusted for preprandial glucose levels
Bolus insulin is adjusted for postprandial levels
How to prevent diabetic foot ulcers
Control blood glucose levels
Physicians who believe a colleague has committed negligence should report the event through the
appropriate hospital protocols
Tumor markers:
Prostate-specific antigen (PSA)
Carcinoembryonic antigen (CEA)
Cancer antigen (CA19-9)
Cancer antigen (CA125)
Alpha-fetoprotein (AFP)
Calcitonin
Prostate-specific antigen (PSA): prostate
Carcinoembryonic antigen (CEA): colon
Cancer antigen (CA19-9): pancreatic
Cancer antigen (CA125): ovarian
Alpha-fetoprotein (AFP): hepatocellular or germ cell
Calcitonin: medullary thyroid
What is autoimmune adrenalitis
Primary adrenal insuffiiciency is MC caused by autoimmune adrenalitis and can present with symptoms of fatigue, anorexia, and decreased libido that may mimic psychiatric diagnoses such as MDD or adjustment disorder. Other findings that strongly suggest PAI over psychiatric diagnoses is hypotension, hyperpigmentation, hypoglycemia, and/or electrolyte abnormalities
If parents refuse essential medical treatment for their child despite careful explanation, the physician should
seek a court order to allow for treatment of a child
Fever, tachycardia, hypotension, warm moist skin and history of 12 kg weight loss (right before surgery) after her cholecystectomy
Thyroid storm
An acute event such as surgery can precipitate thyroid storm in patients with untreated or poorly controlled hyperthyroidism. Immediate treatment for patients with thyroid storm includes thionamides (PTU or methimazole), beta-blockers (propranolol) and glucocorticoids (hydrocortisone)
Iodine should be given >1 hour after the first dose of thionamide is taken
This reduces the risk of iodine producing new thyroid hormone instead of preventing the release of thyroid hormone
In patients undergoing thyroid surgery, particularly patients with decreased bone density or conditions predisposing to decreased bone density, such ass a prior history of gastric bypass surgery, it is important to
take extra care to identify and preserve the parathyroid tissue during thyroid surgery
Serum calcium levels, as well as symptoms of hypocalcemia should be closely monitored after thyroidectomy
Treatment of lithium induced nephrogenic diabetes insipidus
Amiloride which blocks epithelial sodium channels in principal cells and thereby prevents lithium from entering these cells
Lithium can cause nephrogenic DI by entering principal cells of the collecting ducts to interfere with aquaporin-2 water channels
Menopausal patient who wants to start estrogen but has a history of hypothyroidism and is taking levothyroxine
Increase levothyroxine dose
This patient has common symptoms of menopause, including insomnia, vasomotor symptoms (eg, hot flashes), and mood swings. In the absence of contraindications (eg, history of breast cancer, tobacco use), first-line treatment for severe menopausal vasomotor symptoms is oral estrogen-based hormone therapy.
However, estrogen has notable effects on thyroid metabolism. More than 99% of circulating thyroid hormone is bound to plasma proteins, primarily thyroxine-binding globulin (TBG). Estrogen upregulates the production of TBG in the liver; an increase in estrogen activity (eg, pregnancy, oral contraceptive use, menopausal hormone therapy) raises circulating TBG levels, causing a corresponding reduction in free T4 and T3 levels (Choice C).
In patients with a normal hypothalamic-pituitary-thyroid axis, lower free thyroid hormone levels trigger a transient increase in TSH release, leading to increased thyroid hormone production until the additional TBG becomes saturated with thyroid hormone and free hormone levels are restored. However, patients with hypothyroidism are dependent on exogenous thyroid hormone and are unable to increase production to compensate for the increased TBG. Therefore, patients on thyroid replacement therapy who are prescribed oral estrogens require a compensatory adjustment in levothyroxine dose.
Labs for PAI
High renin, low aldosterone
Hyponatremia, hyperkalemia, hypoglycemia, lower DHEA-s, non-gap metabolic acidosis
Hypocalcemia EKG
Prolongation of the QT interval
Panhypopituitarism will lead to decreased
ACTH, TSH, LH, FSH, prolactin, GH
HHS will have normal
serum beta hydroxybutyrate
Clitoromegaly, partially fused labia, hyponatremia, hypoglycemia, normal uterus and ovaries
21-hydroxylase deficiency deficiency
Tx: correction of electrolyte abnormalities, supplement with glucocorticoids and mineralocorticoids to prevent adrenal crisis
In subacute thyroiditis (de Quervain) some patients become
hypothyroid before they recover
Give _ with isoniazid to prevent
pyridoxine (B6)
Nausea, vomiting, epigastric abdominal pain, early satiety, bloating, weight loss, labile glucose (DM), epigastric dissension & succession splash dx and tx?
Gastroparesis
Causes:
-DM (autonomic neuropathy)
-Medications (eg, opioids, anticholinergic drugs)
-Traumatic/postsurgical injury (ie, vagus nerve injury)
-Neurologic (eg, multiple sclerosis, spinal cord injury)
-Idiopathic/postviral
Diagnosis:
-Exclude obstruction with upper endoscopy +/- CT/MR enterography
-Upper endoscopy may reveal food in the stomach despite an overnight fast
-Assess motility with nuclear gastric-emptying study
Treatment
-Frequent small meals (low fat, soluble fiber only)
-Promotility drugs (eg, metoclopramide, erythromycin)
-Gastric electrical stimulation and/or jejunal feeding tube (refractory symptoms)
How will central precocious puberty present and why does it occur
Results from early activation of the hypothalamic-pituitary-gonadal (HPG) axis. Pulsatile GnRH secretion stimulates elevated FSH and LH levels
Patients with true precocious puberty will have increased estrogen/testosterone levels that accelerate skeletal maturation, resulting in advanced bone age and increased growth velocity
Patient will have onset of secondary sexual characteristics in girls age <8 and boys age <9
Require MRI brain to evaluate for a hypothalamic or pituitary tumor activating the HPG axis
If negative, the cause is most likely idiopathic precocious puberty and GnRH therapy can be initiated- it desensitizes the pituitary and suppresses FSH and LH secretion to slow pubertal progression and maximize height potential
How will peripheral precocious puberty present and what causes it
Caused by gonadal or adrenal release of excess sex hormones
Basal levels of FSH and LH are typically low due to negative feedback and remain low following GnRH agonist stimulation
Secondary adrenal insufficiency labs
Low cortisol and ACTH
Normal aldosterone
Mechanism: disruption of HP axis
Etiologies: chronic glucocorticoid therapy, infiltrative disease, ischemia of the anterior pituitary
Will present with less severe symptoms, euvolemia, minimal electrolyte disturbance, no hyperpigmentation. Potassium is normal
Primary adrenal insufficiency
Low cortisol and aldosterone
High ACTH
Mechanism: destruction of bilateral adrenal cortex
Etiologies: autoimmune adrenalitis, infection, malignancy
Etiologies: more severe symptoms, hypovolemia, hyperkalemia, hyponatremia, hyperpigmentation
Treat with glucocorticoids (eg, hydrocortisone, prednisone) and mineralocorticoids (eg, fludrocortisone)
Adrenal crisis give hydrocortisone or dexamethasone and rapid IV volume repletion
Patients with chronic kidney disease are at an increased risk of hypoglycemia due t
delayed clearance of insulin by the kidneys
Labs in celiac
Low calcium and phosphate
High PTH
Because of vitamin D deficiency and secondary hyperparathyroidism
Causes of male secondary hypogonadism
Pituitary tumors, hyperprolactinemia, medications like opioids, glucocorticoids, exogenous androgens (withdrawal phase), infiltrative disease (eg, hemochromatosis), chronic/severe illness, eating disorders, severe weight loss
Clinical feature care fatigue, decreased libido, testicular atrophy, will have low testosterone and low/normal LH
Primary will have gynecomastia
Glucagonoma
Weight loss, necrolytic migratory erythema (erythematous papule that coalesce to form large, indurated plaques with central clearing), DM/hyperglycemia, GI symptoms like diarrhea, anorexia, abdominal pain
Diagnosis: markedly elevated glucagon level, abdominal imaging (MRI or CT scan)
Cardiovascular effects of thyrotoxicosis
Sinus tachycardia, premature atrial and ventricular complexes, atrial fibrillation/flutter, systolic hypertension and increased pulse pressure, increased contractility and cardiac output, decreased systemic vascular resistance, increased myocardial oxygen demand, high output heart failure, exacerbation of preexisting low-output failure, coronary vasospasm, preexisting coronary atherosclerosis
Vitamin D deficiency in children
Labs:
Low 25-hydroxyvitamin D, urine calcium, phosphorus
Elevated alkaline phosphatase, PTH Low/normal calcium
Clinical manifestations
Decreased muscle tone & delayed development
Delayed fontanelle closure, frontal bossing
Widening of epiphyses
Hypertrophy of costochondral joints
Short stature, femoral & tibial bowing
Thyroid storm
Occurs in patients with undiagnosed or inadequately treated hyperthyroidism
Caused by rapid increase in serum thyroid hormone levels or increased sensitivity to thyroid hormone
-Thyroid or nonthyroidal surgery
-Acute illness (eg, trauma, infection), childbirth
-Acute iodine load (eg, iodine contrast)
-Fever as high as 40-41.1 C (104-106 F)
-Tachycardia, hypertension, congestive heart failure, cardiac arrhythmias (eg, atrial fibrillation)
-Agitation, delirium, seizure, coma
-Goiter, lid lag, tremor, warm & moist skin
-Nausea, vomiting, diarrhea, jaundice
-β blocker (eg, propranolol) to ↓ adrenergic manifestations
-PTU followed by iodine solution (SSKI) to ↓ hormone synthesis & release (give iodine at least 1 hour after PTU to prevent excess iodine incorporation into thyroid hormone)
-Glucocorticoids (eg, hydrocortisone) to ↓ peripheral T4 to T3 conversion & improve vasomotor stability
-Identify trigger & treat, supportive care
Long term side effect of methimazole
Severe neutropenia
VIPoma
Watery diarrhea
Hypo- or achlorhydria due to decreased gastric acid secretion
Associated flushing, lethargy, nausea, vomiting, muscle weakness/cramps
Labs: hypokalemia, hypercalcemia, hyperglycemia, stool studies show secretory diarrhea with increased sodium and osmolal gap <50
CT or MRI scan of the abdomen to localize the tumor in pancreas (usually in pancreatic tail)
Laboratory evaluation for hypertension
-Serum electrolytes
-Serum creatinine
-Urinalysis
-Urine albumin/creatinine ratio (optional)
-Fasting glucose or hemoglobin A1c
-Lipid profile
-TSH
-ECG
-Echo (optional)
-CBC
-Uric acid (optional)
Reason for treating 7mm hyperprolactinemia
to prevent bone loss
Prolactin suppresses GnRH in the hypothalamus leading to decreased FSH and LH so decreased estrogen.. you need estrogen to build bone
To assess diabetic patients risk for foot ulcers use
monofilament testing
Euthyroid sick syndrome T3, T4 and TSH levels
Early/mild
T3- decreased
T4- normal
TSH- normal
Prolonged/severe
T3- decreased
T4- decreased
TSH- decreased
how do you know treatment is working in someone with DKA?
serum anion gap
Cardiovascular features in acromegaly
Concentric left ventricular hypertrophy, cardiomyopathy, heart failure
Osteomalacia labs
Increased alkaline phosphatase, PTh
Decreased serum calcium and phosphorus, urinary calcium, 25(OH)D levels
Conditions that increase thyroid binding globulin
Estrogens (eg, pregnancy, OCs, HRT) & estrogenic medications (eg, tamoxifen), acute hepatitis
Rapid eye movement (REM) behavior disorder (RBD) is a risk factor for
Parkinson disease
PCOS treatment to regulate cycles
OCPs
Letrozole for ovulation induction
Effect of intensive glycemic control in T2D
Microvascular complications (eg, nephropathy, retinopathy)- improves
Macrovascular complications (eg, acute MI, stroke)- no change (short-term)
Mortality- no change or increased
Which thyroid nodules do you biopsy with FNA
Hypofunctioning (“cold”) nodules
X-linked (Bruton) agammaglobulinemia
Defect in Btk (Bruton agammaglobulinemia tyrosine kinase) which results in impaired B lymphocyte maturation and decreased levels of immunoglobulins of all classes. Patients present after age 6 months with recurrent sinopulmonary and gastrointestinal infections
Laryngotracheobronchitis
Croup (parainfluenza MC, RSV, influenza, adenovirus)
Inspiratory stridor, barking cough
Children 6 months-3 years
Low grade fever
Steeple sign
Mild cases treat with cool mist therapy and rest and moderate to severe cases are treated with immediate nebulizer racemic epinephrine to open the airway and oral/intramuscular/intravenous dexamethasone to reduce swelling
Hospitalization may be required for serial racemic epinephrine treatments and supplemental oxygen
*moderate to severe is defined as presence of stridor at rest
Epiglottitis
Toxic looking, drooling
High fever
Thumbprint sign
Retropharyngeal abscess
Soft tissue swelling posterior to the pharynx
Toxic, drooling
Hot potato voice
High fever
Bacterial tracheitis
Expiratory stridor
Prolonged prodromal phase, followed by acute decompensation over a period of hours
3 months-2 years
Subglottic narrowing
Active TB treatment
4 months of RIPE (rifampin, isoniazid, pyrazinamide, ethambutol)
2 months of isoniazid and rifampin
Latent TB treatment
4 months of rifampin
TB drugs SE
RIPE
ONGO
Rifampin- orange urine
Isoniazid-
Pyrazinamide
Respiratory isolation
TB
Measles
Chickenpox
COVID-19
Disseminated herpes zoster
Patient had blunt force chest trauma and had multiple bruises on chest and crepitus. Decreased breath sounds on the left. A tube was placed which produced loud expulsion of air and stabilization of vitals. Over next few hours patients oxygen sat decreases. Repeat exam shows decreased breath sounds on the left and repeat radiograph shows subcutaneous emphysema, reaccumulation of air in the right pleural space and pneumomediastum. What is the diagnosis
Tracheobronchial injury (eg, bronchial rupture)
suspect when a patient has a persistent pneumothorax and/or pneumomediastinum despite tube thoracostomy (chest tube)
Diagnose with bronchoscopy
Manage with surgical repair
Dyspnea ddx
Palpitations + tachycardia = arrhythmia
Chest pain + hypotension = myocardial infarction
Productive cough + fever = pneumonia
Chest pain + tachycardia = pulmonary embolism
Disseminated intravascular coagulation (DIC)
Usually occurs in the setting of sepsis or another serious acute medical condition. Characterized by diffuse activation of the coagulation system leading to consumptive coagulopathy and subsequent spontaneous bleeding
Labs are low platelet and fibrinogen level, elevated PT, aPTT and D-dimer and evidence of microangiopathic hemolytic anemia (low hemoglobin/hematocrit, schistocytes, helmet cells on blood smears)
PIC
Vasovagal syncope
aka neurocardiogenic syncope
MC cause of syncope among adults, especially in those without apparent cardiovascular or neurologic disease.
Pathophysiology is thought to be related to a temporary and self-limited symptomatic hypotension mediated by decreased sympathetic tone resulting in bradycardia or peripheral vasodilation. Occurs while sitting or standing since supine position maintains cerebral perfusion. Younger patients are more likely to have the classic triggers such as emotional or orthostatic stress, painful stimulus, prolonged standing or physical exertion
Rule out these life-threatening causes of syncope prior to diagnosis of vasovagal episode
Arrhythmia: v tach, long QT syndrome, Brugada syndrome, sinus arrhythmias
Ischemia: acute coronary syndrome, myocardial infarction
Structural abnormalities: valvular disease, cardiomyopathy, atrial myxoma, tamponade, dissection
Hemorrhage: trauma, GI bleeding or other source of bleeding
Pulmonary embolism
Subarachnoid hemorrhage
Treatment for ST elevation myocardial infarction with acute right ventricular infarction includes
Isotonic IV fluids (to increase preload and cardiac output)
Aspirin therapy
Emergent cardiac catheterization (to decrease mortality and allow for revascularization)
No preload reducers like furosemide or nitrates because they can further reduce CO
Hypotension and JVD that worsen with inhalation (Kussmaul sign) are signs of RV infarction
Sinus bradycardia (resting HR < 60/min) is common in patients treated with the medications that affect the SA or AV nodes. These include
ABCD
Adenosine
Beta blockers (B1)
Calcium channel blocks (non-DHP- verapamil and diltiazem)
Digoxin
Anemia (dyspnea on exertion, fatigue, orthostasis), conjunctival pallor, lymphocytosis, splenomegaly, lymphadenopathy and mild tachycardia
Chronic lymphocytic leukemia
MC in older men, often found incidentally.
Immunophenotypic analysis with flow cytometryis the key diagnostic component. Will see smudge cells on peripheral smear
Mitral valve stenosis is a risk factor for atrial fibrillation which can result in complications such as
Cardioembolic disease (eg, stroke, acute mesenteric ischemia) and acute decompensated heart failure
CHADVASc
PIC
Amyloidosis
Multisystem disease that often presents with cardiac, GI, hematologic and renal manifestations. It is a form of restrictive cardiomyopathy that primarily presents with signs of right heart failure. Echo will reveal concentric LVH, left atrial enlargement and preserved ejection fraction
Aortic stenosis
Syncope, exertion angina, exertional dyspnea
Pulsus parvus et tardus - low volume and slow rising pulse
Risk factors for vasospastic angina (Prinzmetal angina)
Cocaine use, sumatriptan, and smoking
Presents as intermittent chest pain with ST segment elevation when symptomatic and normal ECG when asymptomatic
First line tx is with diltiazem or amlodipine
Hemorrhagic shock
Decreased cardiac index and central venous pressure
Increased systemic vascular resistance
Normal to low pulmonary artery and pulmonary capillary wedge pressures
Examination may reveal hypotension, tachycardia, narrow pulse pressure and extremities that are cool and pale
Initial treatment of toxic shock syndrome
IV fluids when hemodynamic compromise is present
PIC
Metoprolol side effects
Metabolic side effects including weight gain, dyslipidemia and impaired glucose tolerance (leading to type 2 diabetes mellitus)
In patients who have undergone percutaneous coronary intervention with new or chronic atrial fibrillation, the most recent guidelines recommend
double therapy with a P2Y12 inhibitor (eg, clopidogrel) to prevent stent thrombosis and a direct oral anticoagulant (eg, rivaroxaban) for embolic stroke prophylaxis
Sideroblastic anemia
Microcytic anemia, elevated serum iron, ferritin and transferrin saturation and a low TIBC
Isoniazid can interfere with pyridoxine (vitamin B6) metabolism, leading to a functional pyridoxine deficiency. This can result in impaired heme synthesis, presenting as sideroblastic, microcytic anemia
What to do if patient has signs of hypertensive disease despite a normal BP examination in the office
Ambulatory blood pressure monitoring
Medications tha cause Htn
Venlafaxine
Fluoxetine
TCAss
Caffeine
Decongestants like pseudoephedrine and phenylephrine
Herbal supplements like licorice and St. John’s wort
Hormonal birth control OCPs
NSAIDs
Stimulants
What med to add on to someone on one HTN medication and still needs BP lower
DHP-CCB like amlodipine
Tx for resistant hypertension secondary to renal artery stenosis
RAS is most commonly caused by atherosclerosis
Once BP is controlled in RAS, preventative measures 9eg, an HMG-CoA reductase inhibitor, smoking cessation, low-dose aspirin) should be initiated to prevent further cardiovascular disease
For hemodynamically unstable patients with SVT
Urgent cardioversion
For patients with SVT that is not associated with sevre symptoms or hemodynamic collapse:
1. Vagal maneuvers
2. IV adenosine
3. IV non-DHP CCB or IV BB
4. Cardioversion in selected persistent cases or if the patient is unstable
What to do with a patient with STEMI or new LBBB in the setting of chest pain at a hospital with no PCI capabilities
Patients should be transferred to a nearby hospital for definitive management, as long as their initial evaluation-to-balloon time is within 90 minutes
Patients with infectious mononucleosis are at risk for
Splenic rupture secondary to splenomegaly caused by leukocyte infiltration
Patients should avoid contact sports for at least 4 weeks and avoid vigorous exercise for 21 days from the onset of symptoms
First line therapy for HTN in patients with evidence of proteinuria or CKD
ACE-I (regardless of ethnicity)
What to do when a pulmonary nodule is incidentally seen on chest radiograph
- make a comparison with prior radiographs (if available)
- If prior radiographs are not available or if the nodule is new, a CT of the chest should be obtained
Test for mitral regurgitation
TTE is typically initial test of choice
TEE provides better diagnostic accuracy and can be performed initially in certain clinical situations and in patients with prosthetic heart valves
CML
BCR-ABL
philadelphia chromosome abnormal chromosome 22
t(9;22)
Tx with tyrosine kinase inhibitors like imatinib
Transfusion
One unit of packed RBC increases the hemoglobin level by 1 g/dl and the hematocrit by 3%. The recommended transfusion hemoglobin threshold is <7 g/dL
So if a patients hgb is 4 then give them 3 units of packed RBC
What to give patient with BB overdose
glucagon or atropine
Medication contraindicated in vasospastic angina
Nonselective beta-blockers like propranolol because they can worsen vasoconstriction through unopposed alpha-1 activity. Vasospastic angina should be treated with CCB and nitrates
Autoimmune metaplastic atrophic gastritis (AMAG) causes
vitamin B12 deficiency
WPW
Short PR interval
Delta wave
Prolonged QRS
Patients who have uncertain diagnosis based on ECG and other noninvasive testing need to undergo electrophysiology study
Succinylcholine
Paralytic
AE include hyperkalemia, hypercalcemia and malignant hyperthermia
The most common sequela of heparin induced thrombocytopenia
Venous thrombosis (not arterial)
Treatment choice for renal artery stenosis secondary to fibromuscular dysplasia
Percutaneous transluminal angioplasty
Most harvested arteries for coronary artery bypass graft surgery are the
internal mammary arteries and these arteries arise from the anterior surface of the subclavian arteries
Persistent tachycardia and new arrhythmia (eg, premature ventricular contractions) after blunt chest trauma are concerning for blunt cardiac injury. Patients with these findings are admitted for
Continuous cardiac monitoring and echo
Patients with ECG abnormalities and/or elevated troponin –> admit for continuous cardiac monitoring
V tach
Cardioversion used if pulse is palpable
Defibrillation is used if a pulse is not palpable
Superior vena cava syndrome
First step after securing the airway is end-vascular treatment with or without stent placement
Presents ass SOB, cough, facial plethora, headache, respiratory distress with stridor, Pembertons sign (face becoming erythematous when bringing arms up to face)
Non small cell carcinoma followed by small cell carcinoma along with non-hodgkin’s lymphoma is the most common malignancies causing SVC compression
Patient with 4mm painful mass under his axilla. He has experienced lumps like this before but not as large as this one. The lumps would leak pus and go away on their own. What is the most appropriate management?
Incision and drainage along with antibiotics
Patient has a cutaneous abscess- presents as a painful, fluctuant nodule with surrounding erythema
Necrotizing enterocolitis
Abdominal distension and tenderness, rectal bleeding and/or diarrhea, vomiting and lethargy. It produces the pathognomonic sign of bowel wall gas (pneumatosis intestinalis) on abdominal x-ray
Weakness of external rotation of the arm against resistance is most likely caused by teres minor or infraspinatus muscle dysfunction. These nerves supply these muscles a
Infraspinatus- suprascapular nerve
Teres minor- axillary nerve
These muscles are commonly torn in pitchers
Severe eyelid swelling, profuse purulent discharge and chemosis (conjunctival edema) in a newborn first 2-5 days of life
Gonococcal conjunctivitis
Diagnosis is with positive culture on Thayer-Martin agar (gold standard)
Treatment is with a single intramuscular dose of a 3rd generation cephalosporin such as cefotaxime
This condition can be prevented with appropriate maternal screening (and treatment of any maternal infection) plus topical erythromycin prophylaxis for all infants
Local anesthetic toxicity presentation
Tinnitus, metallic taste, perioral numbness, tachycardia and hypertension. Many patients can develop seizures and/or life threatening cardiovascular collapse
Management consists of immediate drug cessation, lipid emulsion rescue therapy, supportive care and treatment with benzodiazepines for seizure control
Drugs that cause hyperkalemia
TMP-SMX, ACE-I, NSAID
Neutrophilic inflammation is associated with
Lymphocytic inflammation is associated with
Bacterial infections
Viral and fungal infections
Gold standard for the diagnosis of nephrolithiasis is
CT abdomen without contrast (won’t be able to see the stone with contrast)
Renal ultrasound in pregnant patients
Loss of balance, loss of vibratory sensation, decreased proprioception, scoliosis, high plantar arches
Fredreich ataxia
Progressive degenerative disease affecting the dorsal columns and sspinocerebellar tract
Repeats of GAA lead to disruption of the frataxin gene on chromosome 9; frataxin regulates iron chaperoning and detoxicfation
Hypertrophic cardiomyopathy is a common complication and the most common cause of death in these patients
Airborne isolation precautions
-COVID-19
-Measles
-Tuberculosis
-Varicella
Contact isolation precautions
-Colonization with multidrug-resistant organisms (eg, methicillin-resistant Staphylococcus aureus)
-Enteric infections (eg, E. coli O157:H7, C. diff)
-Parasitic infections
-Viral respiratory infections (eg, respiratory syncytial virus, COVID-19, influenza)
Droplet isolation precautions
-Adenovirus
-Bacterial meningitis
-Influenza
-Mycoplasma pneumoniae
Neutropenic isolation precautions
Immunosuppressed patients
Transudative ascites with SAAG > 1.1 g/dL
-Cirrhosis
-Alcoholic hepatitis
-Heart failure
-Budd-Chiari syndrome
-Portal vein thrombosis
-Tamponade
Exudative ascites with SAAG < 1.1 g/dL
-Pancreatitis
-Serositis
-Nephrotic syndrome
-Peritoneal tuberculosis
-Peritoneal carcinomatosis
Indications for initiating antibiotics in patients with ascites
-Temperature > 37.8 or 100F
-Abdominal pain and/or tenderness
-Altered mental status
-Polymorphonuclear leukocytes (PMNs) count > 250 cells/mm3
Treat with 3rd gen cephalosporin like cefotaxime
When should spontaneous bacterial peritonitis be suspected
Patients with ascites, fever, abdominal pain, altered mental status and/or polymorphonuclear leukocytes >250 cells/mm3
Treat with 3rd gen cephalosporin
Posterior cerebral artery infarct
Contralateral homonymous hemianopia (inability to see half of the visual field on the opposite side of the lesion)
Cortical blindness (occipital lobe) and/or memory deficits and behavior changes (temp
PCA supplies the occipital and medial temporal lobe
Lacunar stroke
Pure motor symptoms but also be purely sensory or cause ataxic hemiparesis
Middle cerebral artery occlusion
Face and arms
Contralateral hemiparesis, paresthesia and hemianopia (blindness in half of the visual field) and preference of gaze toward the side of the lesion
Agnosia (inability to name objects) may also be seen
Lateral medullary (Wallenburg) syndrome
Occlusion of PICA
Hoarseness, dysphagia, vertigo, ipsilateral ataxia, dysmetria, horner syndrome, loss of pain and temperature sensation on the ipsilateral face and contralateral body
MC cause of PICA infarct is a vertebral artery dissection
Malignant hyperthermia crises are life-threatening conditions caused by uncontrolled release of
calcium from the sarcoplasmic reticulum of skeletal muscle cells this leads to excessive accumulation of calcium ions within the intracellular space of these cells, resulting in sustained muscle contraction and hyper metabolism
Tx with dantrolene
Distal biceps tendon rupture
Confirmed with ultrasound or MRI but MRI allows for optimal detailed visualization of soft tissue structures and can determine partial vs. complete tears as well as the degree of retraction, which is useful information for surgical repair
Upper GI bleed management
NPO
IV fluid administration
IV PPIs
PIC
Treating endometrial hyperplasia without atypic
Progestin therapy or hysterectomy
with atypia or endometrial cancer then hysterectomy
Plantar fasciitis initial therapy
Rest, ice and strengthening and stretching exercises
If symptoms persist, professional orthotics or OtC arch support soles can be recommended
Glucocorticoid injections may be used for refractory pain and surgery may be considered be pts who do not respond to conservative therapy
HOCM
Increased left ventricular wall thickness and asymmetric septal hypertrophy
TTE
Timeline for brief psychotic disorder, schizophreniform disorder and schizophrenia
Brief psychotic disorder: >1 day and < 1 month (no negative symptoms part of diagnostic criteria)
Schizophreniform disorder: > 1 month and < 6 months
Schizophrenia: > 6 months
Schizoaffective vs mood disorder with psychotic features
Schizoaffective = major mood episode (depressive episode or manic) + criterion A symptoms of schizophrenia
Mood disorder with psychotic features =
Opioid overdose
reduces central respiratory drive causing hypoventilation and acute respiratory acid
Insomnia caused by MDD treatment
SSRIs
like citalopram
Mirtazpine
Treatment for benzodiazepines withdrawal
Lorazepam
Antipsychotics lower the seizure threshold and should not be used to treat psychosis that occurs secondary to benzodiazepine withdrawal
Cluster A personality disorders
Paranoid: holding grudges, suspicions of others true motives, resistance in confiding in others, and fidelity or loyalty. Quick to interpret benign remarks as demeaning
Schizoid: detached from relationships, restricted range of emotional expression
Schizotypal: magical thinking, odd or eccentric appearance, social and interpersonal deficits
Cluster B personality disorders
Antisocial: belief of inadequacy that interferes with interpersonal relationships and prevents engaging in a new relationship, social situation or activity, disregard and violation of the rights of others, lack of remorse and empathy
Borderline: mood changes are abrupt (within hours), usually triggered by a stressor. Fear of abandonment and nonsuicidal self-harming injuries
Histrionic: excessive emotionality, attention seeking behavior
Narcissistic: sense of grandiosity, need for admiration, jealousy of others
Cluster C personality disorders
Avoidant: feelings of inadequacy, social inhibition, believing they are inferior to others, this belief prevents them from engaging in social activities or new relationships
Dependent: excessive need to be taken care of by others, leads to submissive behavior, difficulty expressing disagreement, feeling lost when alone and the inability to make simple everyday decisions independently or assume responsibilities
Obsessive-compulsive personality: preoccupation with organization, perfectionism that interferes with task completion, excessive time spent on work, difficulty delegating tasks to others, inability to discard objects with no monetary value and being strict with money and morals
TCA overdose presentation and treatment
Wide complex tachycardia, hyperthermia, hypotension, flushed skin and hypoventilation
Cardiotoxicity related to TCAs is treated with sodium bicarbonate
Ethylene glycol treatment
Fomepizole (competitive inhibitor of alcohol dehydrogenase)
Lamotrigine and carbamazepine are mood stabilizers that can be used ass adjuvant treatment for severe affecting dysregulation in personality disorders. Both medications can lead to potentially life-threatening
SJS/TEN
Frontotemporal dementia history
Pick bodies consisting of hyperphosphorylated tau proteins
MOA of first line therapy for hepatic encephalopathy
Lactulose MOA is reducing intraluminal pH which promotes the conversion of ammonia to ammonium ion. Ammonium ions cannot be absorbed in the gut and are thus excreted in the stool, resulting in reduced serum ammonia levels
Stages of alcohol withdrawal
6-12 hours = tremor, tachycardia, hypertension
12-48 hours = seziures
2-7 days = delirium tremens
SSRIs can cause which electrolyte abnormality
hyponatremia
Treatment for bacterial meningitis in neonates < 1month, children to adults < 50 years of age, adults >50, immunocompromised host (regardless of age)
Neonates <1month: ampicillin + cefotaxime (same for empiric)
Children to adults < 50 years of age: ceftriaxone + vancomycin + dexamethasone
Adults >50: ceftriaxone + vancomycin + ampicillin + dexamethasone (same for empiric)
Immunocompromised: vancomycin + ampicillin + cefepime or meropenem + dexamethasone
Empiric: vanc + 3rd gen cephalosporin like ceftriaxone or cefotaxime + post exposure prophylaxis for close contacts with rifampin
Indications for electroconvulsive therapy
Used for treatment of severe depression, treatment-refractory depression or both. It is safe for use in pregnancy
Risk factors that mandate long-term or lifelong antidepressant therapy include
> 3 episodes of depression
Strong family history of depression
> 1 severe episode (an episode with several symptoms in excess of the required 5)
Comorbid, nonaffective psychiatric diagnosis or chronic medical disorder
First line for mild to moderate dementia or those newly diagnosed with dementia
Acetylcholinesterase inhibitors such as donepezil, galantamine and rivastigmine
Memantine is used in moderate to severe cases, it blocks over excited N-methyl-D-aspartate glutamate receptors
Acute mania in pregnancy treatment
Haloperidol
Primary vs secondary acute angle closure glaucoma
Sudden onset eye pain, blurry vision, redness with an elevated IOCP, unilateral headache, non-reactive pupil, can be triggered by anti-cholinergic medications
Shallow anterior chamber, inadequate drainage of aqueous humor
Gonioscopy is gold standard
Ocular emergency and must be treated promptly to prevent blindness (oral acetazolamide, topical timolol, apraclonidine, pilocarpine)
Primary = patients are automatically predisposed with no identifiable cause
Secondary = primary process (eg, fibrovascular membrane, mass, hemorrhage) is responsible for narrowing or closure of the anterior chamber angle
Open-angle glaucoma
Elevated IOCP, asymptomatic, found incidentally
Optic nerve injury presentation
Can be caused by either direct, penetrating trauma or indirectly following head/orbit trauma
Present with acute, ipsilateral vision loss and a relative afferent pupillary defect on PE (Marcus gunn pupil which is when light shined in affected eye, both pupils dilate and when light shined in unaffected eye both pupils constrict)
Diagnosis is confirmed via CT imaging of the orbit
Optho consult +/- surgical decompression
Management of malignant hyperthermia during surgery
Medical emergency triggered by inhalational anesthetics (sevoflurane) or succinylcholine
Presents with autonomic instability (hyperthermia, hypertension, tachypnea), hypercarbia (difficult ventilation, increased end tidal carbon dioxide), generalized muscle rigidity, cardiac arrhythmias, rhabdomyolysis and delirium
Treatment is immediate removal of the offending agent followed by administration of IV dantrolene
Periorbital cellulitis vs. orbitial cellulitis
Periorbital cellulitis is an infection of the soft tissues of the orbit that is differentiated from orbital cellulitis by a lack of vision changes and pain with eye movement
Periorbital = eyelid swelling +/- erythema, +/- eye pain/tenderness, +/- fever or leukocytosis
Orbital = eyelid swelling +/- erythema, eye pain/tenderness, painful eye movement, proptosis likely present, vision impairment likely present, chemosis (edema of conjunctiva) may be present, fever or leukocytosis
So PAIN with eye movement = orbital
Which class of drugs to avoid in dementia with Ley bodies
Antipsychotics as they can precipitate Parkinsonism or acutely worsen pre-existing Parkinsonism
Wernicke encephalopathy
Alcohol use disorder, nystagmus, confusion
Caused by thiamine deficiency which is also linked with wet and dry beriberi
Wet beriberi is characterized by dilated high-output cardiomyopathy and heart failure
Dry beriberi is characterized by distal peripheral polyneuropathy
Rett syndrome
X-linked mutation in the MECP2 gene
Stereotypic hand-wringing movements, intellectual and verbal disability like loss of spoken language, decelerated head growth, epilepsy, growth failure, gait and motor abnormalities, breathing abnormalities
Benzo MOA
Enhance the activity of GABA-A receptors
Clostridium botulinum moa
bacterial toxin blocks the release of presynaptic neurotransmitters, leading to weakness, hypotonia and possibly respiratory failure
What test to do if a patient has a suspected corneal abrasion
Slit lamp test
Fluorescein can be a useful adjunct to simple slit lamp examination when the diagnosis is unclear
Rare side effect of sildenafil
Cyanopsia (blue-tinted vision0 via inhibition of PDE-6 in the retina
Valproic acid SE
First line tx for juvenile mycoclonic epilepsy
AE: acute pancreatitis, hepatotoxicity, tremor and eight gain
Can also cause neural tube defects and should not be used during pregnancy
Which drugs cause drug-induced pancreatitis
Azathioprine
Corticosteroids
Didanosine
Diuretics (loop and thiazide)
Valproic acid
First line tx for ALS
Glutamate antagonist (eg, riluzole) to aid with increased life expectancy secondary to reducing glutamate receptor excitotoxicity
Drug induced Parkinsonism
tremor is often bilateral vs parkinson disease starts unilateral
CAG
CGG
CTG
GAA
GCC
CAG = huntingtons
CGG = fragile x
CTG = myotonic dystrophy
GAA = Friedrich ataxia
GCC = FRAAXE mental retardation
Management in febrile seizures in kids
Reassurance, supportive care, including antipyretics
Abortive therapy (eg, diazepam) if seizure lasts > 5 minutes
Lithium SE
hyperparathyroidism –> hypercalcemia
Thyroid dysfunction (hypothyroidism)
Nephrogenic diabetes insipidus
Chronic kidney disease
Teratogenic (Ebstein anomaly)
Sacral dysfunction in post partum patient
Bilateral sacral flexion
Negative standing and seated flexion tests
Deep sacral sulci
Shallow ILAs
Anterior sacral rotation about a middle transverse axis
innominate rotation occurs at which motion
inferior transverse axis
Hamstrings
Semitendinosus
Semimembranosus
Biceps femoris
They all do knee flexion and hip extension
Semitendinosus & semimembranosus = hip internal rotation
Biceps femoris = hip external rotation
Sacral axis
Superior transverse:
Middle transverse:
Inferior transverse:
Oblique:
Motion
Superior transverse: craniosacral
Middle transverse: anatomic
Inferior transverse: innominate
Oblique: torsion
Specific test for ACL
Lachman
First line tx for migraines during pregnancy
Acetaminophen
Then aspirin and NSAIDs
MC of sepsis in those under 7 days of age
Consider sepsis in any neonate presenting with temperature instability and lethargy. The most common cause of sepsis in those under 7 days of age is group B strep which is a gram positive cocci
Treatment for patients with a postdural puncture headache
Mild (can tolerate upright position and care for their baby) –> increased hydration, bed rest as needed, oral pain meds, antiemetics
If the headache continues to be debilitating then can give –> epidural blood patch (performed 24 hours following placement of epidural catheter). Second line includes transnasal sphenopalatine block using topical intranasal anesthetic to provide temporary relief or greater occipital nerve block to interrupt pain transmission
Felty syndrome
RA + splenomegaly + neutropenia
Caplan syndrome
RA + pneumoconiosis
Treatment for guillain barre syndrome
Plasmapheresis
GBS is an immune mediated polyneuropathy
Drugs that cause aplastic anemia
Carbamazepine
Phenytoin
Chloramphenicol
Sulfonamides
Methimazole
Propylthiouracil
Indomethacin
Treatment of choice for patients with a cerebellar hemorrhagic stroke who are deteriorating neurologically
Immediate surgical decompression
Lewy body dementia
Visual hallucinations, parkinsonism, fluctuating mental status
Classic eosinophilic cytoplasmic inclusion bodies within the substantia nigra and locus coeruleus
Tx with cholinesterase inhibitors
Osmotic demyelination syndrome is diagnosed by MRI of brain however it may take up to 4 weeks after onset of symptoms for MRI scans to become abnormal. Thus when the syndrome is suspected clinically,
brain MRI should be repeated at a later time if initial imaging is normal
Most common bacterial etiology of an infection of a ventriculoperitoneal shunt placed to manage hydrocephalus is
Staph epidermis which is a gram positive coagulase negative bacteria
Blurry vision, conjunctival erythema after suffering ocular trauma is consistent with sympathetic ophthalmia, which is an
Autoimmune condition that is caused by T cell sensitization to self-antigens
Type IV hypersensitivity
Can affect injured and uninjured eye
Prevent via enucleation of the injured eye
Manage via glucocorticoids and biologic agents
GBS CSF
Normal WBC, RBC, negative gram stain or culture
Elevated protein
Definitive treatment for third degree heart block
Permanent pacemaker because they have an increased risk of sudden cardiac death
Before giving tPA in someone that has acute ischemic stroke and their blood pressure is uncontrolled,
Blood pressure first has to be reduced to the target range typically SBP < 185 mmHg and diastolic pressure < 110 mmHg
IV labetalol and nicardipine are common anti HTN agents used for BP reduction prior to tPA
Subarachnoid hemorrhage
CT head without
Once hemorrhage is identified by CT then cerebral angiography or CT angiography is preferred
If the angiography is negative then an MRI of the head is indicated
All patients with suspected stroke should have what immediately
Oxygen saturation
Finger stick glucose level check
Noncon brain CT
If there is no evidence of hemorrhage on CT and the patient is within the therapeutic window, tPA should be administered
Window ranges from < 3 hours up to 4.5 hours
Optic neuritis management
IV methylprednisolone
What to do first in suspected salicylate toxicity
Arterial blood gas
A mixed respiratory alkalosis and metabolic acidosis would support the diagnosis
Salicylate = aspirin
Acetaminophen = Tylenol
Acute angle-closure glaucoma
Chronic fatigue syndrome
Fatigue, post-exertional malaise, unrefreshing sleep, cognitive impairment, orthostatic related symptoms persisting for > 6 months. May begin suddenly after an infection or may develop gradually
In a patient with suspected pseudotumor cerebri, evaluation begins with
Urgent head MRI done before lumbar puncture to rule out other potential causes of increased ICP
psuedotumor cerebri
This patient’s pulsating, unilateral headache with nausea and vomiting is very typical of acute migraine headache, which can sometimes vary in intensity and response to treatment. Many migraines are adequately treated with simple analgesics (eg, nonsteroidal anti-inflammatory drugs, acetaminophen). For refractory cases, triptans (eg, sumatriptan) can be used as first-line abortive therapy. However, triptans (as well as ergots) are 5-hydroxytryptamine (5-HT1B/D) agonists that can cause vasoconstriction; therefore, they should be avoided in patients with cardiovascular or atherosclerotic disease due to the potential risk for triggering a serious vasoocclusivecomplication (eg, myocardial infarction, stroke) (Choice E).
In patients with significant cardiovascular history, metoclopramide is often used. It blocks dopamine (D2) receptors and does not have significant vasoconstrictive adverse effects. It is particularly effective in the treatment of migraines with significant associated nausea/vomiting, so it is also sometimes used for patients without a cardiovascular history if nausea and vomiting are prominent symptoms of the acute migraine. Diphenhydramine is usually coadministered to prevent the occurrence of extrapyramidal effects (eg, akathisia, dystonia).
Meniere
Vertigo, tinnitus, sensorineural hearing loss (eg, weber lateralizes to the left)
Low frequency hearing loss
Caused from reduced resorption of endolymph
Acute multiple sclerosis exacerbation first line management
IV methylprednisolone (+ PPI (as with any patient receiving glucocorticoids to prevent gastritis))
Patients who do not respond to methylprednisolone should be treated with plasmapheresis
Patient has right and left cerebellopontine angle tumors, what is this patient at greatest risk for
Patient has bilateral acoustic neuromas which is consistent with NF2
NF2 can also cause meningiomas, schwannomas of other cranial nerves and ependymomas
Other NF2 findings are bilateral cataracts, seizures, skin nodules, cafe au lait spots
Acoustic neuromas are caused by compression of vestibulocochlear nerveas a result of the tumor extending into the internal acoustic meatus
Once myasthenia gravis is diagnosed with acetylcholine receptor assay, the next step is to
CT scan the chest to check for a thymoma
PYRIDOstigmine (cholinesterase inhibitor) is the treatment
Patient has right sided facial drooping and complete paralysis of right upper and lower extremities. Circumduction gait, sometimes dysarthria. Which vessel is the case
Contralateral lenticulostriate artery
A pure motor stroke is caused by infarction in the posterior limb of the internal capsule which contains the corticospinal and corticobulbar fibers that innervate the motor nuclei on the contralateral side
Epidural hematoma
Middle meningeal artery
Initial LOC followed by a lucid interval
Middle cerebral artery embolism manifests as
focal neurologic deficits (hemiparesis), altered mental staatus, vomiting
Does herpes simplex encephalitis require prophylactic therapy
No
Central vs peripheral vertigo
Central: brainstem stroke, cerebellar stroke/tumor, nystagmus is immediate and in any direction (vertical, horizontal, rotary), no auditory findings, often has neurological findings, head position doesn’t change
Peripheral: semicircular canal debris, BPPV, meniere disease, nystagmus is horizontal and unidirectional, occasionally will have auditory findings, no neurological findings, and head position is worsened by changing
With central look for rotary or vertical nystagmus
ALS diagnosis and treatment
Involves UMN and LMN signs in at least 3 body segments (muscle wasting and weakness, atrophy, spasticity, abnormally active reflexes, pathological reflexes)
UMN: spasticity (including spastic dysarthria), hyperreflexia and/or sustained clonus, hoffman sign, extensor planar response, pseudobulbar effect
LMN: flaccid muscle tone, muscle atrophy and wasting, muscle cramping, bulbar signs (dysphagia, dysarthria, respiratory weakness), fasciculations
Diagnosis: EMG to confirm diagnosis and to exclude mimics- will show fibrillations and loss of innervation in multiple muscle groups
Treatment is Riluzole
Amaurosis fugax
schemia in the territory of the central retinal artery
Presenting sign of carotid stenosis
Treatment for Wilsons
Penicillamine
Rifampin MOA and SE
MOA: bacterial DNA dependent RNA polymerase and therefore inhibits bacterial protein production
SE: discoloration of body fluids, hepatotoxicity
Posterior communicating artery aneurysms
Can compress the oculomotor nerve causing oculomotor nerve palsy
Anterior communicating artery aneurysms
Can compress the optic chiasm causing bitemporal heteronymous hemianopsia
Posterior inferior cerebellar artery
Wallenberg syndrome
Decreased pain and/or temperature of the ipsilateral face and contralateral body
Patients may also have dysphagia, slurred speech, vertigo, and nystagmus
Treatment for solitary brain metastasis when patients have no evidence of extracranial disease and a good performance status
Surgical resection
Whole-brain radiation is recommended for patients with multiple brain metastases, poor performance status and/or extracranial metastasis
Which are associated with higher and lower risk of Alzheimers
Lower = apoE2
Higher = apoE4, amyloid precursor protein gene mutations, presinilin 1 and 2, trisomy 21
Cryptococcal meningitis
Immunocompromised such as those with HIV infection and a CD4+ count < 100 cells/mcl
Latest agglutination test of CSF will be positive
The combination of amphotericin B and flucytosine is used for induction therapy for the first 2 weeks, followed by fluxonazole for at least 8 weeks and then low dose fluconazole for at least 1 year
Migraines pathophys
Result of primary neuronal dysfunction with the main pathophysiologic mechanism being activation of the trigeminovascular system. This activation leads to the release of vasoactive neuropeptides (substance P, calcitonin gene related peptide, neurokinin A) that trigger neuroinflammation and pain
Succinylcholine MOA
Depolarizing neuromuscular blocker that acts as an acetylcholine receptor agonist
It has a rapid onset and short duration of action
Due to the cellular potassium efflux, transient fasciculations may be seen
Bilateral conductive hearing loss, positive family history of hearing issues
Tuning fork placed on mastoid, the patient can sense vibration longer than when hearing the tuning fork when it is placed near the ear
Otosclerosis
Loss of stapedial reflex is a common finding
Von hippel Lindau diseaase
Retinal and cerebellar hemangioblastoma
Renal cell carcinoma
Pheochromocytoma
Surveillance with MRI of brain and spine, MRI of abdomen regular eye examinations, measurement of serum and/or metanephrines
MC neurologic deficit of untreated bacterial meningitis
Hearing loss
High dose corticosteroids administered prior to antibiotics have been shown to reduce this risk
Maroon-colored stools (hematochezia), bright red blood per rectum, clots in stool is suggestive of
Black tarry stools (melena) is suggestive of
Lower GI bleed
Upper GI bleed
Internal hemorrhoid
Presents as anal pruritus, prolapse and occasionally painless rectal bleeding
Seen proximal to the dentate line and arise from the superior hemorrhoid veins
Painless
ENDOderm
Treatment is fiber, fluids and possibly laxatives to improve bowel habits
Note that when the prolapse is out of the anal canal with defecation or straining WITHOUT reduce spontaneously then manual reduction is required
External hemorrhoid
Located distal to the dentate line and arise from the inferior hemorrhoid veins
Painful
Arises from ECTOderm
Treatment for symptomatic thrombosed (dark blue purple color) external hemorrhoids is surgical excision
Conservative management like sitz baths, topical treatment and antidiarrheal agents are reserved for less symptomatic cases or for patients who present > 72 hours after onset of symptoms
ZES
Functional gastrin-secreting tumor that occurs most commonly in the pancreas and/or duodenum
Severe GERD, frequent recurrent gastric and duodenal ulcers, recurrent bleeding ulcers, chronic abdominal pain, diarrhea, weight loss
Multiple ulcers, ulcers distal to the duodenal bulb, negative testing for H pylori
Dx with casting serum gastrin level or positive secretin stimulation test
Secretin decreases gastrin secretion from normal G cells but increases gastrin secretion from gastrinoma cells
First line drug treatment its PPIs (a somatostatin analog like octreotide can be used if the patient doesnt respond to PPI therapy)
Definitive treatment is surgery
Girl with bulimia has painful swallowing and vomiting. Earlier that evening she forced herself to vomit after eating which she noticed blood in the vomit and a severe sharp pain in her chest. PE shows enlarged parotid glands bilaterally and crepitus on palpation of upper chest. What’s the most appropriate diagnostic test
Gastrograffin swallow which is esophagography with a water soluble contrast agent
Barium swallow is avoided when possible as leakage of barium through a perforation can cause severe inflammation of the mediastinum or pleural cavities
Patient likely has a ruptured esophagus (Boerhaave syndrome), crepitus is indicative of subcutaneous emphysema which is a common finding of a transmural tear (ie, rupture) of the esophagus
Perianal abscess
Etiology: infection of an occluded anal crypt gland
Risk factors: anoreceptive intercourse, constipation
Pain with defecation, anal pruritis, progression can lead to contrast pain and systemic signs of infection such a s low grade fever
PE: indurated, erythematous, painful mass near the anal orifice
Treatment: incision and drainage should be performed in order to prevent fistula formation
C diff pathogenesis
Pathogenesis: Disruption of normal colonic flora, allowing for proliferation of toxin producing strains of C diff
MC occurs with a hx of antibiotic use but can occur in patients with IBD without history of antibiotic use
Enzyme immunoassay for glutamate dehydrogenase (GDH) antigen is sensitive but not specific. EIA for GDH should be followed by a more specific test such as EIA for c diff toxins A and B (stool sample). If one of thosr is positive and the other is negative then do a NAAT testing
Treatment: oral vancomycin or oral fidaxomycin (RNA polymerase inhibitor that is bactericidal)
Food protein induced allergic proctocolitis (FPIAP)
Suspected when a child aged younger than 6 months presents with blood-streaked stools and no evidence of anal fissure on exam
For breastfed infants –> elimination of dairy from mothers diet
Formula-fed infants –>< switched to a hydrolyzed formula
Eosinophilic inflammation of the rectosigmoid colon, non-IgE mediated, triggers include cows milk and soy proteins, risk factors include eczema and FH of food allergies
AE of first line medication given for hepatic encephalopathy
Ammonia is directly related to encephalopathy and is MC treated with lactulose
Lactulose may cause a non-anion gap metabolic acidosis as side effect in the setting of diarrhea from large volume losses of bicarbonate
Other SE include dehydration, hypernatremia, hypokalemia, abdominal cramps, distension, excessive diarrhea, flatulence, nausea/vomiting
Acute cholecystitis management
Ultrasound then HIDA (hepatobiliary iminodiacetic acid scan)
Secondary lactase deficiency
Result of intestinal epithelial cell damage following viral gastroenteritis
Symptoms due to carbohydrate malabsorption
Abdominal pain, bloating and flatulence, watery diarrhea
Tx with temporary dietary modification with restriction of dairy products, typically resolve within weeks to months
Vascular ring
Congenital malformations of the aortic arch system. Symptoms are caused by tracheal and/or esophageal compression
Tracheal compression by a vascular ring will present with biphasic stridor that worsens when crying and feeding and improves with neck extension. Esophageal compression can cause vomiting and dysphagia
Diagnosis: CT scan, evaluate for other abnormalities (eg, echo, laryngoscopy)
Treatment: surgical division of the ring
Autoimmune hepatitis
Adolescent or middle-aged females with elevated liver enzymes and antinuclear antibodies, esp those with another autoimmune disorder
Anti-smooth muscle antibiodies aare he most specific blood tesst and diagnosis caan be confirmed with aa liver biopsy
High-volume, watery diarrhea and electrolyte derangements following travel to an endemic area (eg, Latin America, Southern Asia)
Caused by the bacterial organism Vibrio cholera and symptoms are the result of a bacterial exotoxin (enterotoxin) that causes impaired intestinal electrolyte absorption
Stool microscopy shows no leukocytes or erythrocytes
Treatment: aggressive fluid resuscitation and electrolyte replacement +/- antimicrobial therapy
Zenker diverticulum
Pathophysiology: impaired relaxation of cricopharyngeal muscle –> increase intraluminal pressure –> herniation of mucosa and submucosa –> pseudodiverticulum (false diverticulum)
Located between the 2 parts of the inferior pharyngeal constrictor muscle: thyropharyngeus and cricopharyngeus muscles (Killian triangle)
Presentation: progressive dysphagia, halitosis, regurgitation of undigested food, neck mass, aspiration (pneumonia, lung abscess)
Initial diagnostic test is barium esophagram
Treatment is surgery (diverticulectomy +/- cricopharyngeal myotomy)
H pylori treatment
Two options:
PPI + clarithromycin + amoxicillin (metronidazole in patients allergic to penicillins)
PPI + bismuth subsalicyclate + tetracycline + metronidazole 9used in patients with increased likelihood of clarithromycin-resistant disease such as those previously treated with macrolides or living in a region with high clarithromycin resistance rate (>15%))
Hirschsprung disease (congenital aganglionic megacolon)
Congenital absence of both the myenteric and submucosal plexuses in the colon
Rectal biopsy (distal to the dilated segment of bowel) is the definitive diagnostic test
In GERD the epithelium of the distal esophagus changes from
stratified squamous cells to simple columnar cells
Peptic ulcer disease
Gastric ulcer- abdominal pain occurs shortly after eating as food stimulates the release of gastric acid
Duodenal ulcers- pain improves with eating because of bicarbonate release into the duodenum and the buffering effects of food
Most common origin of carcinoid tumors
Small intestine (appendix and terminal ileum)
Carcinoid syndrome arises from neuroendocrine tumors that have metastasized to the liver. After spreading to the liver carcinoid tumors can metastasize to the lung, bones, skin and other organs. Can also cause valvular abnormalities including tricuspid regurgitation and right sided heart failure
What is colonic pseudo-obstruction aka Ogilive syndrome
Acute pseudo-obstruction and dilation of the colon in the absence of mechanical obstruction in severely ill patients
Budd-chiari
Obstruction of hepatic venous outflow
MC associated with hypercoagulable states as can occur with OCP use, pregnancy, malignancies and thrombophilias
Diagnosis is usually confirmed by Doppler ultrasound of the RUQ
Serology for patients who have recovered from hepatitis B
Positive HBsAb and HBcAb
AIDS defining illness
PIC
Infantile GERD
Arching the back while feeding, spitting up, normal height and weight, may also present with emesis following meals, irritability and occasionally a cough
Diagnosis is through H&P
Although rarely needed to confirm the diagnosis, the gold standard for diagnosing infantile GERD if esophageal pH monitoring
Esophageal manometry if motility disorder is suspected
EGD used for biopsy if the diagnosis is still unclear
Treatment: smaller and more frequent meals, thickening the feeding formula with rice cereal, keep infant upright after feeding, H2 receptor antagonists
Acute cholecystitis-
Ascending cholangitis-
Choledocholithiasis-
Gallstone ileus-
Acute cholecystitis- RUQ pain, tenderness on RUQ palpation, radiates to right shoulder, worse after meals, Murphy sign (tenderness to the RUQ that worsens on inspiration)and gallstones in cystic duct. No jaundice (or mild)
Ascending cholangitis- bacterial infection of the biliary tree usually occurs from obstruction of common bile duct, ill-appearing, Charcot triad of RUQ pain, jaundice and fever. Reynold pentad is Charcot triad + septic shock and altered mental status)
Choledocholithiasis- gallstones in common bile duct. Elevated alk phos and total bilirubin
Gallstone ileus- small bowel obstruction resulting from the passage of aa large gallstone into the bowel through a cholecystoduodenal fistula, usually occurs at the ileocecal valve, signs and symptoms of SBO and have pneumobilia or on abdominal radiographs
Candida esophagitis treatment
Oral fluconazole (can do IV if patient cannot tolerate swallowing)
Ulcerative colitis first line medication
Meslamine (5-aminosalicylate) is first line for induction of remission as well as maintenance of remission
If remission is not acheived with meslamine alone, prednisone is typically added
First line treatment to slow the rate of accumulation of ascites in patients with hepatic cirrhosis
Dietary sodium restriction
Diuretic therapy with furosemide + spironolactone is also required in many patients
Transjugular intrahepatic portosystemic shunt (TIPS) is an option for some patients with refractory ascites due to hepatic cirrhosis
Portal hypertension is the first step in the development of ascites secondary to hepatic cirrhosis. Patients with cirrhosis and a normal portal venous pressure do not develop ascites. Portal HTN leads to splanchnic vasodilation resulting in decreased splanchnic blood flow and systemic vasodilation resulting in low arterial blood pressure
To maintain perfusion pressures, the RAAS system is activated, ADH secretion increases and sympathetic NS activity increases. The result is avid sodium and water retention by the kidneys, causing hypervolemic hyponatremia, accumulation of ascites fluid and peripheral edema
A patient with crohns presents to ED with similar presentation to acute appendicitis, what’s the next step
CT abdomen and pelvis since crohn flare and acute appendicitis presents similarly
Initial testing for carpal tunnel
Electromyogram and nerve conduction studies
Treatment for mild disease = PT, glucocorticoid injections, cock-up wrist splint
Severe = surgical decompression
Two scenarios and nerves leading to wining of scapula
- damage to long thoracic nerve (C5-C7) during mastectomy causes medial winging of the scapula via serratus anterior
- damage to the spinal accessory nerve (CN 11) during radical neck dissection of lymph node metastasis, causing lateral winging of the scapula via trapezius
Osteosarcoma treatment
Chemotherapy and limb-salvage therapy
If there is any question of scaphoid fracture union prior to return to high-impact activities, what do you order
CT scan is the best study to verify osseous union
Right anterior innominate muscle energy set up
Flexing and ADDucting the hip on the affected side to the restrictive barrier with the patient attempting to extend the hip against the physician’s equal and opposite counterforce. Performed 3 to 5 times with each contraction lasting 3 to 5 seconds. The hip is flexed to the new barrier after relaxation of each isometric contraction
Lead poisoning treatment
Chelation with dimercaptosuccinic acid or EDTA
Muscle energy
Direct
Patient contracts toward position of ease
Metatarsal adductus
Medial deviation of the metatarsals with the metatarsals pointing toward the midline relative to the hind foot
Congenital clubfoot deformity
CAVE
Cavus: exaggerated arch of the midfoot
Adductus: forefoot in adduction
Varus: hindfoot rotated inward
Equinus: ankle/foot fixed in plantar flexion
Sjogren syndrome is associated with an increased risk of developing
non-Hodgkin lymphoma
Developmental dysplasia of hip
Presents as a clunk sound upon elevation and abduction as well as depression and adduction of the newborn hip joint
Risk factors include the 5 F’s: femaale, footling (breach), firstborn, flexible (hyperlaxity), family history
Diagnosis is confirmed by ultrasound performed from approximately 6 weeks to 4 months of age (<6 weeks then defer imaging until >6 weeks of age)
Plain radiographs are used for diagnosis after 4 months of age when the femoral heads and acetabula ossify
Treatment for De Quervain tenosynovitis if conservative measures are inadequate
Surgical release of the abductor pollicis longus tendon
DEXA screening
Woman at age 65 or at an earlier age in postmenopausal women with risk factors for osteoporosis
Whipple’s disease
History of chronic malabsorptive diarrhea (steatorrhea, flatulence, abdominal distension), protein-losing enteropathy, weight loss, migratory non-deforming arthritis, lymphadenopathy and a low-grade fever
PAAS + macrophages in the lamina propria containing non-acid-fast gram-positive bacilli (T. whipped)
Initial management of osteoarthritis
Weight loss, regular moderate activity, topical or oral NSAIDs
Exercises to strengthen the quadriceps muscles can reduce abnormal loading on the joint and protect the articular cartilage from further stress
Strongest risk factor for rheumatoid arthritis
HLA-DR4
Others are smoking and female gender
Anti-cyclic citrullinated peptide antibodies = most specific diagnostic markers
for RA Rheumatoid factor = most sensitive marker
Polymyalgia rheumatica treatment
Low-dose prednisone
Dantrolene MOA
Binds to the RYR1 receptor to inhibit calcium release from the sarcoplasmic reticulum of skeletal muscle
Labs for:
Pagets
Osteoporosis
Osteomalacia
Osteitis fibrosa cystica
Pagets: increased alk phos, normal calcium, vitamin D, parathyroid, phosphate
Osteoporosis
Osteomalacia
Osteitis fibrosa cystica
Femoral neck fracture
Elderly patients that fall laterally onto hip
Unable to ambulate, shortened and externally rotated lower extremity on the affected side
Anterior vs posterior hip dislocations
Anterior is much less common, affected limb is usually externally rotated and appears longer than the unaffected limb
Posterior hip dislocations are usually caused by major traumas such as MVAs, the affected limb is shortened and internally rotated. Sciatic nerve is the only major nerve located posterior to he hip joint- injury in a posterior hip dislocation would result in weakness of knee flexion, ankle plantarflexion, ankle dorsiflexion, toe flexion and toe extension
Slipped capital femoral epiphysis
Proximal femoral epiphysis at the growth plate, resulting in displacement of the femoral hed posteriorly and medially regarding the femoral neck
PE: patient will hold affected hip in passive external rotaton thaat is exaggerated with hip flex. Internal rotation at the hip is limited and often painful
Legg-Calve-Perthes disease
AKA avascular necrosis of the femoral head
Characterized by atraumatic limp in young children with impaired internal rotation and abduction of the affected hip
Typically occurs in younger children with peak incidence at approx 5-6yo
Plain radiographs are the best diagnostic tool and will show evidence of femoral head necrosis
Avascular necrosis of the lunate (Kienbock disease) presentation
Caused by repetitive microtrauma to the carpal bones
presents with dorsal wrist pain, decreased grip strength and reduced range of motion
Priority listing of the use of language interpreters
-Physician (if fluent in the patient’s preferred language)
-Qualified (ie, trained formal interpreters): in-person, teleconferencing, video
-Unqualified ad hoc (eg, bilingual family and staff members)
-Written
Which standard DMARD for RA? What should you monitor throughout therapy?
Methotrexate
Monitor CBC, can cause myelosuppression
Osteoarthritis
Older ages, chronic joint pain, morning stiffness of < 30 minutes duration, swelling at t he end of the day
Radiographic findings include joint space narrowing, subchondral sclerosis and osteophytes
Firist like pharmacological traetment is NSAIDs (unless CI like in HTN, peptic ulcer disease, chronic kidney disease) or do not help alleviate pain,
ORal duloxetine or intra-articular corticosteroid injection should be considered
Calcium pyrophosphate deposition disease (aka pseudogout
Rhomboid shaped crystals with positive birefringence
Color when parallel to light = blue
Color when perpendicular to light = yellow
Predispositions to develop CPPD: hemochromatosis, hyperparathyroidism, hypomagnesemia, hypophosphatasia, familial chondrocalcinosis, familial hypocalciuric hypercalcemia
Bisphosphonates
Decreases osteoclast activity
Take on an empty stomach and don’t lie down for 30 to 60 minutes after taking to prevent esophageal irritation
Pes anserine bursitis
Anteromedial knee pain that occurs during lateral movements which are commonly observed in agility sports like soccer, basketball and field hockey
Initial management of polymyalgia rheumatica
Oral glucocorticoids
Common peroneal (fibular) nerve entrapment
Injury causes foot drop and an inverted and plantarflexed foot at rest with lack of eversion and dorsiflexion
PED = peroneal everts and dorsiflexes
Most specific antibody for: Dermatomyositis
Polymyositis
Multiple sclerosis
Rheumatoid arthritis
Type 1 diabetes
CREST syndrome
Crohn disease
Dermatomyositis: Anti-Mi-2
Polymyositis: Anti-Jo-1
Multiple sclerosis: Anti-myelin
Rheumatoid arthritis: Anti-CCP
Type 1 diabetes: Anti-glutamic acid decarboxylase
CREST syndrome: Anti-centromere
Crohn disease: Anti-Saccharomyces cerevisiae
Posterior fibular head dysfunction
Talus = internally rotated
Foot = inverted, plantarflexed and adducted (supinated)
Gold standard for diagnosing carpal tunnel
Electrodiagnostic testing (electromyography and nerve conduction studies)
Gout joint fluid aspirate
Cloudy, negatively birefringent, needle-shaped crystals with a WBC between 2,000 to 20,000 cells/mm3
Approach for subacromial joint injection
Insert the needle inferior to the lateral edge of the acromion and direct the needle medially and parallel to the acromion
Pseudomonas treatment
Penicillin
If allergic then aztreonam
ALL confirmatory test
Bone marrow biopsy
+myeloperoxidase
+TdT
ITP
For children with ITP and no or only mild bleeding, such as this patient with self-limited epistaxis and scattered petechiae, the American Society of Hematology 2019 guidelines recommend observation, irrespective of platelet count. Spontaneous resolution occurs in the majority of pediatric patients with ITP, often within six months, and severe bleeding is rare, even in patients with severe thrombocytopenia (i.e., < 30,000/mm3), because the function of circulating platelets is not impaired in patients with ITP.
ITP is a diagnosis of exclusion that is made in patients with isolated thrombocytopenia (i.e., no concurrent anemia or leukocytosis) after other potential causes have been ruled out. It is most commonly diagnosed in children and women of childbearing age. Unlike in children, in whom the indication for pharmacological intervention is based exclusively on clinical presentation, treatment initiation is generally recommended in adults with ITP with a platelet count < 30,000/mm3.
Acute hemolytic reaction
ABO incompatibility usually due to clerical error
Intravascular hemolysis
Onset within minutes-24 hr of transfusion
Fever, chills, hypotension
+ direct coombs test
Hemolysis (increased LDH and indirect bilirubin)
Splenectomy
Strep pneumo, H flu, Neisseria meningitides
polysaccharide exterior that conceals antigenic epitopes and resists innate phagocytosis. Therefore, these pathogens are largely eliminated via the humoral immune response with antibody-mediatedphagocytosis(opsonization) and antibody-mediated complement activation. Much of this is dependent on splenic macrophages and the generation of splenic opsonizing antibodies. As such, patients with asplenia are at high risk for fulminant infection with encapsulated organisms. These patients should be immunized with pneumococcal, meningococcal, and H influenzae type B vaccines and take oral antibiotics early in the course of any febrile illness.
Treatment for thalassemia minor
Do not require specific treatment
47 yo M comes in with occasional daytime headaches, dizziness and nausea, works in a underground parking garage, smoked 2 packs of cigarettes a day for 25 years, hematocrit 60%
This patient, who is exposed to automobile exhaust in an enclosed space, has intermittent headaches, dizziness, nausea, and polycythemia (elevated hematocrit), most likely due to chronic carbon monoxide (CO) poisoning.
CO is a byproduct of combusting organic matter (eg, oil, gas, wood). Exposure to toxic levels is more likely in enclosed or poorly ventilated areas. CO tightly binds hemoglobin - forming carboxyhemoglobin - with an affinity much greater than that of oxygen. Nonsmokers have low levels (<3%) of carboxyhemoglobin (due to normal enzymatic reactions). Cigarette smokers may have carboxyhemoglobin levels as high as 10%. Even though patients at this level are generally asymptomatic, small additional amounts of CO exposure may cause toxicity manifesting as headache, malaise, and nausea.
Carboxyhemoglobin shifts the oxygen dissociation curve to the left, impairing the ability of heme to unload oxygen at the tissue level. This results in tissue hypoxia. The kidney responds to tissue hypoxia by producing more erythropoietin (EPO). EPO stimulates the bone marrow to differentiate more red blood cells. Chronic CO toxicity is a cause of secondary polycythemia.
Pulse oximetry does not differentiate between carboxyhemoglobin and oxyhemoglobin; it cannot be used in the diagnosis of CO poisoning. Diagnosis is made by arterial blood gas with cooximetry.
Treat with high-flow 100% oxygen and in severe cases intubation/hyperbaric oxyge
Elderly patient with severe lymphocytosis combined with hepatosplenomegaly, lymphadenopathy and bicytopenia (anemia, thrombocytopenia) strongly suggests
CLL
Diagnosed by flow cytometry (showing a clonality of mature B cells)
Superior vena cava syndrome work up
Chest x-ray
If abnormal then chest CT and histology to determine tumor type and guide therapy
MC cause of obstruction is malignancy like lung cancer or non-hodgkin lymphoma
SVC syndrome is obstruction of the SVC impedes venous return from the head, neck and arms to the heart
Signs and symptoms include dyspnea, venous congestion aand swelling of the head, neck and arms
Male with a persistent palpable firm neck mass, referred otalgia, smoking history and no preceding infection most common cause
Malignancy is extremely likely in a patient with a persistent (>2 weeks), palpable (>1.5 cm), firm neck mass; a smoking history; and no preceding infection. By far the most common malignancy in an upper cervical node is mucosal head and neck squamous cell carcinoma (SCC). Indeed, the first (and only) apparent manifestation may be a palpable cervical lymph node, representing regional nodal metastasis. Referred otalgia is another common presenting symptom, facilitated by either the glossopharyngeal nerve (CN IX) (innervates both the base of tongue and the external auditory canal [EAC]) or the vagus nerve (CN X; innervates parts of the larynx/hypopharynx and the EAC).
Identification of the primary source of head and neck SCC is essential to direct treatment. Thorough examination includes endoscopic visualization using laryngopharyngoscopy as well as neck imaging (CT with contrast) to evaluate the primary site and characterize the cervical nodal disease. Fine-needle aspiration of the lymph node is advised over open biopsy to avoid tumor seeding.
