CCP 218 GU Reproductive System Emergencies

Question 1

What is the most reliable marker for GU end-organ perfusion?

Answer 1

Urine output

Question 2

primary complications of acute renal failure

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Answer 2

1. hyperkalemia
2. severe metabolic acidosis
3. volume overload
4. uremia

Question 3

treatment pathway for hyperkalemia

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Answer 3

1. Stabilize cardiac cell membrane (Calcium)
2. Shift potassium intracellularly (dextrose, insulin, bicarb, ventolin, MgSO4)
3. Remove potassium from body (IV fluids, lasix, dialysis, GI binding agents [kayexalate])

Question 4

treatment pathway for severe metabolic acidosis

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Answer 4

1. Support perfusion
2. Support ventilation
3. Bicarb IV
4. Hemodialysis

Question 5

treatment pathway for volume overload

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Answer 5

1. Positive pressure ventilation
2. Nitrates
3. Lasix
4. hemodialysis

Question 6

Acute renal failure/acute kidney injury (AKI) definition

Answer 6

abrupt decrease in kidney function, which encompasses both injury (structural damage) and impairment (loss of function)

1. Absolute increase in serum creatinine ≥26.4 μmol/L
2. Increase in serum creatinine ≥1.5x above baseline
3. Oliguria (urine output <0.5 mL/kg per hour) for >6 hours.

Question 7

three different categories of AKI

Answer 7

1. prerenal
2. intrinsic
3. postrenal

Question 8

Key Diagnostic Elements of pre-renal AKI

Answer 8

1. Historical: Volume loss, decreased cardiac output, or third spacing.
2. Physical Exam: Dry mucous membranes, orthostatic hypotension, decreased urination

Question 9

Key Diagnostic Elements of intra-renal AKI

Answer 9

1. Historical: Use of nephrotoxins, IV contrast dye, rhabdomyolysis, pulmonary renal diseases.
2. Physical Exam: Edema, purpura

Question 10

Key Diagnostic Elements of post-renal AKI

Answer 10

1. Historical: Obstructive process such as a mass, distal kidney stones, alternating oliguria and polyuria
2. physical exam: Distended bladder, anuria

Question 11

Indications for emergent hemodialysis (mnemonic: AEIOU)

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Answer 11

1. Acidosis (eg, cardiac instability associated with acidosis)
2. Electrolyte abnormality (ie, hyperkalemia)
3. Ingestions (toxins)
4. Overload (pulmonary edema with hypoxia)
5. Uremia

Question 12

treatment goals for pre-renal AKI

Answer 12

1. Optimize renal preload and perfusion with IV fluids +/- pressors and blood products

Question 13

treatment goals for intra-renal AKI

Answer 13

1. Stop any causative agents

2. treat infections (eg, Legionella, cytomegalovirus)

Question 14

treatment goals for post-renal AKI

Answer 14

1. Relieve obstruction

Question 15

pathophysiology of pre-renal AKI

Answer 15

1. Renal glomerular filtration is dependent on renal blood flow and is controlled by auto-regulation
2. A decrease in blood flow to the kidneys leads to pre-renal AKI

Question 16

causes of pre-renal AKI

Answer 16

1. Decreased intravascular volume
2. Volume redistribution with cardiorenal and hepatorenal syndrome
3. systemic vasodilation from sepsis or neurogenic shock
4. Drugs affecting glomerular blood flow, such as NSAIDs and ACE-inhibitors

Question 17

causes of intra-renal AKI

Answer 17

1. differentiated into conditions of the vessels, glomerulus, tubules, and interstitium
2. Intrinsic vascular disease can affect small vessels due to vasculitides
3. Large vessels can be affected by systemic thromboembolism, renal atheroembolic disease, and aortic dissection
4. Glomerular disease can be idiopathic, rheumatologic, or drug-induced
5. Acute tubular necrosis is related to nephrotoxins or ischemia in the setting of hypotension and shock
6. Acute interstitial nephritis is primarily caused by medications

Question 18

how does CKD increase the risk of AKI

Answer 18

1. renal autoregulation failure
2. abnormal vasodilatation
3. side effects of medications such as diuretics and antihypertensive agents

Question 19

primary systemic manifestations of AKI

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Answer 19

1. augmented inflammatory response and immunocompromise
2. volume overload and pulmonary edema
3. metabolic acidosis (reduced excretion of acid and reabsorption of bicarbonate)
4. electrolyte abnormalities (potassium, calcium, phosphorus)
5. GI edema, gut ischemia
6. acute lung injury/ARDS

Question 20

ECG findings associated with hyperkalemia

Answer 20

1. Peaked T-waves
2. Wide QRS complexes
3. AV blocks and unusual bradydysrhythmias
4. Sine wave pattern

Question 21

testicular torsion definition

Answer 21

1. testicular torsion results from inadequate fixation of the lower pole of the testis to the tunica vaginalis
2. testis may torse (twist) on the spermatic cord, potentially producing ischemia from reduced arterial inflow and venous outflow obstruction
3. may occur after an inciting event (eg, trauma, vigorous physical activity) or spontaneously

Question 22

classic case presentation on history for testicular torsion

Answer 22

1. sudden onset of unilateral testicular pain associated with nausea/vomiting (90%) after vigorous physical activity or minor trauma
2. high-riding testicle, edema, erythema, swelling, and tenderness

Question 23

emergency maneuver for testicular torsion

Answer 23

1. manual detorsion for testicular torsion to resume blood flow to the affected testis
2. rotate testes from the medial to lateral side (open book rotation)

Question 24

Urolithiasis pathophysiology

Answer 24

1. Urolithiasis occurs when the concentration of urinary electrolytes supersaturates the urine, resulting in crystal formation
2. Stones can obstruct urinary flow, resulting in increased intrarenal and intraureteral pressure
3. This increased pressure causes a prostaglandin-mediated ureteral spasm resulting in renal colic. The location of pain varies based on stone location
4. Hematuria develops as stones migrate through the urinary tract, damaging the urothelium
5. Most stones become obstructed at the ureteropelvic junction or the ureterovesicular junction
6. Obstructions of the urinary tract can lead to hydronephrosis
7. The most concerning complication of stone obstruction is sepsis from an infected stone

Question 25

Urolithiasis definition

Answer 25

1. the presence of renal calculi (stones) within the urinary tract

Question 26

classic case presentation for Urolithiasis

Answer 26

1. colicky flank pain 2. hematuria 3. nausea/vomiting

Question 27

Uremia induced metabolic acidosis

Answer 27

1. related to several unmeasured strong ions not incorporated into the normal anion gap calculation (phosphatase, sulfates, Krebs cycle derivatives) 2. BUN level notifies clinician that renal failure may play a role in an elevated anion gap acidosis

Question 28

Pelvic causes of abdominal pain in women

Answer 28

1. Ectopic pregnancy 2. Pelvic inflammatory disease 3. Ovarian torsion 4. Ruptured ovarian cyst 5. Endometriosis

Question 29

Glomerulonephritis definition

Answer 29

acute or chronic nephritis that involves inflammation of the capillaries of the renal glomeruli

Question 30

Cystitis definition

Answer 30

1. inflammation of the bladder | 2. Most often caused by a bacterial UTI

Question 31

pyelonephritis definition

Answer 31

infection of the renal pelvis and kidney

Question 32

AKIN Classification for Acute Kidney Injury 💵💵💵💵 MONEY SLIDE 💵💵💵💵

Answer 32

Classifies severity of acute kidney injury, similar to RIFLE Criteria To be diagnosed with acute kidney injury by the AKIN definition, patient must have at least one of the following within the past 48 hours 1. Absolute increase in serum creatinine ≥26.4 μmol/L 2. Increase in serum creatinine ≥1.5x above baseline 3. Oliguria (urine output <0.5 mL/kg per hour) for >6 hours.

Question 33

RIFLE Criteria for Acute Kidney Injury (AKI) 💵💵💵💵 MONEY SLIDE 💵💵💵💵

Answer 33

1. Classifies severity of acute kidney injury, similar to AKIN Classification

Question 34

pathophysiology of creatinine

Answer 34

1. Creatinine is an amino acid derivative 2. waste product of creatine and phosphocreatine 3. found almost exclusively (90%) in skeletal muscle tissues 4. freely filtered through the glomerulus 5. increase in serum creatinine to ≥1.5-fold the presumed baseline or an increase in serum creatinine by ≥26.5 µmol/L over 48 h

Question 35

pathophysiology of blood urea nitrogen

Answer 35

1. measures the amount of urea nitrogen, a waste product of protein metabolism 2. Urea is formed by the liver, carried by the blood to the kidneys for excretion 3. Because urea is cleared by the kidneys, measuring how much urea nitrogen remains in the blood can be used as a test of renal function 4. confounders include protein breakdown, hydration status, and liver failure

Question 36

pathophysiology of urine osmolality test

Answer 36

1. measures renal tubular concentrating ability 2. index of the concentration of osmotically active particles (Cl-, Na+, urea, K+, glucose) 3. measure of the solute-to-water ratio 4. depends on the number of osmotically active ions and molecules dissolved in a kilogram of body water 5. expressed as "xx" milliosmoles per kilogram of water (mOsm/kg water) 6. The difference between the calculated value and measured value is known as the osmolar gap

Question 37

how does Urine osmolality relate to renal function

Answer 37

1. Healthy kidneys can concentrate urine to an osmolality 4 times greater than serum and dilute urine to 1/4 the osmolality of serum 2. impaired renal function disrupts the ability to concentrate urine 3. in AKI urine osmolality can fall to approach that of serum, approximately 290mOsm/Kg

Question 38

osmoreceptor/vasopressin pathway (fluid balance homeostasis)

Answer 38

1. osmoreceptors in the hypothalmus sense the diffusion of water into or out of receptor cells caused by changes in serum osmolality 2. hypothalamus directs the pituitary to increase or decrease the release of vasopressin from the posterior pituitary 3. vasopressin causes increased water resorption in the distal tubules and collecting ducts of the kidney (reduces water loss and concentrates urine) 4. dehydration increases vasopressin release leading to water conservation and urine concentration 5. Fluid overload decreases vasopressin release which leads to diuresis

Question 39

osmolar gap definition

Answer 39

1. Expected serum osmolality assumes that sodium salts (chloride and bicarbonate), glucose, and urea nitrogen are the primary solutes in the serum 2. A difference from the expected and actual serum osmolarity values is the osmolar gap 3. The gap reflects an expected solute composition abnormality or the addition of an unexpected solute such as ethylene glycol and methanol

Question 40

Ectopic pregnancy definition

Answer 40

1. a fertilized ovum that implants outside the uterine cavity (≥90% of ectopic pregnancies implant in the fallopian tube)

Question 41

classic clinical presentation for ruptured ectopic pregnancy

Answer 41

1. hypotension/tachycardia/shock 2. sudden onset of severe and persistent abdominal pain 3. vaginal hemorrhage

Question 42

medical management for ectopic pregnancy

Answer 42

1. methotrexate (folic acid antagonist)

Question 43

treatment pathway for ruptured ectopic pregnancy

Answer 43

1. Volume Resuscitation (may require MTP) 2. Analgesia 3. STAT surgical consult

Question 44

AEIOU Indications for Dialysis in Patients with Acute Kidney Injury

Answer 44

1. A – Acidosis – metabolic acidosis with a pH <7.1 2. E – Electrolytes – refractory hyperkalemia with a serum potassium >6.5 mEq/L or rapidly rising potassium levels 3. I – Intoxications – use the mnemonic SLIME to remember the drugs and toxins that can be removed with dialysis: salicylates, lithium, isopropanol, methanol, ethylene glycol 4. O – Overload – volume overload refractory to diuresis 5. U – Uremia – elevated BUN with signs or symptoms of uremia, including pericarditis, neuropathy, uremic bleeding, or an otherwise unexplained decline in mental status (uremic encephalopathy)

Question 45

common modes of RRT 💵💵💵💵 MONEY SLIDE 💵💵💵💵

Answer 45

1. Continuous RRT (CRRT) 1. Slow Continuous Ultrafiltration (SCUF) 2. Continuous Venovenous Hemodialysis (CVVHD) 3. Hemofiltration (CVVHF) 4. Hemodiafiltration (CVVHDF) 5. Continuous Arterio-Venous Hemofiltration (CAVHF), 6. Slow low-efficiency daily dialysis (SLEDD) 3. Peritoneal dialysis (PD) 4. Plasmapheresis or plasma exchange 5. Intermittent Hemodialysis (IHD)

Question 46

IHD vs CRRT

Answer 46

IHD: Name: Intermittent hemodialysis Mechanism and molecules removed: Dialysis – mostly low Molecular Weight Use: Ambulatory CRF, Hyperkalemia Blood flow: 300 - 400 mL/min Dialysate flow: 500 mL/min or 30 L/hr Efficiency: High Urea clearance: (mL/min) 150 Hemodynamic stability: Poor (hypotension common) Duration: 3-4 h 3x/week Access: Fistula or vascath (must be good!) Anticoagulation: Not needed Dialysis Dysequilibrium Syndrome (DDS): Insufficient time for equilibration between compartments can cause cerebral edema Drugs and toxicology: Risk of rebound if high VD. Better for low VD (e.g. toxic alcohols) Logistics: Need tap water supply, need hygienic effluent removal, Technically difficult CRRT: Name: Continuous renal replacement therapy Mechanism and molecules removed: Small + middle molecules with CVVHDF Use: Critically ill/Non-ambulatory Blood flow: 150 - 200 mL/min Dialysate flow: CVVHF: nil/CVVHDF: 1 L/h Efficiency: Low (but increased clearance of high VD molecules over time) Urea clearance: (mL/min) 30 (CVVHDF) Hemodynamic stability: Good Duration: Continuous (24h/filter) Access: Vascath only Anticoagulation: Important (if filter clots can lose ~150 mL blood) Dialysis Dysequilibrium Syndrome (DDS): N/A Drugs and toxicology: Slower removal Logistics: High workload, clearance limited by interruptions, costly sterile dialysate bags, immobility

Question 47

SIADH versus CSW 💵💵💵💵 MONEY SLIDE 💵💵💵💵

Answer 47

SIADH 1. hyponatremia (decreased serum Na+, increased urine Na+) 2. euvolemia/slight hypervolemia (NORMAL VOLUME) 3. CVP normal-high 4. decreased urine output (Restrict fluid) 5. Replace salt (3% HTS) 6. water retention d/t elevated ADH levels 7. increased urine sodium CSW 1. hyponatremia (decreased serum Na+, increased urine Na+) 2. hypovolemia/dehydrated (patient is DRY) 3. CVP low 4. increased urine output 5. Replace fluids (0.9% NS) 6. excess secretion of sodium + water 7. increased urine sodium