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CCP 218 GU Reproductive System Emergencies Flashcards

1
Q

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

A

Urine output

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2
Q

primary complications of acute renal failure

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

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

treatment pathway for hyperkalemia

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  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])
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4
Q

treatment pathway for severe metabolic acidosis

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Support perfusion
  2. Support ventilation
  3. Bicarb IV
  4. Hemodialysis
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5
Q

treatment pathway for volume overload

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Positive pressure ventilation
  2. Nitrates
  3. Lasix
  4. hemodialysis
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6
Q

Acute renal failure/acute kidney injury (AKI) definition

A

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

  1. Absolute increase in serum creatinine β‰₯26.4 ΞΌmol/L
  2. Increase in serum creatinine β‰₯1.5x above baseline
  3. Oliguria (urine output <0.5 mL/kg per hour) for >6 hours.
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7
Q

three different categories of AKI

A
  1. prerenal
  2. intrinsic
  3. postrenal
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8
Q

Key Diagnostic Elements of pre-renal AKI

A
  1. Historical: Volume loss, decreased cardiac output, or third spacing.
  2. Physical Exam: Dry mucous membranes, orthostatic hypotension, decreased urination
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9
Q

Key Diagnostic Elements of intra-renal AKI

A
  1. Historical: Use of nephrotoxins, IV contrast dye, rhabdomyolysis, pulmonary renal diseases.
  2. Physical Exam: Edema, purpura
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10
Q

Key Diagnostic Elements of post-renal AKI

A
  1. Historical: Obstructive process such as a mass, distal kidney stones, alternating oliguria and polyuria
  2. physical exam: Distended bladder, anuria
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11
Q

Indications for emergent hemodialysis (mnemonic: AEIOU)

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Acidosis (eg, cardiac instability associated with acidosis)
  2. Electrolyte abnormality (ie, hyperkalemia)
  3. Ingestions (toxins)
  4. Overload (pulmonary edema with hypoxia)
  5. Uremia
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12
Q

treatment goals for pre-renal AKI

A
  1. Optimize renal preload and perfusion with IV fluids +/- pressors and blood products
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13
Q

treatment goals for intra-renal AKI

A
  1. Stop any causative agents

2. treat infections (eg, Legionella, cytomegalovirus)

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14
Q

treatment goals for post-renal AKI

A
  1. Relieve obstruction
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15
Q

pathophysiology of pre-renal AKI

A
  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
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16
Q

causes of pre-renal AKI

A
  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
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17
Q

causes of intra-renal AKI

A
  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
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18
Q

how does CKD increase the risk of AKI

A
  1. renal autoregulation failure
  2. abnormal vasodilatation
  3. side effects of medications such as diuretics and antihypertensive agents
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19
Q

primary systemic manifestations of AKI

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  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
20
Q

ECG findings associated with hyperkalemia

A
  1. Peaked T-waves
  2. Wide QRS complexes
  3. AV blocks and unusual bradydysrhythmias
  4. Sine wave pattern
21
Q

testicular torsion definition

A
  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
22
Q

classic case presentation on history for testicular torsion

A
  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
23
Q

emergency maneuver for testicular torsion

A
  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)
24
Q

Urolithiasis pathophysiology

A
  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
25
Q

Urolithiasis definition

A
  1. the presence of renal calculi (stones) within the urinary tract
26
Q

classic case presentation for Urolithiasis

A
  1. colicky flank pain
  2. hematuria
  3. nausea/vomiting
27
Q

Uremia induced metabolic acidosis

A
  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
28
Q

Pelvic causes of abdominal pain in women

A
  1. Ectopic pregnancy
  2. Pelvic inflammatory disease
  3. Ovarian torsion
  4. Ruptured ovarian cyst
  5. Endometriosis
29
Q

Glomerulonephritis definition

A

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

30
Q

Cystitis definition

A
  1. inflammation of the bladder

2. Most often caused by a bacterial UTI

31
Q

pyelonephritis definition

A

infection of the renal pelvis and kidney

32
Q

AKIN Classification for Acute Kidney Injury

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A

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 β‰₯26.4 ΞΌmol/L
  2. Increase in serum creatinine β‰₯1.5x above baseline
  3. Oliguria (urine output <0.5 mL/kg per hour) for >6 hours.
33
Q

RIFLE Criteria for Acute Kidney Injury (AKI)

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Classifies severity of acute kidney injury, similar to AKIN Classification
34
Q

pathophysiology of creatinine

A
  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 β‰₯1.5-fold the presumed baseline or an increase in serum creatinine by β‰₯26.5 Β΅mol/L over 48 h
35
Q

pathophysiology of blood urea nitrogen

A
  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
36
Q

pathophysiology of urine osmolality test

A
  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 β€œxx” milliosmoles per kilogram of water (mOsm/kg water)
  6. The difference between the calculated value and measured value is known as the osmolar gap
37
Q

how does Urine osmolality relate to renal function

A
  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
38
Q

osmoreceptor/vasopressin pathway (fluid balance homeostasis)

A
  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
39
Q

osmolar gap definition

A
  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
40
Q

Ectopic pregnancy definition

A
  1. a fertilized ovum that implants outside the uterine cavity (β‰₯90% of ectopic pregnancies implant in the fallopian tube)
41
Q

classic clinical presentation for ruptured ectopic pregnancy

A
  1. hypotension/tachycardia/shock
  2. sudden onset of severe and persistent abdominal pain
  3. vaginal hemorrhage
42
Q

medical management for ectopic pregnancy

A
  1. methotrexate (folic acid antagonist)
43
Q

treatment pathway for ruptured ectopic pregnancy

A
  1. Volume Resuscitation (may require MTP)
  2. Analgesia
  3. STAT surgical consult
44
Q

AEIOU Indications for Dialysis in Patients with Acute Kidney Injury

A
  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)
45
Q

common modes of RRT

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A
  1. Continuous RRT (CRRT)
  2. Slow Continuous Ultrafiltration (SCUF)
  3. Continuous Venovenous Hemodialysis (CVVHD)
  4. Hemofiltration (CVVHF)
  5. Hemodiafiltration (CVVHDF)
  6. Continuous Arterio-Venous Hemofiltration (CAVHF), 6. Slow low-efficiency daily dialysis (SLEDD)
  7. Peritoneal dialysis (PD)
  8. Plasmapheresis or plasma exchange
  9. Intermittent Hemodialysis (IHD)
46
Q

IHD vs CRRT

A

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

47
Q

SIADH versus CSW

πŸ’΅πŸ’΅πŸ’΅πŸ’΅ MONEY SLIDE πŸ’΅πŸ’΅πŸ’΅πŸ’΅

A

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

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