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Surgery 2 Flashcards

1
Q

What is an extraperitoneal bladder injury (EPBI)?

A

Either contusion or rupture of the neck, anterior wall, or anterolateral wall of the bladder

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2
Q

Presentation of extraperitoneal bladder injury (EPBI)?

A

In the case of rupture, extravasation of urine into adjacent tissues causes localized pain in the lower abdomen and pelvis. Pelvic fracture is almost always present. Sometimes a bony fragment can puncture and rupture the bladder.

  • NO peritoneal signs
  • Gross hematuria
  • Urinary retention
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3
Q

What is intraperitoneal bladder rupture?

A

Rupture of the dome of the bladder (superior and lateral bladder walls, directly abuts the peritoneal space)

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4
Q

Presentation of intraperitoneal bladder rupture?

A

Causes intraperitoneal urine leakage, leads to chemical peritonitis (eg, diffuse abdominal tenderness, guarding, rebound)
Pelvic fracture is often present, but less common than EPBI

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5
Q

Presentation of renal laceration?

A

May have hematuria; urinary tension would be unusual

Flank pain and hemorrhage into the retroperitoneal space

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6
Q

What is the most common cause of ureteral injury?

A

Iatrogenic trauma during abdominal surgery; injury due to blunt trauma is relatively rare

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7
Q

Most common site of ureteral injury 2/2 blunt trauma?

A

UPJ

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8
Q

Presentation of ureteral injury?

A

Hematuria

Fever, flank pain, renal mass (from hydronephrosis) several hours after injury

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9
Q

Presentation of urethral injury?

A

Blood at the urethral meatus
High-riding prostate
Inability to pass Foley into the bladder

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10
Q

List 6 indications for cystoscopy.

A
  1. Gross hematuria with no evidence of glomerular disease or infection
  2. Microscopic hematuria with no evidence of glomerular disease or infection but increased risk for malignancy
  3. Recurrent UTIs
  4. Obstructive symptoms with suspicion for stricture or stone
  5. Irritative symptoms without UTI
  6. Abnormal bladder imaging or urine cytology
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11
Q

DDx - microscopic hematuria?

A
  • Renal (renal cell cancer, IgA nephropathy, etc.)
  • Ureteral (stricture, stone, etc.)
  • Bladder (cancer, cystitis, etc.)
  • Prostate/urethral (BPH, prostate cancer, urethritis)
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12
Q

Risk factors for bladder cancer?

A 
Cigarette smoking
Certain occupational exposures (painters, metal workers, etc.)
Chronic cystitis
Iatrogenic causes (cyclophosphamide)
Pelvic radiation exposure
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13
Q

What is the most important risk factor for bladder cancer?

A

Cigarette smoking

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14
Q

Maximal urinary flow rate testing can diagnose BPH. Flow rates > ___ usually exclude significant bladder outlet obstruction. This is considered an optional test for most patients.

A

15 mL/sec

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15
Q

What is a porcelain gallbladder and what is it associated with?

A

Calcium-laden gallbladder wall with bluish color and brittle consistency

Chronic cholecystitis

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16
Q

Pathogenesis of porcelain gallbladder?

A

Remains unclear, but it is thought that calcium salts are deposited intramurally due to the natural progression of chronic inflammation or irritation from gallstones

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17
Q

Appearance of porcelain gallbladder on XR and CT?

A

XR - rim-like calcification in the area of the gallbladder

CT - calcified rim in the gallbladder wall with a central bile-filled dark area

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18
Q

Porcelain gallbladder has been associated with increased risk for ___. Management?

A

Gallbladder adenocarcinoma; choelcystectomy, especially if symptomatic or incomplete mural calcification

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19
Q

Ruptured ___ cyst can cause anaphylaxis with eventual shock. Presentation and appearance on CT?

A

Echinococcal cyst; travel outside the US. Cystic liver lesions (sometimes with calcification but without gallbladder involvement)

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20
Q

Causes of liver abscess?

A

Portal vein bacteremia
Systemic bacteremia
Ascending cholangitis
Trauma

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21
Q

Who should have an immediate appendectomy without imaging and why?

A

Patients with a classic presentation (migratory pain, N/V, fever, leukocytosis, McBurney point tenderness, Rovsing sign); prevent appendiceal rupture

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22
Q

When are imaging studies useful in patients with suspected appendicitis?

A

Non-classic symptoms, other possible causes of RLQ (diverticulitis, ileitis, IBD, etc.), equivocal findings on initial assessment, delayed presentation

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23
Q

Management of patients with appendicitis who have had symptoms for >5 days?

A

Usually have a phlegmon with an abscess that has walled off; manage conservatively with IV ABX, bowel rest, delayed appendectomy weeks later

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24
Q

How can BPH increase risk for recurrent UTIs?

A

Gradually compress the prostatic urethra, leading to incomplete bladder emptying

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25
Q

Staghorn calculi are caused by what types of bacteria?

A

Urease-producing organisms (Proteus, Klebsiella, etc.)

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26
Q

What is suggested in a patient s/p abdominal surgery with new RUQ pain, fever, leukocytosis, and pulmonary manifestations (SOB, hiccups, R-sided effusion)?

A

Subphrenic abscess

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27
Q

Most common complication of appendectomy?

A

Infection

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28
Q

True or false - risk of intra-abdominal abscess is significantly greater with laparotomy than with laparoscopic appendectomy.

A

False - risk is significantly greater with lap appendectomy

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29
Q

Dx and Rx intra-abdominal abscess?

A

CT scan; drainage and IV ABX

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30
Q

Most cases of hospital-acquired pneumonia occur how many days post-operativelyl?

A

5 or less

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31
Q

Presentation and timing of post-operative atelectasis?

A

Common up to 5 days after abdominal procedures, often presents with hypoxemia and dyspnea

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32
Q

Symptoms of hypocalcemia? Cause of symptoms?

A 
Perioral tingling and numbness
Muscle cramps
Tetany
Carpopedal spasms
Seizures
Prolongation of QT interval

Caused by neuromuscular irritability

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33
Q

Causes of primary hypoparathyroidism?

A
  1. Post-surgical
  2. Autoimmune
  3. Cogenital absence of maldevelopment of the parathyroid glands (eg, DiGeorge syndrome)
  4. Defective calcium-sensing receptor on the parathyroid glands
  5. Non-autoimmune destruction of the parathyroid gland due to infiltrative diseases such as hemochromatosis, Wilson disease, and neck radiation
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34
Q

Most common cause of primary hypoparathyroidism?

A

Post-surgical (thyroidectomy, sub-total parathyroidectomy)

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35
Q

Most common non-surgical cause of primary hypoparathyroidism?

A

Autoimmune

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36
Q

Lab findings in hypoparathyroidism?

A

Hypocalcemia
Hyperphosphatemia
Normal renal function

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37
Q

Explain the PTH, vitamin D, and calcium axis.

A

PTH release -> increased bone resorption and calcium release + increase calcium resorption and phosphate excretion (kidneys) + increased production of 1,25-dihydroxyvitamin D (kidneys) -> increased GI calcium and phosphorus absorption -> increased circulating calcium -> negative feedback on PTH (also negative feedback from increased 1,25-)

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38
Q

What is syringomyelia?

A

Disorder caused by disruption of CSF drainage from the central canal, leading to formation of a fluid-filled cavity (syrinx) that compresses the surrounding tissue. Cavity can enlarge over time and destroy adjacent portions of the spinal cord.

Symptoms may present months to years after the initial insult

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39
Q

Causes of syringomyelia?

A

Most commonly seen with Arnold-Chiari type 1 malformations (extension of the cerebellar tonsils into the foramen magnum)

Sequela of meningitis
Inflammatory disorders
Tumors
Trauma

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40
Q

Presentation of syringomyelia?

A

Can occur at any level, most commonly involves cervical or thoracic spine -> upper extremity symptoms -> progressive loss of pain and temperature sensation in dermatomes corresponding to the level of involvement (cape-like)
Touch, vibration, proprioception preserved if syrinx is small enough. Expansion into the motor fibers may result in progressive weakness and flaccid paralysis within the affected area. Over time, central pain, incontinence, and lower extremity manifestations may develop.

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41
Q

Pathogenesis of syringomyelia?

A

Destruction of crossing fibers of the spinothalamic tract in the ventral white commissure

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42
Q

Dx and Rx syringomyelia?

A 
MRI (shows intramedullary cavity)
Surgical intervention (shunt placement)
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43
Q

Presentation - upper and lower motor neuron deficits with no loss of sensory function?

A

ALS

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44
Q

What is cervical spondylosis?

A

Chronic degeneration of the intervertebral discs and facet joints

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45
Q

Presentation of cervical spondylosis?

A

Usually occurs in older individuals, though it can affect younger patients with prior spine injury

Neck pain and stiffness
Cord compression may occasionally be seen but typically causes weakness below the affected spinal cord level, not regional loss of pain and temperature sensation

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46
Q

Presentation of herniated cervical disk?

A

Radiculopathy due to compression of the nerve root; unilateral pain and weakness in the distribution of the involved nerve
Dissociated sensory findings do NOT occur

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47
Q

MOA of succinylcholine?

A

Depolarizing neuromuscular blocker, binds to post-synaptic acetylcholine receptors to trigger influx of sodium ions and efflux of potassium ions through ligand-gated ion channels. Depolarization occurs and temporary paralysis ensues (delayed repolarization of the skeletal muscle membrane).

48
Q

Use of succinylcholine?

A

Often used during rapid-sequence intubation, as it has a rapid onset (45-60 seconds) and offset (6-10 minutes) of action

49
Q

What patients can have life-threatening cardiac arrhythmias due to severe hyperkalemia when managed with succinylcholine?

A

Patients who have experienced an extensive skeletal muscle crush injury -> increased risk of hyperkalemia due to rhabdomyolsis.

In addition, skeletal muscle injury, burn injury, disuse muscle atrophy, and denervation (stroke, Guillain-Barre, critical illness polyneuropathy) all can upregulate post-synapatic ACh receptors, which can result in masssive efflux of potassium follow succinylcholine administration -> hyperkalemia

50
Q

What should be used instead of succinylcholine when there is increased risk for life-threatening hyperkalemia?

A

Non-depolarizing neuromuscular blocking agents (vecuronium, rocuronium, etc.) - don’t affect post-synaptic ligand-gated ion channels

51
Q

Side effects of halothane?

A

Acute liver failure due to production of hepatotoxic intermediary compounds (now rarely used, adult women at greatest risk)

52
Q

Side effect of etomidate?

A

Adrenal insufficiency 2/2 inhibition of 11-beta-hydroxylase (elderly and very sick patients are susceptible)

53
Q

Side effect of nitrous oxide?

A

Inactivates vitamin B12 -> inhibition of methionine synthase activity -> neurotoxicity in patients with pre-existing vitamin B12 deficiency

54
Q

Side effects of propofol?

A

Severe hypotension due to myocardial depression (avoid/use with extreme caution in patients with ventricular systolic dysfunction)

55
Q

What is the role of Vitamin K in hemostasis?

A

Cofactor in the enzymatic carboxylation of glutamic acid residues on prothrombin complex proteins

56
Q

Most common causes of vitamin K deficiency?

A 
Inadequate dietary intake (eg, no enteral nutrition post-op)
Intestinal malabsorption (eg, broad-spectrum ABX wiping out gut bacteria)
Hepatocellular disease causing loss of storage sites
57
Q

The liver can normally store a ___ supply of vitamin K, but an acutely ill person with underlying liver disease can become deficient in as little as ___ days.

A

30-day; 7-10

58
Q

Vitamin K deficiency decreases plasma levels of which proteins? What is the affect on coag labs?

A

All prothrombin complex proteins (factors 2, 7, 9, 10, protein C and S); initially increases PT, followed by prolonged PTT.

59
Q

Management of vitamin K deficiency?

A

Administration of vitamin K rapidly replenishes stores in 8-10 hours; FFP may be used to manage acute hemorrhage in the interim

60
Q

Presentation of DIC?

A

Causes depletion of clotting factors and secondary fibrinolysis -> bleeding, acute kidney and liver injury, hypotension, tachycardia

Thrombocytopenia, prolonged PT and PTT, decreased fibrinogen, schistocytes on peripheral smear

61
Q

Presentation of lupus anticoagulant?

A

Prolonged PTT

Increased risk of venous thrombosis

62
Q

Factor V Leiden causes a hypercoagulable state due to ___.

A

Activated protein C resistance

63
Q

Factor VIII deficiency is an X-linked inherited plasma coagulation disorder that primarily affects what lab?

A

Prolongs PTT

64
Q

Presentation of hypersplenism?

A

Patients with cirrhosis, portal HTN, splenomegaly

Thrombocytopenia; rarely develop clinical bleeding or prolonged PT/PTT

65
Q

Presentation of thrombotic thrombocytopenic purpura?

A

Rare form of consumptive thrombocytopenia caused by widespread platelet thrombi that form in the microcirculation

Presents with thrombocytopenia, microangiopathic hemolytic anemia, fever, neuro findings (AMS, etc.)

66
Q

Most frequently diagnosed inherited bleeding disorder in adults?

A

Von Willebrand disease

67
Q

Lab findings in von Willebrand disease?

A

Increased bleeding time and PTT

Normal PT

68
Q

Presentation of rotator cuff impingement or tendinopathy?

A

Pain with abduction and external rotation
Subacromial tenderness
Normal range of motion
Positive impingement tests (Neer, Hawkins, etc.)

NO weakness

69
Q

Presentation of rotator cuff tear?

A

Similar to rotator cuff tendinopathy
Pain at the lateral shoulder worse with raising arm overhead or with rotation/abduction
WEAKNESS with abduction and external rotation
Drop arm sign (inability to smoothly control shoulder adduction)
Age >40
Fall on an outstretched arm

70
Q

Dx rotator cuff tear?

A

MRI - can visualize the soft tissues around the humeral head and accurately diagnose a rotator cuff tear

71
Q

Rx rotator cuff tear?

A

Surgery, best results if performed within 6 weeks of injury

72
Q

Causes of acalculous cholecystitis?

A

Most often seen in severely ill patients in the ICU with multiorgan failure, severe trauma, surgery, burns, sepsis, or prolonged parenteral nutrition

73
Q

Likely pathogenesis of acalculous cholecystitis?

A

Cholestasis and gallbladder ischemia leading to secondary infection by enteric organisms and resultant edema and necrosis of the gallbladder

74
Q

Rx acalculous cholecystitis in critically ill patients?

A

ABX followed by perc cholecystotomy under radiologic guidance

Definitive therapy with improvement in medical condition - cholecystectomy with drainage of any associated abscesses

75
Q

Presentation and diagnosis of duodenal perforation?

A

Sudden-onset diffuse abdominal pain; rigid abdomen with later distention.

imaging - free air under the diaphragm

76
Q

Presentation of mesenteric ischemia?

A

Sudden periumbilical abdominal pain out of proportion to exam findings

77
Q

Risk factors for mesenteric ischemia?

A

Older age, AF, CHF, atherosclerotic vascular disease

78
Q

Dx mesenteric ischemia?

A

CT Abdomen with focal or segmental bowel wall thickening, small-bowel dilation, mesenteric stranding

79
Q

Presentaiton of SBO?

A

Abdominal distension, high-pitched hyperactive bowel sounds, dilated loops of bowel with air-fluid levels on imaging, and no or minimal air in the colon and rectum

80
Q

Compare the etiologies of SBO vs. ileus.

A

SBO - prior surgery (weeks to years)

Ileus - recent surgery (hours to days), metabolic (eg, hypokalemia), medication induced

81
Q

Compare the exam findings of SBO vs. ileus.

A

SBO - distention, increased bowel sounds

Ileus - possible distension, reduced/absent bowel sounds

82
Q

Compare the small and large bowel dilation seen in SBO vs. ileus.

A

Small bowel dilation present in both. Large bowel only present in ileus.

83
Q

Ddx - initial hematuria?

A

Urethritis

Trauma (eg, catheterization)

84
Q

Ddx - terminal hematuria?

A 
Urothelial cancer
Cystitis (infectious, post-radiation)
Urolithiasis
BPH
Prostate cancer
85
Q

DDx - hematuria throughout urinary stream?

A 
Renal mass (benign or malignant)
Glomerulonephritis
Urolithiasis
PCKD
Pyelonephritis
Urothelial cancer
Trauma
86
Q

What is the leading heritable cause of renal disease in adults?

A

PCKD

87
Q

Initial hematuria suggests ___ damage. Terminal hematuria indicates ___ damage. Total hematuria indicates ___ damage.

A

Urethral; bladder or prostatic; kidney or ureters

88
Q

Presentation of splenic abscess?

A

Classic triad - fever, leukocytosis, LUQ abdominal pain (splenic fluid collection)

Can also develop left-sided pleuritic chest pain, left pleural effusion, splenomegaly

89
Q

Risk factors for splenic abscess?

A

Infection (eg, infective endocarditis) with hematogenous spread, immunosuppression, IVDU, trauma, hemoglobinopathies

90
Q

Dx splenic abscess?

A

CT abdomen

91
Q

Pathogenesis of splenic abscess 2/2 infective endocarditis?

A

Hematogenous seeding or septic emboli to the spleen.

Common agents include Staph, Strep, Salmonella

92
Q

Rx spelnic abscess?

A

Splenectomy (all patients, as ABX alone have high mortality); perc drainage an option for poor surgical candidates

93
Q

Who has increased risk of endocarditis?

A

Patients with MV prolapse (5x increased risk), fever with systemic manifestations, splenic abscess

94
Q

If endocarditis is suspected, what should be done?

A

BCx

Echo

95
Q

Discuss the development of atelectasis 2/2 left mainstem bronchial mucus plugging.

A

Creates distal air trapping in the alveoli; eventually, the trapped air molecules diffuse into the bloodstream. because no additional air can enter, the alveoli collapse. To occupy the vacated space, mediastinal structures are pulled toward the atelectasis.

96
Q

Presentation of atelectasis?

A

Respiratory distress (dyspnea, tachypnea, tachycardia), hypoxemia, dullness to percussion + absence of breath sounds in the affected lung area on exam

97
Q

CXR findings of atelectasis?

A

Opacification of the affected lung area with mediastinal shifting toward the side of the opacification

Rib spacing becomes narrower

98
Q

What increases risk of mucus plugging? How can it be prevented? Treated?

A

Surgery under anesthesia; smoking

Chest physiotherapy to prevent/treat relatively minor atelectasis

Large-volume requires bronchoscopy to remove the plug

99
Q

Work-up of suspected aortic aneurysm rupture and subsequent treatment?

A

Stable -> CT scan

Unstable -> U/S (limited role)

Both go to the OR

100
Q

Causes of acute adrenal insufficiency (adrenal crisis)/

A

Adrenal hemorrhage or infarction

Acute illness/injury/surgery in patient with chronic adrenal insufficiency or long-term glucocorticoid use

101
Q

Presentation of acute adrenal insufficiency?

A

Hypotension/shock
N/V/abdominal pain
Weakness
Fever

102
Q

Rx of acute adrenal insufficiency?

A

Hydrocortisone or dexamethasone

High-flow IV fluids

Start empirically

103
Q

Lab findings seen in primary adrenal insufficiency?

A

Hyponatremia
Hyperkalemia

(Central adrenal insufficiency - normal potassium)

104
Q

Patients on long-term glucocorticoid therapy who have Cushingoid features are at very high risk of adrenal crisis. However, HPA suppression can be seen in as little as ___ weeks in patients taking ___ prednisone (dose). These patients may not respond appropriately to acute stressors and should be given higher doses of steroids during the acute condition. How should low-dose and intermediate doses be managed?

A

3; 20+ mg/day or equivalent; low-dose (<5 mg/day) have minimal risk and usually do not require stress dosing. Intermediate doses (5-20 mg/day) can cause suppression and require pre-op eval with an early-morning cortisol level to determine risk

105
Q

Risk factors for foot infections in patients with DM?

A

Poor glycemic control (impaired immunity)
Neuropathy (impaired recognition)
PAD (impaired healing)

106
Q

Presentation of foot infections in patients with DM?

A

Localized skin erythema, warmth, tenderness, edema

Deeper infections should be suspected in those with long-standing wounds (>1-2 weeks), systemic symptoms, large ulcer size (2+ cm), elevated ESR, presence or palpation of bone in the ulcer base

107
Q

Expected infectious species involved in patients with deeper infections 2/2 foot infection in DM?

A

Almost always polymicrobial with a mix of GP (S. aureus, S. pyogenes), GN (P. aeruginosa, etc.), and anaerobes

108
Q

True or false - superficial diabetic foot infections may be monomicrobial, but deeper infections are almost always polymicrobial.

A

True

109
Q

In adults, underlying osteomyelitis with an overlying wound is almost always the result of ___ spread.

A

Contiguous

110
Q

Hematogenous osteomyelitis accounts for ____% of osteomyelitis cases in adults and primarily affects what bones?

A

20; vertebrae, pelvis, hips

111
Q

___ (type of cancer) is common in people with a significant history of alcohol and tobacco use. The first manifestation may be a palpable cervical lymph node.

A

Squamous cell carcinoma of the mucosa of the head and neck

112
Q

Best first test to evaluate squamous cell carcinoma of the mucosa of the head and neck?

A

Panendoscopy = esophagoscopy, bronchoscopy, laryngoscopy to detect the primary tumor

113
Q

Next step after panendoscopy to find primary tumor?

A

Biopsy to establish a histologic diagnosis (management and prognosis)

114
Q

Classic clinical presentation of acute arterial occlusion of an extremity (aka acute limb ischemia)?

A 
Pain
Pallor
Poikilothermia (cool extremity)
Paresthesia
Pulselessness
Paralysis
115
Q

Management of suspected acute arterial occlusion with an immediately-threatened limb?

A

Anticoagulation (heparin) while further dx procedures are performed

116
Q

Use of ankle-brachial index (ratio of systolic pressure in ankle to arm)?

A

Screening and/or diagnostic tool in patients with suspected PAD

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