Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 2 > Surgery 6 > Flashcards

Surgery 6 Flashcards

1
Q

Presentation - painful swelling of the parotid gland that is aggravated by chewing; high fever, tender/swollen/erythematous parotid gland, purulent saliva expressed from the duct; leukocytosis

A

Acute bacterial parotitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What can be done to prevent acute bacterial parotitis in the post-op setting?

A

Adequate fluid hydration and oral hygiene in the pre- and post-operative setting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most common infectious agent in acute bacterial parotitis?

A

S. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

___ has been shown to reduce post-operative pulmonary complications by 50%.

A

Incentive spirometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Perioperative use of ___ in patients with CAD decreases the likelihood of MI.

A

Beta-blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Perioperative ABX should routinely be given to patients undergoing ___ surgery.

A

Abdominal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

___ is one of many proven methods of preventing post-operative complications, particularly DVT.

A

Early ambulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Presentation - preceding violent muscle contractions; arm held in adduction and internal rotation, impaired external rotation, flattening of the anterior aspect of the shoulder, prominence of the coracoid process

A

Posterior shoudler dislocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

X-ray appearance of posterior shoulder dislocation?

A

Loss of the normal relation/overlap between the humeral head and glenoid; internal rotation of the humeral head (circular appearance -> light bulb sign), widened joint space (>6 mm) = rim sign, 2 parallel cortical bone lines on the medial aspect of the humeral head (trough line sign)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Management of posterior dislocation?

A

Closed reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Potential complications of posterior shoulder dislocation?

A

Fractures of the proximal humerus, labral injuries, tears to the rotator cuff system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Most common form of shoulder dislocation? Most common injury causing this?

A

Anterior dislocation; direct blow or fall on an outstreched arm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does an anterior dislocation present (appearance of arm)?

A

Slightly abducted and externally rotated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Todd paralysis?

A

Transient unilateral weakness following a tonic-clonic seizure, resolves spontaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is this maneuver and what is it looking for - the physician places the stethosocope over the upper abdomen and rocks the patient back and forth at the hips?

A

Abdominal succussion splash

Retained gastric material >3 hours after a meal will generate a splash sound, indicating the presence of a hollow viscus filled with fluid and gas

Modest sensitivity and specificity for diagnosing gastric outlet obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Initial managemnet of gastric outlet obstruction?

A

NG suctioning to decompress the stomach
IV hydration
Endoscopy for definitive diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Presentation - pain and weakness in the shoulder; with the arm abducted over the head, the patient may be unable to lower the arm smoothly (drop arm test)

A

Rotator cuff tear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Components of the rotator cuff?

A

Tendons of the supraspinatus, infraspinatus, teres minor, and subscapularis muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which part of the rotator cuff is most commonly injured and why?

A

Supraspinatus, due to degeneration of the tendon with age and repeated ischemia induced by impingement between the humerus and the acromion during abduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Dx and Rx rotator cuff tear?

A

MRI; surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Presentation - injury caused by forceful flexion of the arm; sudden pain with an audible pop and a visible bulge (Popeye sign)

A

Biceps tendon tear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Presentation - paralysis of the deltoid and teres minor muscles, sensory loss over the lateral upper arm; bony tenderness, swelling, ecchymosis, or crepitus over the site of injury

A

Fracture of the surgical neck of the humerus -> axillary nerve injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Although the deltoid is responsible for shoulder abduction between 15-90 degrees, deltoid weakness is best appreciated with what maneuver?

A

At extreme extension rather than abduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Presentation - weak serratus anterior with impairment at extreme abduction (>90 degrees) due to inability to rotate scapular upward, caused by penetrating trauma or procedures

A

Long thoracic nerve injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Presentation - weakness and atrophy of the hypothenar and interosseous muscles, claw hand deformity, caused by injury with sudden upward traction on the arm

A

Injury to the lower (inferior) trunk of the brachial plexus (orginates from C8 and T1 cervical roots); affects muscles supplied by the ulnar nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Distinguish between rotator cuff impingement or tendinopathy vs. rotator cuff tear.

A

PAIN with abduction and external rotation vs. WEAKNESS with abduction and external rotation

Impingement/tendinopathy -> normal ROM with positive impingement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Management of amputation injury?

A

Amputated parts should be wrapped in saline-moistened sterile gauze, sealed in a plastic bag, placed on ice, and brought to the ED with patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Who are the best candidates for amputation reimplantation?

A

Younger patients suffering sharp amputations with no crush injury or avulsion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Presentation - new-onset watery diarrhea, fever, leukocytosis, mild abdominal tenderness, recent ABX use

May present as fulminant colitis/toxic megacolon

A

C. difficile colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Risk factors for C. difficile colitis?

A

Recent ABX use (mostly commonly FQs, PCN, cephalosporins, clindamycin)
Hospitalization
PPI use
Advanced age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Dx C. difficile colitis?

A

Stool PCR for toxin (high sensitivity, specificity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Rx C. difficile colitis?

A

Oral metronidazole

Vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Initial management of patient with septic shock?

A
  • Secure an airway if necessary
  • Restore adequate tissue perfusion through IV 0.9% saline (crystalloid) -> IV boluses (500-1000 mL) to improve systolic BP >90 mmHg
  • Identify and Rx the underlying infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Why is crystalloid the fluid of choice to restore volume quickly vs. albumin?

A

It is just as effective as albumin in terms of survival, but less costly and easier to acquire

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When should vasopressors be started to improve perfusion in a patient with septic shock?

A

If a patient fails to respond to adequate IV fluid resuscitation or develops evidence of volume overload without improvement in blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

When is IV hydrocortisone used in septic shock?

A

In patients who do not respond to volume resuscitation and initiation of vasopressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Rx malignant hyperthermia?

A

Dantrolene (skeletal muscle relaxant)

Cooling measures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

X-ray of the ankle is required in what situations based on the Ottawa ankle rules?

A

Pain at the malleolar zone AND:

  • Tender at posterior margin/tip of medial malleolus or
  • Tender at posterior margin/tip of lateral malleolus or
  • Unable to bear weight 4 steps (2 on each foot)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

X-ray of the foot is required in what situations based on the Ottawa ankle rules?

A

Pain at the midfoot zone AND:

  • Tender at the navicular or
  • Tender at the base of the 5th metatarsal or
  • Unable to bear weight 4 steps (2 on each foot)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Presentation - injury caused by forceful inversion of the foot during running, walking on even surfaces, or a fall from a height; swelling of the lateral ankle, tenderness over the ligaments. Range from stable/weightbearing to ecchymosis, anterior or inversion laxity, and impaired weightbearing

A

Lateral ankle sprain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Most commonly injured ligament in a lateral ankle sprain

A

Anterior talofibular ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Management of lateral ankle sprain?

A

If tenderness only over the ligaments distal to the lateral malleoli + bear weight -> conservative management (compression bandage or brace, ice packs, crutches, etc.) without imaging

If Ottowa rules met -> X-ray to rule out a distal fibular fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Classic presentation - insidious onset of constant/gnawing epigastric pain, frequently worse at night, anorexia with weight loss, jaundice due to extrahepatic biliary obstruction

A

Pancreatic cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Risk factors for pancreatic adenocarcinoma

A

Smoking
Hereditary pancreatitis
Non-hereditary chronic pancreatitis
Obesity and lack of physical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Clinical presentation of pancreatic adenocarcinoma

A 
Systemic symptoms (>85%)
Abdominal pain/back pain (80%)
Jaundice (56%)
Recent-onset atypical diabetes mellitus
Unexplained migratory superficial thrombophelbitis (Trousseau sign)
Hepatomegaly and ascites with mets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Lab findings in pancreatic adenocarcinoma

A

Cholestasis (increased alk phos and Dbili)
Increased CA 19-9 (not a screening test)
Abdominal U/S (if jaundiced) or CT (if no jaundice)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is a hiatal hernia?

A

Common disorder that occurs when the contents of the abdominal cavity herniate through the diaphragm into the thoracic cavity at the esophageal hiatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Appearance of hiatal hernia on plain radiography?

A

Retrocardiac opacity (often with an air/fluid level) within the thoracic cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Management of asymptomatic sliding hiatal hernia?

A

Observation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Management of symptomatic sliding hiatal hernia (reflux symptoms vs refractory GERD symptoms)

A

Reflux - medical management (PPIs, etc.)

Refractory - consider anti-reflux surgery (Nissen fundoplication)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What does 24-hour esophageal pH monitoring evaluate?

A

GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What does esophageal manometry evaluate?

A

Suspected esophageal motility diorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the cause of acquired methemoglobinemia?

A

Oxidization of iron in hemoglobin to methemoglobin, which cannot bind oxygen; the remaining normal hemoglobin has an increased affinity for oxygen, resulting in less deelivery to tissues; most commonly due to topical anesthetic agents or dapsone (and nitrates in infants)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Presentation - hypoxia, characteristic pulse oximetry reading of ~85%, large oxygen saturation gap (false elevation on ABG)

A

Acquired methemoglobinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Timing of cyanosis, hypoxia, severe symptoms/death in methemoglobinemia?

A

Methemglobin ~10% of total Hgb -> cyanosis
~20% ->
hypoxia (headache, lethargy)
~50+% -> risk of severe symptoms and death

56
Q

Rx acquired methemeglobinemia?

A

D/C causitive agent

Administer methylene blue

57
Q

Presentation - chest/back and/or epigastri pain, systemic signs (eg, fever); crepitus, Hamman sign (crunching sound on asucultation), pleural effusion with atypical (green, etc.) fluid

A

Esophageal perforation

58
Q

3 main causes of esophageal perforation?

A

Instrumentation, trauma
Effort rupture (Boerhaave syndrome)
Esopahgitis (infectious/pills/caustic)

59
Q

Findings of esophageal perforation on CXR or CT?

A

Widened mediastinum, pneumomediastinum, PT, pleural effusion

CT - esophageal wall thickening, mediastinal fluid collection

60
Q

Dx esophageal perforation?

A

Esophagography or CT scan with water-soluble contrast (Barium contrast more sensitive but can incite granulomatous inflammatory response, only used when water-soluble contrast is inconclusive)

61
Q

Rx esophageal perforation?

A

Emergent surgical consultation + IV ABX and PPIs

Mainstay of treatment - surgical debridement and repair

Select healthy patients (limited leak, minimal symptoms, no signs of sepsis) -> medical management trial

62
Q

How can severe triscuspid regurgitation develop as an adverse effect of a permanent pacemaker?

A

The right ventricular lead of a transvenous implantable pacemaker or cardioverter-defibrillator passes through the SVC into the right atrium and then through the triscupid valve to terminate in the endocardium of the R ventricle; damage to the tricuspid valve leaflets or inadequate leaflet coaptation can occur, leading to severe TR in 10-20% of patients

63
Q

Presentation - right-sided heart failure (distended jugular veins, pulsatile/tender hepatomegaly, abdominal distention with ascites, lower extremity edema), right ventricular heave, holosystolic murmur heard best at the left sternal border, murmur increases with deep inspiration, leg raise

A

Chronic, severe tricuspid regurgitation

64
Q

Presentation - prominent pulmonary edema, holosystolic murmur heard best at the cardiac apex

A

Mitral chordal rupture

65
Q

Presentation - systolic ejection murmur heard best at the left upper sternal border, murmur intensifies with increases in R ventricular preload

A

Pulmonic valve stenosis (most commonly 2/2 congenital defect, often asymptomatic)

66
Q

Squamous cell carcinoma is most often associated with UV (sun) exposure - what is another, less common cause?

A

Chronically wounded, scarred, or inflamed skin (burns, osteomyelitis, radiotherapy scars, venous ulcers, etc.)

67
Q

What is the name for SqCC arising within a burn wound?

A

Marjolin ulcer

68
Q

Presentation - pearly telangiectatic papules with central ulceration

A

Basal cell carcinoma

69
Q

Presentation - scaly, pruritic patches or plaques

A

Cutaneous T-cell lymphoma (aka mycosis fungoides)

70
Q

Clinical signs of type 2 HIT?

A

Suspect with heparin exposure >5 days and any of the following:

  1. Platelet count reduction >50% from baseline
  2. Arterial or venous thrombosis
  3. Necrotic skin lesions at heparin injection sites
  4. Acute systemic (anaphylactoid) reactions after heparin
71
Q

Dx type HIT?

A

Serotonin release assay (gold standard)

72
Q

Manage type 2 HIT?

A

Start treatment prior to confirmatory tests
Stop ALL heparin products
Start a direct thrombin inhibitor (eg, argatroban) or fondaparinux (synthetic pentasaccharide)

73
Q

Pathogenesis of HIT?

A

Heparin induces a conformation change in a platelet surface protein (platelet factor 4), which exposures a neoantigen. HIT antobides form in response to the neoantigen and bind to the surface of platelets, causing platelet aggregation, thrombocytopenia (or drop in platelets 50%), and a prothrombotic state

74
Q

How might HIT present in patients receiving heparin subcutaneously?

A

Skin necrosis at the abdominal injection site

75
Q

What causes acquired protein C deficiency?

A

Warfarin

76
Q

Presentation - classic skin findings affecting the lower extremities, including livedo reticularis, gangrene, and cyanosis; following coronary angiography

A

Cholesterol embolization

77
Q

Most common cause of nosocomial bloodstream infections?

A

Central venous catheters

78
Q

Budding yeast that frequentyl colonizes the skin, mucous membranes, and GI tract?

A

Candida

79
Q

Dx candida bloodstream infections?

A

Blood cultures or biopsy; serum beta-D-glucan antigen -> rapid indicator of possible infection

80
Q

True or false - Candida in a blood culture can be a contaminant.

A

False - it should always prompt a search for a nidus of infection

81
Q

Presentation - diffuse or LUQ abdominal pain, peritonitis, referred left shoulder pain (Kehr sign), hemodynamic instability

A

Atraumatic splenic rupture

82
Q

Risk factors for atraumatic splenic rupture?

A

Hematologic malignancy (leukemia, lymphoma, etc.)
Infection (CMV, EBV, malaria, etc.)
Inflammatory disease (eg, SLE, pancreatitis)
Splenic congestion (eg, cirrhosis, pregnancy)
Medications (eg, anticoagulation, G-CSF)

83
Q

How is splenic rupture diagnosed?

A

Acute anemia

Intraperitoneal free fluid on imaging

84
Q

Rx splenic rupture?

A

If stable -> catheter-based angioembolization

If unstable -> emergency splenectomy

85
Q

Presentation - s/p vascular access during cardiac catheterization, mild localized pain and swelling, continuous bruit/palpable thrill, distal pulses may be diminished in the affected extremity

A

AV fistula

86
Q

What is the most common vascular access point in patients undergoing cardiac cath?

A

Femoral artery

87
Q

How does an AV fistula develop following cardiac cath?

A

Vein can be inadvertently punctured during needle insertion. Inadequate hemostasis may allow persistent bleeding from the arterial puncture site to track into the venous puncture site, creating an AVF

88
Q

Natural history of an untreated AVF?

A

Progressive enlargement, limb edema (2/2 venous hyeprtension), limb ischemia (2/2 redirection of arterial blood flow), high-output HF (2/2 blood returning to the R atrium without passing through peripheral resistance)

89
Q

Dx AVF?

A

Duplex U/S

90
Q

Management of AVF?

A

Small -> observation or U/S guided compression

Large -> surgical repair

91
Q

List the 3 local vascular complications of cardiac catheterization.

A
  1. Hematoma
  2. Pseudoaneurysm
  3. AV fistula
92
Q

Compare the presentations of the 3 local vascular complications of cardiac cath.

A
  1. Hematoma - +/- mass, no bruit
  2. Pseudoaneurysm - bulging, pulsatile mass, systolic bruit
  3. AV fistula - no mass, continuous bruit
93
Q

___ should be suspected in patients with prior blunt thoracoabdominal trauma and abnormal CXR findings (eg, bowel loops in the thorax, mediastinal shift).

A

Diaphragmatic rupture

94
Q

Cause of diaphragmatic rupture?

A

Blunt thoracoabdominal trauma -> sudden and unequal decrease in thoracoabdominal pressure -> tears or avulsion

95
Q

Why is the left diaphragm more prone to injury than the right?

A

2/2 congenital weakness in the diaphragm’s left posterolateral region and the liver’s protective effects on the right side

96
Q

Definitive diagnosis of diaphragm rupture?

A

CT chest and abdomen

97
Q

Presentation - valgus stress or severe twisting injury to the knee, local swelling, ecchymosis, and joint line tenderness at the medial knee, valgus laxity (may be masked by swelling/muscle spasm)

A

Medical collateral ligament tear

98
Q

Acute effusion/hemarthrosis is uncommon in the setting of MCL tear unless there is concurrent injury to the ___.

A

ACL

99
Q

Dx MCL tear?

A

MRI (most sensitive), but generally reserved for patients being considered for surgical intervention

100
Q

Manage uncomplicated MCL tear?

A

Non-operative management - rest, ice, compression, elevation (RICE measures), analgesics with progressive return to activity as tolerated

101
Q

Presentation - anterior laxity, acute/dramatic hemarthrosis with an effusion on exam

A

ACL injury

102
Q

How can an MCL injury be differentiated from a medical meniscal injury?

A

A meniscus injury will also have small joint effusion and crepitus, locking, or catching with ROM; often occur when patients pivot on a flexed knee while the foot is planted

103
Q

Presentation - anterior knee pain and tenderness, normal ligament stress testing

A

Patellar tendonitis

104
Q

Distinguish between primary and secondary polycythemia.

A

Primary polycythemia - decreased EPO

Secondary polycythemia - normal or increased EPO

105
Q

DDx - primary polycythemia

A 
Polycythemia vera (JAK2 mutation)
EPO receptor mutations
106
Q

DDx - secondary polycythemia

A 
Hypoxemia (cardiopulmonary disease, OSA, high altitude)
EPO-producing tumors (renal, hepatic)
Congenital (high-affinity Hgb)
S/p renal transplantation
Andreogen supplementation
107
Q

Define polycythemia

A

Hct level >49% in men or >48% in women

108
Q

What is the main determinant of blood viscosity?

A

Hematocrit

109
Q

Pathogenesis of primary polycythemia.

A

Malignant transofrmation of erythrocyte progenitor cells, leading to unregulated erythrocyte production; elevated RBC mass exerts a negative feedback effect on EPO-producing cells in the renal cortex, leading to low or absent EPO

110
Q

What is Factor V Leiden?

A

Autosomal dominant disease associated with VTE, MI, and stroke; generally suspected with family history of VTE or patient with VTE <50 y/o

111
Q

Why are patients with severe burns susceptible to sepsis?

A

Severe burns disrupt the skin barrier and create an avascular, immunologically poor, protein-rich substrate for the growth and proliferation of bacteria and fungus.

112
Q

Discuss the timing of different types of sepsis in a patient with severe burns.

A

Immediately after a burn, GP organisms (S. aureus, etc.) from hair follicles and sweat glands dominate

> 5 days, most infections are due to GN organisms (P. aeruginosa, etc.) or fungi (eg, Candida)

113
Q

Risk factors for wound infections in patients with burns?

A

Large surface area (>20%) burns

114
Q

Earliest sign of wound infections in burns?

A

Change in appearance of the wound or loss of a viable skin graft

115
Q

Findings seen in burn wound sepsis?

A 
Temperature <36.5 C or >39 C
Progressive tachycardia (>90/min)
Progressive tachypnea (>30/min)
Refractory hypotension (systolic BP <90 mmHg)

Also oliguria, unexplained hyperglycemia, thrombocytopenia, mental status changes

116
Q

Dx burn wound sepsis?

A

Quantitative wound culture (>10E5 bacteria/g of tissue)

Biopsy for histopathology (tissue invasion depth)

117
Q

Rx burn wound sepsis?

A

Empiric, broad-spectrum IV ABX with the addition of potential coverage for MRSA (vancomycin, etc.) or multidrug-resistant P. aeruginosa (eg, an AG)

Local wound care
Debridement

118
Q

Displaced supracondylar fractures of the humerus are at risk of injury to what structures and why?

A

Brachial artery and median nerve, because these structures pass anterior to the humerus and can become entrapped by the anteromedially displaced proximal humerus fragment

119
Q

Most common elbow fractures in children?

A

Supracondylar fractures of the humerus

120
Q

Mechanism of injury leading to a supracondylar fracture of the humerus?

A

Fall on an outstretched hand with a hyperextended elbow

121
Q

What can be injured during proximal humerus fractures?

A

Axillary artery and nerve

122
Q

In a patient on warfarin who needs emergent surgery, what should be done prior to surgery?

A

Reverse anticoagulation with pre-operative infusion of FFP to restore vitamin K-dependent clotting factors

123
Q

___ is given pre-operatively to patients with mild hemophilia A in order to prevent excessive bleeding. How does it work?

A

Desmopressin (indirectly increases factor VIII levels by causing vWF release from endothelial cells

124
Q

What is an effective measure for reducing the risk of CAUTI in patients with neurogenic bladder?

A

Clean intermittent catheterization (periodic insertion and removal of a clean urinary catheter)

125
Q

What are the 2 major causes of CAUTI?

A

Extraluminal ascent of microorganisms due to the ability of some pathogens to form biofilm along the catheter wall, allowing them to reach the bladder within 24 hours of catheter insertion

Intraluminal infection (less common) 2/2 impaired urinary catheter drainage or contaimnation of a urinary collection bag

126
Q

What are the next steps in management of blunt abdominal trauma in hemodynamically unstable patients based on FAST exam results?

A
  1. Positive -> laparotomy
  2. Inconclusive -> DPL
    - If negative -> #3
    - If positive -> #1
  3. Negative -> assess for signs of extra-abdominal hemorrhage (eg, pelvic/long-bone fracture)
    - If yes -> stabilize (angiography, splint, etc.)
    - If no -> stabilize, then CT of abdomen
127
Q

2 most commonly injured organs following blunt abdominal trauma?

A

Liver

Spleen

128
Q

Presentation - early satiety, nausea, non-bilious vomiting, weight loss

A

Gastric outlet obstruction

129
Q

In a patient with a history of acid ingestion presenting with gastric outlet obstruction, what is the most likely cause?

A

Pyloric stricture

130
Q

Common causes of gastric outlet obstruction?

A 
Gastric malignancy
PUD
Crohn disease
Strictures 2/2 ingestion of caustic agents
Gastric bezoars
131
Q

2 broad categories of malignant testicular neoplasms?

A
  1. Germ cell (95%)

2. Stromal (5%)

132
Q

2 types of germ cell testicular neoplasm? 2 types of stromal testicular neoplasm?

A

Germ cell: seminoma, non-seminoma

Stromal - Leydig, Sertoli

133
Q

Distinguish between the 4 types of malignant testicular neoplasms previously discussed (based on presentation and labs)

A
  1. Seminoma - beta-hCG, AFP usually negative; retain features of spermatogenesis
  2. Non-seminoma - beta-hCG, AFP usually positive; 1+ partially differentiated cells
  3. Leydig - often produces excessive estrogen (gynecomastia, loss of libido, ED, etc.) or testosterone (acne, hirsutism, etc.) -> FSH and LH suppression; can cause precocious puberty; do not produce serum tumor markers.
  4. Sertoli - occasionally associated with excessive estrogen secretion (eg, gynecomastia); rare
134
Q

List the 4 types of non-seminoma testicular neoplasm.

A

Yolk sac
Embryonal carcinoma
Teratoma
Choriocarcinoma

135
Q

What type of cell is the primary source of testicular tesosterone?

A

Leydig cells (but are also capable of generating estrogen)

136
Q

Which testicular tumor typically produces beta-hCG?

A

Choriocarcinoma

137
Q

Which testicular tumor typically produces AFP?

A

Yolk sac tumors

Step 2 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions