UWorld Flashcards
Most common site of bladder rupture
Overall = bladder dome is the weakest part, it’s also the only part that is intraperitoneal => rupture of the bladder dome can cause peritonitis (by leakage of urine into the peritoneum) and therefore shoulder pain (shared dermatome C3-C5 of the phrenic nerve)
Most common site of extraperitoneal bladder rupture = bladder neck
45 yo F s/p elective TAH develops N/V/abdominal pain
- Meds: metformin, insulin glargine, prednisone
- round plethoric face, buffalo hump, and central obesity
Cause of acute condition?
Acute adrenal insufficiency = adrenal crisis
Pt w/ Cushingoid features (hump, moon face) are especially at high risk
Primary cause = Addison’s
Secondary cause = chronic (even just 3 wks) of steroid use 2/2 HPA suppression
So chronic steroid use suppresses HPA axis so pt’s body cannot appropriately response to stress (ex: surgery)
29 yo F 3 days s/p full-thickness burn p/w severe pain and itching of the area
- circumferential eschar formation
- hand is tense and tender
(a) Dx
(b) Mechanism of symptoms
(a) Compartment syndrome
- rapidly increasing tense swelling, key is tissue tension
- circumferential eschar can lead to construction of venous/lymphatic drainage
(b) Venous compromise
Don’t confuse this w/ subcutaneous bacterial invasion- cellulitis would have skin worth and gas gangrene (crepitus)
Abdominal Xray findings of paralytic ileus
Uniformly distended, gas-filled both small and large bowel
Organisms responsible for prosthetic joint infections
Early vs. delayed onset infections
Early-onset infections (w/in 3 months of arthroplasty): think Staph aureus, GNR, anaerobes
Delayed-onset (over 3 mo): think coagulase-negative staph (staph epidermidis), propionibacterium, enterococci
Tx for both is implant removal/exchange
Etiology of mediastinal shift that is not pneumothorax
Diaphragmatic hernia- abdominal contents up into thorax causing compression of lungs and mediastinal shift
Clinical presentation of Fitz-Hugh-Curtis syndrome
Acute onset RUQ pain in F worse w/ inspiration, coughing, or laughing (b/c due to perihepatitis as a complication of PID)
-inflamed liver capsule rubbing against diaphragm
= rare complication of PID
Best imaging modality when suspecting perforated peptic ulcer
Upright CXR of chest and abdomen
-see penumoperitoneum (free intraperitoneal air under diaphragm)
Would only do upper endoscopy if acute upper GI hemorrhage, not needed for acute perforated PUD
22 yo M w/ sudden onset SOB x2hrs while watching tv
- 150 lbs, 6ft2
- sharp r. chest pain worse w/ deep inspiration and cough
- CXR: small right apical pneumothorax
(a) Dx
(b) Tx
(a) Dx = primary spontaneous pneumothorax
- rupture of subpleural bleb at rest
- risk factor = tall thin male, cig smoking
(b) Small pneumothorax in stable pt = supplemental O2 to enhance speed of resorption
- if it was large you’d decompress w/ large bore-needle
- if pt was unstable, place chest tube
53 yo M after MVA c/o b/l chest pain and left leg pain, left femur fracture, pH 7.56/pO2 81/pCO2 32
- CXR: alveolar opacities over b/l lung bases
- normal PCWP
Dx causing SOB
Pulmonary contusion complicates 30-75% of severe blunt chest trauma
- often has delayed onset
- hypoxemia causes hyperventilation => respiratory alkalosis and hypocarbia
Xray findings of pulmonary contusion
Patchy alveolar infiltrates
Ddx for fever on POD5
Acute post-op fever (1-7 days after surgery)
- nosocominal infection (pneumonia, catheter associated)
- atelectasis if low grade
- surgical site infection: most commonly group A strep or clostridium perfringens
- noninfections: MI/PE/DVT
Ddx of immediate post-op fever
Immediate post-op fever (first 2 hrs post-op)
- prior trauma/infection
- blood products
- malignant hyperthermia from anesthesia
Ddx for fever on POD14
Subacute (1-4 wks) post op fever ddx
- surgical site infection
- C. dif
- drug fever (diagnosis of exclusion, think if abx allopurinol or anticonvulsants started)
- PE/DVT
Main clinical feature of acute adrenal insufficiency
Severe and often refractory hypotension
- N/V, abdominal pain
- weakness
- fever
Abdominal pain following trauma w/ Xray showing air in both small and large bowel
Dx
Dx = paralytic (adynamic) ileus
2/2: local release of inflammatory mediators, opioid use, increased splanchnic nerve sympathetic tone following peritoneal irritation
Clinical exam finding indicating uncal herniation
Ipsilateral pupil dilation 2/2 oculomotor nerve compression
50 yo M w/ occasional left calf pain when walking
- occasionally legs cramp at rest
- palpable pulses throughout, NSR on EKG
Next step?
Thinking PAD (peripheral artery disease) => next step is ABI
NOT arterial duplex ultrasound- much less sepcific and sensitive for PAD
25 yo in MVA, unable to void despite urge
- blood at urethral meatus and scrotal hematoma
- high-riding prostate, distended bladder on exam
Dx
Dx = posterior urethral injury
-prostate high0riding b/c displaced by pelvic hematoma
Etiology of tic douloureux
Tic douloureux = trigeminal neuralgia
Etiology = external compression of the trigeminal nerve
Clinical presentation after injury to
(a) Radial nerve
(b) Ulnar nerve
(c) Median nerve
(a) Radial nerve injury => wrist drop due to limitation of wrist extension
(b) Ulnar nerve injury => claw hand
(c) Median nerve => loss of sensation to skin over lateral 3 1/2 fingers
Mechanism by which the following lower ICP
(a) Head elevation
(b) Sedation
(c) IV mannitol
(d) Hyperventilation
Interventions to lower ICP
(a) Elevate head of the bed to increase venous outflow from the brain
(b) Sedate the pt to decrease metabolic demand
(c) IV mannitol works as an osmotic diuretic to extract free water from brain tissue
(d) Hyperventilation increases pCO2 which causes cerebral vasoconstriction
65 yo M p/w suden onset severe r. leg pain
- h/o recent anterior wall MI, HTN, DM, HLD
- below the knee r. leg is cool to touch and pale
- DP pulse not palpable, popliteal full
- numbness over dorsum of r. leg and foot
Mechanism of symptoms
Symptoms most likely caused by arterial embolism to the popliteal artery
- you know it’s arterial b/c cool and pale (venous would be swollen and warm from pooled venous blood)
- it’s acute, so you’re thinking embolism over a more chronic process like thrombosis
- embolism from cardiac origin consistent w/ h/o acute MI
- nerve damage alone wouldn’t account for missing pulse or cold/pale
Normal value of mixed venous oxygen saturation
60-80%