inflammation, wound healing, trauma/ICU/Burn Flashcards

1
Q

phases of inflammation

A

injury-> exposed collagen-> plt activating factor release and tissue factor release from endothelium-> platelets bind collagen-> release growth factors (ie-ptl-derived GF PDGR)-> PMN and macrophage recruitment

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2
Q

role of macrophages in wound healing- what do they release

A

dominant role, release PDGF (plt derived GF) and cytokines (IL-1 and TNF-alpha)

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3
Q

Growth and activating factors in inflammation: role of the following

1) PDGF (platelet derived growth factor)
2) EGF (epidermal growth factor)
3) FGF (fibroblastic growth factor)
4) PAF (platelet-activating factor)

A

1) chemotactic and activates inflammatory cells (PMNs and macrophages) and activates fibroblasts-> ECM proteins and collagen. Imp for angiogenesis and epithelialization. Chemotactic for smooth muscle cells. accelerates wound healing
2, 3) Chemotactic, activates fibroblasts, angiogenesis, epithelialization
4) generated by phospholipase in endothelium (a phospholipid) which is chemotactic for inflam cells and inc adhesion mlqs

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4
Q

1) what are the chemotactic factors for inflammatory cells
2) for fibroblasts
3) angiogenesis factors
4) epithelialization factors

A

1) PDGF, IL-8, LTB-4, C5a and C3a, PAF
2) PDGF, EGF, FGF
3) PDGF, EGF, FGF, IL-8 and hypoxia
4) PDGF, EGF, FGF

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5
Q

1) How long do PMNs last in tissues and in blood
2) how long do platelets last
3) lymphocyte role in inflammation

A

1) 1-2 days in tissues, 7 days in blood
2) 7-10 days
3) involved in chronic inflammation (T cells) and Ab production (B cells)

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6
Q

Type 1 hypersensitivity rx:

1) role of eosinophils
2) what type of infections have increased eosinophils
3) role of basophils, where aren’t they found
4) Mast cells role
5) role of histamine
6) role of bradykinin
7) what inactivates bradykinin and where is it found

A

1) release major basic protien once bound to allergin-> stimulates basophils and mast cells to release histamine
2) parasitic
3) main source of histamine in blood (not in tissue)
4) main source of histamine in tissues, primary cell in type 1 hypersensitivity
5) vasodilation, tissue edema, postcapillary leakage; primary effector type in type I hypersensitivity rxs (allergic rxs)
6) peripheral vasodilation, increased permeability, pain, pulm vasoconstriction
7) Angiotensin-converting enzyme located in lung

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7
Q

Nitric oxide

1) what is its precursor
2) what does it activate and end effect
3) another name for it
4) what has the opposite effect of NO

A

1) Arginine
2) guanulate cyclase-> inc cGMP-> vascular smooth muscle dilation
3) endothelium-derived relaxing factor
4) Endothelin-> vascular smooth muscle constriction

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8
Q

cytokines

1) main initial cytokine resonse to injury and infection is release of

A

1) TNF-alpha and IL-1

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9
Q

cytokines

1) largest producer of TNF
2) role of TNF-alpha
3) what can high concentrations of TNF-a cause
4) largest producer of IL-1
5) effects of IL-1 and what does it synergize with
6) which cytokine causes cachexia in CA pts
7) which cytokine is responsible for fever and how?
8) how do NSAIDS reduce fever
9) role of IL-6

A

1) Macrophages
2) increases adhesion mlqs, procoagulant, activates neutrophils and macs-> more cytokine production and cell recruitment
3) circulatory collapse and multisystem organ failure
4) macs
5) same as TNF-alpha, synergizes with TNF-alpha
6) TNF-alpha
7) IL-1 (how alveolar macs cause fever with atelectasis), PGE2 mediated in hypothalamus
8) reduce PGE2 synthesis
9) increases hepatic acute phase proteins (CRP, amyloid A -> activate complement), decreases albumin, pre-albumin and transferrin

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10
Q

Interferons

1) what are they released by
2) what stimulates release
3) effect of release

A

1) lymphocytes
2) viral infection or other stimulants
3) activate macs, NK cells and cytotoxic T cells-> inhibit viral replication

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11
Q

Cell adhesion mlqs- where are they located, what they bind and type of adhesion

1) Selectins
2) Beta-2 integrins (CD11/18 molecules)
3) ICAM, VCAM, PECAM, ELAM

A

1) L-selectins on leukocytes bind E- (endothelial) and P-(platelet) selectins-> rolling adhesion
2) on leukocytes, bind ICAM etc-> anchoring adhesion
3) on endothelial cells, bind beta-2 integrin mlqs located on leukocytes and platelets. Also involved in transendothelial migration

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12
Q

Complement- what activates the following pathways and what factors are only in each one

1) classic pathway
2) alternative pathway
3) what complement factor is common to both pathways
4) what electrolyte is required for both pathways

A

1) (IgG or IgM) Ag-Ab complex activates. Factors C1, C2, C4
2) endotoxin, bacteria, other stimuli activate. Factors B, D and P (properdin)
3) C3
4) Mg

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13
Q

Complement

1) factors that are anaphylatoxins and actions
2) membrane attack complex factors and actions
3) opsonization factors and action
4) factors involved in chemotaxis for inflammatory cells

A

1) C3a, C4a, C5a. increase vascular permeability, bronchoconstriction and activate mast cells and basophils
2) C5b-9b-> cell lysis (usually bacteria) by creating hole in the membrane
3) C3b and C4b- targets Ag for immune response
4) C3a and C5a

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14
Q

Prostaglandins

1) precursor
2) LTC4, LTD4, and LTE4 actions
3) LTB4 actions

A

1) arachidonic precursors
2) slow-reacting substances of anaphylaxis, bronchoconstriction, vasoconstriction followed by increased permeability
3) chemotactic for inflammatory cells

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15
Q

Catecholamines

1) when after injury do they peak
2) where is norepinephrine released?
2) where is epinephrine released?

A

1) 24-48hours
2) sympathetic postganglionic neurons and adrenal medulla
3) adrenal medulla (neural response to injury)

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16
Q

T/F thyroid hormone plays a major role in injury/inflammation

A

false

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17
Q

neuroendocrine response to injury

A

afferent nerves from site of injury stimulate CRF, ACTH, ADH, growth hormone, epi and norepi release

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18
Q

CXC chemokines

1) what are they
2) what is their role
3) what does CXC stand for

A

1) IL-8 and platelet factor 4
2) chemotaxis, angiogenesis, wound healing
3) C=cysteine, X= another amino acid

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19
Q

1) what oxidants are generated in inflammation

2) what are cellular defenses against oxidative species

A

1) superoxide anion radical (NADPH oxidase), hydrogen peroxide (xanthine oxidase)
2)superoxide anion radical- defense is superoxide dismutase
hydrogen peroxide- defence is glutathione peroxidase, catalase

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20
Q

primary mediator of reperfusion injury

A

PMNs

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21
Q

Chronic granulomatous disease:

1) enzyme defect and result

A

NADPH-oxidase system enzyme defect in PMNs-> decreased superoxide radical formation-> increased infection from bacteria and fungi

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22
Q

stages of wound healing- cells involved, what happens during each and time frame

1) Inflammation
2) proliferation
3) remodeling

A

1) days 1-10. PMNs, macs. Epithelialization (1-2mm/day)
2) 5days-3wks. fibroblasts. collagen deposition, neovascularization, granulation tissue formation; type III collagen replaced with type 1
3) 3wk to 1 year. decreased vascularity. net amount of collagen unchanged despite sig production and degradation

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23
Q

rate of

1) epithelialization
2) peripheral nerve regeneration

A

1) 1-2 mm/day

2) 1mm/day

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24
Q

order of cell arrival in wound: PMNs, lymphoctes, macs, fibroblasts, platelets

A

1) platelets
2) PMNs
3) Macrophages
4) lymphocytes
5) fibroblasts

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25
Q

role of the following in wound healing

1) macrophages
2) fibronectin
2) fibroblasts

A

1) release growth factors, cytokines, etc
2) chemotactic for macs; anchors fibroblasts
3) replace fibronectin-fibrin with collagen

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26
Q

predominant cell type by day:

1) day 0-2
2) days 3-4
3) days 5+

A

1) PMNs
2) macrophages
3) fibroblasts

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27
Q

1) composition of the platelet plug
2) composition of provisional matrix
3) what wounds show accelerated wound healing

A

1) platelets and fibrin
2) platelets, fibrin and fibronectin
3) reopened wounds bc healing cells already present

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28
Q

Open wounds

1) most imp factor in healing open wounds
2) where does epithelium migrate from

A

1) epithelial integrity
2) hair follicles (#1 site), wound edges and sweat glands
- dependent on granulation tissue in wound
- unepithelialized wounds leak serum and protein and promote bacteria

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29
Q

closed wounds

1)most imp factor in healing

A

tensile strength- depends on collagen eposition and cross-linking of collagen

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30
Q

1) which layer of bowel provides the strength

2) what is weakest time point for small bowel anastamosis

A

1) submucosa

2) 3-5days

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31
Q

myofibroblasts- what are they, how do they communicate and what part of wound healing are they involved in

A

smooth muscle cell fibroblast. communicate by gap junction. Involved in wound contraction and healing by secondary intention.

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32
Q

t/F: perineum has better wound contraction than leg

A

true

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33
Q

which type of collagen is:

1) MC type, found in skin, bone and tendons. Primary collagen in healed wound
2) widepread, particularly found in cornea
3) increased in healing wound, also in blood vessels and skin
4) basement membranes
5) cartilage

A

1) type I
2) type V
3) type III
4) type IV
4) type II

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34
Q

1) what aa improves wound tensile strength
2) which of the following are not required for hydroxylation and subsequent cross-linking of proline residues: Alpha-ketoglutarate, Magnesium, Vitamin C, Oxygen and Iron

A

1) proline cross-linking. collagen has proline every 3rd aa.

2) Magnesium

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35
Q

cause of scurvy

A

Vit C deficiency

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36
Q

1) max tensile strength of healed wound compared to pre-wound skin
2) what is predominant collagen over days 1-2
3) collagen over days 3-4
4) at what point has all of the type of collagen in #2 been replaced by the collagen in #3
5) when does wound reach max tensile strength
6) what inhibits collagen cross-linking

A

1) 80%
2) III
3) I
4) 3 weeks
5) 8 weeks
6) d-Penicillamine

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37
Q

optimal wound healing

1) is dry or moist environment better
2) how to inc O2 delivery
3) effect of edema
4) which vitamin counteracts the effects of steroids on wound healing
5) what amount of bacteria impedes wound healing and why
6) what drugs impair wound healing in 1st 14d after injury

A

1) moist
2) optimize fluids, no smoking, pain control, supp O2, arterial revascularization
3) avoid it by leg elevation
4) vit A
5) >10^5 2/2 dec O2 content, collagen lysis, prolonged inflammation
6) cytotoxic drugs- 5FU, methotrexate, cyclosporin, FK-506

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38
Q

1) how does DM contribute to poor wound healing
2) what albumin level sig risk for poor wound healing
3) mechanism via which steroids inhibit wound healing

A

1) impedes early-phase inflammation response (hyperglycemia causes poor leukocyte chemotaxis)
2) dec tensile strength

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39
Q

Diseases associated with abnormal wound healing- name the defect

1) Osteogenesis Imperfecta
2) Ehlers-Danlos syndrome
3) Marfan’s syndrome
4) Epidermolysis bullosa and rx
5) Scurvy
6) what extraintestinal manifestation of IBD is associated with abnl wound healing

A

1) Type I collagen defect
2) 10 types identifies, all collagen
3) fibrillin defect (connective tissue protein)
4) excessive fibroblasts. rx- phenytoin
5) vit C def
6) Pyoderma gangrenosum

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40
Q

Diabetic foot ulcers

1) where they most commonly occur
2) 2/2 what?
3) cause of 90% of leg ulcers and rx

A

1) Charcot’s joint (2nd MTP joint) MC, also on toes
2) peripheral neuropathy (can’t feel-> pressure from walking-> ischemia)
3) venous insufficiency. rx- Unna boot (elastic wrap)

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41
Q

1) what are scars made of
2) when to do scar revisions
3) what pts heal with little to no scarring

A

1) proteoglycans, hyaluronic acid and water
2) wait 1 year to allow for maturation, may improve with age
3) infants

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42
Q

1) how does cartilage get nutrients and oxygen
2) does denervation effect wound healing
3) does chemo affect wound healing

A

1) diffusion. Doesn’t have blood vessels
2) no
3) no effect on healing after 14 days

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43
Q

Keloids

1) inheritance pattern
2) difference bw them and hypertrophic scars
3) rx
4) rx hypertrophic scars
5) when do hypertrophic scars occur

A

1) autosomal dominant, more common in dark skinned ppl
2) in keloids collagen goes beyond original scar where as hypertrophic scar collagen is confined to original scar
3) intra-lesion steroid injection, silicone, pressure garments, XRT
4) steroid injection, silicone, pressure garments
5) burns or wounds that take a long time to heal

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44
Q

Platelet granules:

1) what are the alpha granules and what is their role
2) dense granules
3) platelet aggregation factors

A

1) platelet factor 4- aggregation
beta thrombomodulin- binds thrombin
platelet derived growth factor- chemoattractant
Transforming growth factor beta (TGF-beta)- modulates above responses
2) adenosine, serotonin and Ca
3) TXA2, thrombin, platelet factor 4

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45
Q

Trauma deaths by time after injury

1) when does 1st peak occur and associated injuries
2) when does 2nd peak occur and associated injuries
3) when does 3rd peak occur and associated injuries

A

1) 0-30min- lac of heart, aorta, brain, brainstem, spinal cord. no hope to save
2) 30min-4hr-head injury (#1), hemorrhage (#2)- golden hour. pts can be saved with rapid assessment
3) days to weeks-multi system organ failure and sepsis

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46
Q

1) what % of trauma is blunt injury and what is most commonly injured organ
2) most commonly injured organ in penetrating injury
3) biggest predictors of survival after fall
4) what is the median lethal dose for fall (LD50)

A

1) 80%. Liver (although some texts say spleen)
2) small bowel (some texts say liver
3) age and body orientation
4) 4 stories

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47
Q

kinetic energy calculation

A

1/2 MV^2; M=mass, V=velocity

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48
Q

1) when will you see a change in BP with hemorrhage?

2) resuscitation- when to switch to blood

A

1) >30% blood loss

2) 2L LR then switch to blood

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49
Q

MC cause of

1) death after reaching ER alive
2) death long term
3) upper airway obstruction

A

1) head injury
2) infection
3) tongue

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50
Q

1) injuries from seat belts
2) best site for cutdown for venous access
3) positive DPL- what makes it +
4) what does DPL miss
5) where to do DPL if pelvic fracture
6) when might you get a false negative FAST

A

1) small bowel perf, lumbar spine fx, sternal fx
2) saphenous vein at ankle
3) >10cc blood, >100,000 RBCs/cc, food particles, bile, bacteria, >500WBC/cc
4) retroperitoneal bleeds, contained hematomas
5) supraumbilical
6) free fluid

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51
Q

1) where might pts with hypoTN and neg FAST be bleeding
2) when do you need a CT scan following blunt trauma
3) what might a CT scan miss in trauma
4) when to go to OR for laparotomy (which doesn’t require it: peritonitis, evisceration, positive DPL, uncontrolled visceral hemorrhage, free air, diaphragm injury, indeterminant FAST, intraperitoneal bladder injury, contrast extravasation from hollow viscus, specific renal/pancreas/biliary tract injuries

A

1) pelvic fx, chest, extremity
2) abdominal pain, need for gen anesthesia, closed head injury, intoxicants on board, paraplegia, distracting injury, hematuria, negative DPL
3) hollow viscus or diaphragm injury
4) negative FAST

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52
Q

1) abdominal injuries- when do you need to go to the OR
2) first step after pt with penetrating anterior abd trauma, no obv peritonitis/eviscer and local wound exploration shows fascial violation or equivocal

A

1) any penetrating abd injury (GSW, evisceration), local wound exploration with fascial violation or equivocal. If no fascial violation can observe
2) diagnostic laparoscopy. If peritoneal violation-> explore. if no peritoneal violation-> d/c after recovery

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53
Q

Abdominal compartment syndrome

1) when do you see it
2) bladder pressure
3) cause of decreased cardiac output
4) result of low Cardiac output
5) effect on ventilation/why?
6) rx

A

1) after massive fluid resuscitation, trauma or abdominal surgery
2) >25-30
3) IVC compression
4) visceral and renal malperfusion-> dec UOP
5) upward displacement of diaphragm affects ventilaton
6) decompressive laparotomy

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54
Q

1) when to use Pneumatic antishock garment
2) when to do ER thoracotomy after
a-blunt trauma
b-penetrating tauma
3) how to perform thoracotomy
4) when should pt be transfered to OR after ED thoracotomy

A

1) pts with SBP70mmHg, if not situation is futile

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55
Q

1) when do catecholamines peak after injury
2) change in ADH, ACTH and glucagon after trauma
3) type specific blood- why do ppl get reactions to it
4) What should you do for all GCS </= 8

A

1) 24-48 hours
2) fight or flight response-> increase ADH, etc
3) blood is nonscreened, non cross-matched so can get effects from abs to HLA minor Ag in the donated blood
4) Head CT
5) Intubate
6) ICP monitor

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56
Q

Epidural hematoma

1) artery injured MC
2) shape on head CT
3) clinical picture
4) when to operate

A

1) middle meningeal artery
2) lenticular deformity
3) LOC-> lucid interval-> sudden deterioration (vomiting, LOC, restlessness)
4) significant neurologic degeneration or significant mass effect (shift >5 mm)

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57
Q

subderal hematoma

1) vessel injured
2) shape on CT
3) when to go to OR
4) who gets chronic subdural hematomas

A

1) tearing of venous plexus (bridging veins bw dura and arachnoid)
2) crescent-shaped
3) sig neurologic degeneration or mass effect (>1cm shift)

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58
Q

intracerebral hematoma-

1) where does it usually occur
2) when to operate
3) type of injury with coup and countrecoup lesions

A

1) frontal or temporal
2) significant mass effect
3) cerebral contusion

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59
Q

1) treatment for traumatic intraventricular hemorrhage

2) how to dxs diffuse axonal injury, treatment and prognosis

A

1) ventriculostomy if causing hydrocephalus

2) MRI better than CT. Tx- supportive, craniectomy if elevated ICP, very poor prognosis

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60
Q

How to calculate Cerbral Perfusion Pressure (CPP)

A

CPP=MAP- ICP (intracranial pressure)

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61
Q

When to use an ICP monitor

A

GCS<=8, suspected inc ICP (dec ventricular size, loss of sulci, loss of cisterns) or pt with moderate to severe head injury and inability to follow clinical exam (ie- intubated pt)

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62
Q

1) Normal ICP
2) When to treat ICP
3) where to keep CPP

A

1) 10
2) >20
3) >60

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63
Q
How to increases Cerbral perfusion pressure? which of the following won't:
sedation and paralysis
lower head of bed
relative hyperventilation (CO2 30-35)
Mannitol
Barbituate coma
ventriculostomy with CSF drainage
craniotomy decompression
A

must RAISE the head of the bed to increase CPP

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64
Q

1) which side is the temporal pressure increased in for a dilated pupil
2) when does peak ICP occur
3) what can be given prophylactically to prevent seizures with moderate to severe head injury
4) how to dose mannitol
5) what level to keep Na and serum Osm in head injury pts

A

1) same side (CNIII, oculomotor compression)
2) 48-72hr after injury
3) keppra and fosphenytoin
4) load 1g/kg, give 0.25mg/kg q4hr after that (draws fluid from brain)
5) Na 140-150. Serum Osm 295-310 (may need to use hypertonic saline)

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65
Q

1) What do Racoon eyes signal?
2) Battle’s sign? and what is management
3) Nerve injured in basal skull fracture
4) nerves injured in temporal skull fx
5) what kind of blows are associated with temporal skull fx
6) when to operate for skull fx
7) cause of coagulopthy in traumatic brain injury
8) most common site of fascial nerve injury

A

1) per-orbital ecchymosis, anterior fossa fx
2) mastoid echymossis- middle fossa fx; can injure facial nerve CNVII. rx-if acute facial nerve injury, need exploration and repair. if delayed, likely 2/2 edema and exploration not needed
3) CN VII
4) CNVII and VIII (vestibulocochlear nerve)
5) orbital or lateral skull blows
6) if signficantly depressed (>1cm), contaminated, or persistant CSF leak no responding to conservative therapy (lumbar CSF drainage)
7) release of tissue factor
8) geniculate ganglion

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66
Q

Spine trauma

1) Jefferson fracture- what level, cause, rx
2) Hangman’s fracture- level, cause, rx
3) odontoid fx- level, 3 types and rx
4) Facet fx/dislocation- how they occur and what else can be injured?

A

1) C1 burst 2/2 axial loading. Tx- rigid collar
2) C2- caused by distraction and extension. rx- traction and halo
3) C2. Type 1- above base, stable; Type 2- at base, unstable (need fusion or halo); Type 3- extends into vertebral body (needs fusion or halo)
4) Can cause cord injury; associated with hyperextension and rotation with ligamentous disruption

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67
Q

Thoracolumbar Spine

1) what comprises the 3 columns of the thoracolumbar spine?
2) when is thoracolumbar spine considered unstable
3) what column is affected by compression (wedge) fx?
4) what fx is unstable and rx
5) what fx is stable

A

1) Anterior- anterior logitudinal ligament and anterior 1/2 of vertebral body
Middle- posterior 1/2 of vertebral body and posterior logitudinal ligament
Posterior- facet joints, lamina, spinous processes, interspinous ligament
2) if >1 column disrupted
3) anterior column only, stable
4) Burst fractures (>1 column) require spinal fusion
5) Compression (wedge) fx

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68
Q

1) bones that are at risk for injury in upright fall
2) when in spinal injury should you get an MRI?
3) indications for emergent spinal decompression

A

1) calcaneous, lumbar, wrist/forearm
2) neuro defects w/o bony injury to eval for ligamentous injury
3) fracture/dislocation not reducible with distraction, open fx, soft tissue or bony compression of cord, progressive neuro dysfnc

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69
Q

1) most common cause of facial nerve injury in trauma
2) technique for repairing facial lacerations
3) Le Fort Classification of Facial Fractures I-III. describe. what is the rx

A

1) temporal bone fx
2) preserve skin and don’t trim edges
3) Le Fort I- maxillary fx straifht across (-). rx- reduce, stabilize, intramaxillary fixation (IMF) +/- circumzygomatic and orbital rim suspension wires.
Le Fort II- lateral to nasal bone, underneath eyes, diagonal toward maxilla (/ ). rx same as I
Le Fort III-lateral orbital walls (- -). rx-suspension wiring to stablize frontal bone, may need external fixation

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70
Q

1) what type of facial fx have a 70% CSF leak and rx of CSF leak
2) rx of nose bleeds

A

1) nasoethmoidal orbital fx. conservative therapy for up to 2 weeks. Can try epidural catheter to dec CSF pressure and help leak close, may need surgical closure of dura if above fail
2) anterior- packing
posterior- try balloon tamponade 1st. May need angioembolization of internal maxillary artery or ethmoidal artery

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71
Q

1) rx of orbital blowout fx and who needs repair
2) Tripod fx- what is it and how to repair
3) T/F: pts with maxillofacial fx are at high risk for cervical spine injuries

A

1) repair pts with upward gaze or diplopia with upward vision. rx- restoration of orbital floor with bone fragments or bone graft
2) Zygomatic bone fx- ORIF for cosmesis
3) True

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72
Q

1) what is the #1 indicator of Mandibular injury
2) how to diagnose mandibular injury
3) rx

A

1) malocclusion
2) fine0cut facial CT with reconstruction
3) IMF (intramaxillary fixation- metal arch bars to upper and lower dental arches for 6-8wks) or ORIF

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73
Q

Neck Trauma

1) 3 neck zones of injury
2) study to get in asymptomatic pt with blunt injury
3) in asymptomatic penetrating (by 3 neck zones)
4) in symptomatic blunt or penetrating injury (shock, bleeding, expanding hematoma, losing or lost airway, subq air, stridor, dysphagia, hemoptysis, neuro defect

A

1)ZOne I- clavical to cricoid cartilage. Zone II- Cricoid to angle of mandible. Zone III- angle of mandible to base of skull
2) neck CT
3) Zone I- (greater potential for intrathoracic great vessel injury) angiography, bronchoscopy, esophagoscopy and barium swallow. pericardial window may be indicated. May need medium sternotomy to reach lesions
ZOne II-neck exploration in OR
Zone III-angiography and laryngoscopy. May need jaw subluxatin/digastric and SCM muscle release/mastoid sinus resection to reach vascular injuries in this location
4) neck exploration in OR immediately

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74
Q
Esophageal injury
1) how to diagnose
2) rx of contained injuries
3) rx of non-contained injuries if:
a- small injury, minimal contamination
b- extensive injury or contamination
4) Approach to esophageal injuries in:
a- the neck
b- upper 2/3 of thoracic esophagus
c- lower 1/3 of thoracic esophagus
A

1) hardest neck injury to find. Do esophagoscopy and esophagogram (finds 95% of injuries when combined)
2) observe
3) a-primary closure. b-if in neck- just place drain (will heal). if in chest- chest tubes to drain injury and place spit fistula in neck (eventually will need esophagectomy)
4) a-left side, b- right thoracotomy, c- left thoracotomy

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75
Q

Laryngeal fracture and tracheal injuries

1) sx
2) are these non-urgent, urgent or emergent?
3) rx

A

1) stridor, crepitus, resp compramise
2) emergent
3) secure airway in ER (usually cricothydoidotomy). then primary repair (can use strap muscle for airway support) _ tracheostomy for most to allow edema to subside and check for stricture (convert the cric to a trach)

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76
Q

1) rx of thyroid gland injury
2) rx of recurrent laryngeal nerve injury
3) management of shotgun injures to neck
4) of vertebral artery bleeds
5) common carotid bleeds and complication

A

1) control bleed and drain (NOT thyroidectomy)
2) try to repair or reimplant in cricoarytenoid muscle)
3) get angiogram and neck CT, esophagus and trach evaluation
4) embolize or ligate without any sequela
5) ligation causes stroke in 20%

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77
Q

Chest trauma:

1) when to go to OR for thoracotomy after CT placement
2) how quickly do you need to drain blood in hemothorax and why
3) management of unresolved hemothorax after 2 well-placed drains

A

1) >1500 cc after initial insertion in one side, >250cc/hr for 3 hours, >2500cc/24 hr or bleeding with instability
2)

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78
Q

Sucking chest wound

1) how big does it need to be to be clinically significant
2) rx

A

1) >2/3 diameter of trachea

2) cover wound with dressing that has tape on 3 sides to prevent tension pneumo

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79
Q

1) what should you think about if pt has worsening oxygenation after chest tube placement
2) T/F Bronchus injuries are more common on the right
3) dx of thracheobronchial injury
4) rx- indications for repair and how to repair (type of incision)

A

1) tracheobronchial injury. one of the few indications to clamp NGT
2) True
3) bronchoscopy
4) may need to mainstem intubate pt on unaggected side repair if large air leak and respirator compromise or after 2 weeks of persistent air leak.
- right thoracotomy for right mainstem, trachea and and proximal left mainstem injuries (avoids aorta)
- left thoracotomy for distal left mainstem injuries

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80
Q

Injuries of the diaphragm

1) where are they more common?
2) more common in blunt or penetrating trauma?
3) signs on CXR
4) type of approach for repair

A

1) on left
2) blunt trauma
3) air-fluid level in chest from stomach herniation
4) transabdominal if 1wk bc will have to take down adhesions in the chest. May need mesh

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81
Q

1) what am I: widened mediastinum, 1st or 2nd rib fx, apical capping, loss of aortopulmonary window, loss of aortic contour, left hemothorax, trachea deviation to the right

A

1) aortic transection

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82
Q

1) where is aortic transection most common
2) how good is CXR at diagnosing?
3) when should you do aortic evaluation if nl CXR
4) Dx of aortic transection
5) operative approach
6) if pt has aortic transection and + DPL twhat should be addressed first

A

1) ligamentum arteriosum (just distal to subclavian takeoff) is MC. also seen near ortic valve and where aorta traverses diaphragm
2) nl in 5%
3) significant mechanism (head on car crash >45 mph, fall >15ft)
4) CT angio chest
5) left thoracotomy and repair with left heart bypass of place covered stent endograft (distal transections only)
6) abdominal ex-lap first. Rx other life-threatening injuries first.

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83
Q

What am I?: widened mediastinum, 1st or 2nd rib fx, apical capping, loss of aortopulmonary window, loss of aortic contour, left hemothorax, trachea deviation to the right

A

aortic transection

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84
Q

Aortic transection

1) MC place for tear and other places
2) How good is CXR at detecting
3) Diagnostic study
4) operative approach
5) T/F: you can not defer treatment to treat other life-threatening injuries or positive DPL first

A

1) ligamentum arteriosum just distal to subclavian takeoff (MC). Also, near aortic valve where aorta traverses diaphragm
2) misses 5%, need evaluation of aorta for pts with sig mech (head on car crash >45mph or fall >15ft
3) CT angio chest
4) left thoracotomy and repair with partial L heart bypass or place a covered stent endograft (distal transections only)
5) false, you can defer for other life-threatening injuries

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85
Q

what operative approach should you use for the following injuries:

1) ascending aorta, innominate artery, proximal right subclavian artery, inominate vein, proximal left common carotid
2) left subclavian artery, descending aorta
3) distal right subclavian artery

A

1) median sternotomy
2) left thoracotomy
3) midclavicular incision with removal of medial clavical

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86
Q

Myocardial contusion

1) what is MC cause of death
2) MC arrhythmia seen
3) how long to monitor and when is risk highest

A

1) v-tach and v-fib
2) SVT
3) risk highest in 1st 24 hours, monitor for 24-48hrs

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87
Q

1) flail chest ddefinition and rx and biggest pulm impairment
2) T/F: aspiration produces immediate CXR findings

A

1) 2+ consecutive rib fx with 2+ break sites. rx- occlusive dressing taped at 3 sides. can result in underlying pulm contusion
2) false- may not be immediate

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88
Q

Penetrating Chest injuries

1) first imaging study in stable pts
2) penetrating “box” injuries- location and studies to do to dx injuries
3) penetrating chest wound outside box w/o pneumo or hemothorax- what to do
4) what to do if find blood on doing pericardial window?
5) when do you need to go to OR for laparoscopy or laparotomy

A

1) CXR (if pneumothorax or hemothorax place a chest tube)
2) borders are clavicles, xiphoid process, nipples
- do pericardial window, bronchoscopy, esophagoschopy, barium swallow
3) need chest tube if pt req intubation otherwise just follow serial CXR
4) median sternotomy to fix possible injury to heart or great vessels, place pericardial drain
5) penetrating injuries anterior-medial to midaxillary line below the nipples (may also need penetrating box injury eval)

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89
Q

1) traumatic causes of cardiogenic shock
2) tension pneumo: what do you see for BP, airway pressures, breath sounds, neck veins, trachea
3) cause of cardiac compromise in tension pneumo
4) pts with what type of fx are at high risk for cardiac contusion
5) what fx put pt at high risk for aortic transection

A

1) tension pneumo, cardiac tamponade, cardiac contusion
2) hypotension, inc airway pressures, dec breath sounds, bulging neck veins, tracheal shift
3) 2/2 ICV/SVC compression-> dec venous return
4) sternal
5) 1st and 2nd rib fx

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90
Q

Pelvic trauma

1) what to do with hemodynamically unstable with pelvic fx and negative DPL, CXR and not other signs of blood loss or reason for shock
2) what other structures may be injured
3) 3 types of fx, mortality and bld loss

A

1) stabilize pelvis (C-clamp, external fixator, sheet) and go to angio for embolization
2) genitourinary and abdominal injuries
3) Type I- crush, unstable, mortality 20-30%, blood loss >10units
Type II- verticle incision completely transecting, unstable, mortality 8-12%, blood loss 2-10u
Type III- fx in rami, etc that doesn’t transect entire pelvis. stable.

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91
Q

Pelvic trauma

1) can repair be delayed for other injuries
2) Intra-op management of penetrating injury pelvic hematomas
3) Intra-op management of blunt injury pelvic hematomas

A

1) yes
2) open (can angio)
3) leave. if expanding or unstable-> stabilize fx, pack if in OR and go to angio for embolization. remove packs after 24-48hr

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92
Q

Duodenal Trauma

1) MC cause of injury
2) MC area injured
3) MC rx
4) for what section is segmental resection with primary end-to-end closure not possible
5) mortality
6) MC source of morbidity

A

1) blunt (crash or deceleration injury)
2) 2nd portion (descending portion near ampulla of Vater)
3) 80% get debridement and primary closure
4) second portion of duodenum
5) 25%
6) fistulas

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93
Q

1) rx of intra-op paraduodenal hematomas and where they are located with blunt injury
2) presentation, dx and rx of paraduodenal hemotomas

A

1) 2+cm is significant- open for both blunt and penetrating (usually in third portion of duodenum overlying spine in blunt injury)
2) SBO 12-72 hrs after injury, UGI shows stacked coins or coiled spring appearance (make sure no contrast extravasation). rx- conservative (NGT, TPN)- cures 90% over 2-3wk (hematoma resorbed)

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94
Q

1) what to do if at laparotomy and duodenal injury suspected

A

1) Kocker maneuver (to mobilize the duodenum) and open lesser sac through omentum. Chekc for hematoma, bile, succus and fat necrosis and if you see any do formal inspection of entire duodenum

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95
Q

1) how to diagnoses suspected duodenal injury

A

1) CT abd with contrast-1st then UGI (best)
CT- bowel wall thickening, hematoma, fre air, contrast leak or retroperitoneal fluid/air. If CT worrisome but non diagnostic, can repeat CT in 8-12 hours

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96
Q

1) Tx of duodenal trauma

2) What to do if in 2nd portion of duodenum and can’t do primary repair->

A

try to get primary repair/anastamosis

  • may have to divert with pyloric exclusion and gastrojejunostomy to allow healing.
  • place distal feeding jejunostomy and possibly proximal draining jejunostomy tube that threads back to injury site. Place drains.
    1) place jejunal serosal patch over hole (may need whipple in future), do pyloric exclusion and gastrojejunostomy, consider feeding and draining jejunostomies, leave drains

-Trauma whipple rarely if ever indicated (v high mortality)

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97
Q

1) when to remove drains after duodenal injury repair

1) rx of fistulas

A

1) when pt tol diet without increasing drainage

2) bowel rest, TPN, octreotide, conservative management for 4-6wks.

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98
Q
Colon trauma
1) MC type of injury
2) repair for:
a- right colon
b- transverse colon
c-left colon
d-paracolonic hematomas
A

1) penetrating injury
2) a and b- perform primary repair/anastomosis
c-primary repair/anastamosis, diverting ileostomy
d-both blunt and penetrating need to be opened

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99
Q

rectal trauma

1) MC type of injury
2) repair of high rectal injuries
3) repair of low rectal injuries (<5cm)
4) when to place diverting ileostomy

A

1) penetrating
2) extraperitoneal- generally not repaired bc of inaccessibility. can do serial debridement or consider diverting ileostomy
intraperitoneal- rx- repair defect, presacral drainage, consider diverting ileostomy
3) repair transanally
4) shock, gross contamination, extensive injury

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100
Q

Liver trauma

1) T/F- often need to do lobectomy
2) can you ligate the common hepatic artery?
3) what is the pringle maneuver? does it stop bleeding from hepatic veins?
4) when to use an atriocaval shunt?
5) management of portal triad hematoma

A

1) F
2) yes- gastroduodenal artery has collaterals
3) clamping portal triad. Does not stop bleeding from hepatic veins
4) for retrohepatic IVC injury. Allows for control while performing repair
5) explore

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101
Q

Liver trauma cont

1) ideal repair of common biled duct injury
2) repair of portal vein injury and should you ligate portal vein
3) when to use omental graft
4) should you leave drains?

A

1) if 50% circumference or complex injury- do choledochojejunostomy. May need intraop cholangiogram to define injury. ALSO- place drains bc 10% of duct anastamoses leak
2) if you need to transect through pancreas to get to the injury in the portal vein need to perform distal pancreatectomy. Ligation of portal vein is associated with 50% mortality
3) place in liver lac to help with bleeding and prevent bile leaks.
4) yes!

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102
Q

Conservative management of blunt liver injuries

1) activity level allowed for pt
2) when should you go to the OR

A

1) bedrest for 5 days
2) -if pt becomes unstable despite aggressive resucitation (HR>120 or SBP4u needed to keep HCT>25)
- if active blush on CT abd or pseudoaneurysm: if posterior may be better going to angiogram (but if doubt go to OR), if anterior go straight to OR

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103
Q

spleen injury

1) how long does it take spleen to fully heal
2) when is postsplenectomy sepsis risk greatest
3) T/F splenic salvage is associated with increased transfusions
4) when to go to the OR/when has conservative management failed
5) activity level with conservative management
6) in what pts is threshold for splenectomy much higher
7) what immunizations do you need after trauma splenectomy

A

1) 6 weeks
2) greatest within 2 years of splenectomy
3) true
4) -pt unstable despite aggressive fluid resucitation (HR>120 or SBP2u needed to keep HCT>25)
- if active blush on CT abd or pseudoaneurysm
5) bedrest x 5days
6) children
7) Strept pneumo (pneumococcal), H flu (Hib), meningococcal

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104
Q

Pancreatic Trauma

1) MC injury type
2) what type of injury can cause pancreatic duct fractures and typical orientation of fx
3) what are CT signs of injury
4) rx of pancreatic contusion
5) rx of distal pancreatic duct injury
6) rx of pancreatic head injury that is not reparable
7) how do you decide bw a whipple vs distal pancreatectomy

A

1) penetrating accounts fo 80%
2) bunt injury-> fx perpendicular to duct
3) edema or necrosis of peripancreatic fat
4) leave if stable, place drains if in OR
5) distal pancreatectomy (can take up to 80% of the gland)
6) place drains initially. delayed whipple or possible ERCP with stent may eventually be necessary
7) based on duct injury in relation to SMV

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105
Q

Pancreatic Trauma

1) should you leave drains?
2) what maneuver helps evaluate the pancreas operatively
3) rx for pancreatic hematoma
4) what lab value should make you suspect missed pancreatic injury
5) when to use ERCP

A

1) YES!
2) Kocher
3) both blunt and penetrating need to be opened
4) rising or persistent amylase
5) good at finding ductal injuries and may be able to treat with temporary stent

106
Q

Vascular Trauma

1) repair before or after ortho repair?
2) when to go to the OR
3) when to go to angio
4) indications for saphenous vein graft
5) what vein injuries need repair?
6) what should you consider doing if ischemia>4-6hr

A

1) repair vascular injury 1st (or vascular shunt)
2) if major signs of injury go to OR: active hemorrhage, pulse deficit, expanding of pulsatile hematoma, distal ischemia, bruit, thrill (may need to go to angio to define injury)
3) if moderate/soft signs of injury go to angio: h/o hemorrhage, deficit of anatomically related nerve, large stable/nonpulsatile hematoma, ABI 2cm missing (use vein from contralateral leg when fixing lower extremity arterial injuries
5) vena cava, femoral, popliteal, brachiocephalic, subclavian and axillary
6) fasciotomy

107
Q

1) rx for transection of single artery in the calf in otherwise healthy pt
2) at what compartment pressure should you consider compartment syndrome
3) clinical signs of compartment syndrome
4) most common injuries leading to comp syndrome
5) how to rx

A

1) ligate
2) >20mmHg or clinical exam
3) pain-> paresthesia-> anesthesia-> paralysis-> poikliothermia-> pulselessness (late finding)
4) suprachondylar humeral, tibial, crush injuries or injuries with disruption and then restoration of blood flow after 4-6hr
5) fasciotomy- incisions are anterolateral and posteromedial

108
Q

IVC injury

1) how to best control bleeding, should you clamp it?
2) how to repair

A

1) proximal and distal pressure- don’t clamp bc can tear
2) primary repair if residual stenosis is <50% the diameter of the IVC, otherwise do saphenous vein graft or synthetic patch.
- posterior wall injury repaired through anterior wall (may need to cut through anterior IVC to access)

109
Q

Ortho trauma
1) how much blood can be lost from femur fx
2) which of the following is not an ortho emergency: pelvic fx in unstable pt, spine injury with deficit, open fx, dislocations or fx with vascular compromise, compartment syndrome, calcaneal fx
3) pt w femoral neck fx are at high risk for?
4) rx of long bone fx or dislocation with loss of pulse or weak pulse
a-first step
b- if pulse doesn’t return->
c- if pulse is weak ->
4) rx monogram for knee dislocations
5) fx associated with upright falls

A

1) >2L
2) calcanear fx, unless associated with lumbar fx with neuro impairment
3) avascular necrosis
4) a- Immediate reduction and reassessment of pulse
b- go to OR for vascular bypass or repair (may need OR angio to define injury)
c-go to antio
4) all knee dislocations go to angiogram unless pulse is absent in which case you go to OR
5) lumbar, distal forearm (radial ulnar), calcaneous

110
Q

what is the concomitant nerve/artery injury UE

1) Anterior shoulder disloc
2) Posterior shoulder disloc
3) Proximal humerus fx
4) midshaft humerus fx (or spiral humerus fx)
5) distal humerus fx (supracondylar
6) Elbow dislocation
7) Distal radius fx

A

1) axillary nerve
2) axillary artery
3) axillary nerve
4) radial nerve
5) brachial artery
6) brachial artery
7) median nerve

111
Q

what is the concomitant nerve/artery injury LE

1) anterior hip disloc
2) posterior hip disloc
3) distal (supracondylar) femur fx
4) posterior knee disloc
5) fibula neck fx

A

1) femoral artery
2) sciatic nerve
3, 4) popliteal artery
5) common peroneal nerve

112
Q

what is the concomitant nerve/artery/organ injury

1) temoral or parietal bone fx
2) maxillofacial fx
3) sternal fx
4) 1st or 2nd rib fx
5) scapula fx
6) Left ribs 8-12 fx
7) Right ribs 8-12 fx
8) pelvic fx

A

1) middle meningeal injury-> epidural hematoma
2) cervical spine fx
3) cardiac contusion
4) aortic transection
5) pulmonary contusion, aortic transection
6) spleen lac
7) liver lac
8) bladder rupture, urethral transaction

113
Q

Renal trauma

1) best indicator of kidney injury
2) what imaging study should all pts with hematuria have
3) if you are going immediately to the OR without abdominal CT scan, what other study is useful to identify the presence of a functional contralateral kidney

A

1) hematuria
2) abd CT
3) intravenous pyelogram

114
Q

Renal trauma

1) T/F the left and right renal vein can be ligated near the IVC
2) what are the renal hilum structures from anterior to posterior
3) T/F- 95% of injuries are treated nonperatively
4) T/F- all urine extravasation injuries require operation
5) indications for operation in acute injury
6) indications for OR after acute phase

A

1) False, only the left renal vein can be ligated near IVC because it has adrenal and gonadal collaterals. The Right renal vein doesn’t have these collaterals
2) VAP= vein artery pelvis
3) True
4) false
5) ongoing hemorrhage with instability
6) major collecting system dysruption, non-resolving urine extravasation, severe hematuria

115
Q

Renal Trauma
1) with exploration in OR what should you try to get bleeding control of first
2) should you place drains intra-op?
3) how to check for leak at end of case
How would you treat if at exploration for another blunt injury or penetrating trauma you find:
4) blunt renal injury with hematoma
5) Penetrating renal injury with hematoma
How do you rx:
6) Trauma to flank and IVP shows no uptake in stable pt

A

1) vascular hilum control
2) yes! especially if collecting system is injured
3) methylene blue die
4) leave unless pre-op CT/IVP shows no function or significant urine extravasation
5) open unless pre-op CT/IVP shows good function without significant urine extravasaton
6) angiogram (can stent if flap present)

116
Q

Bladder Trauma

1) best indicator that the bladder is injured
2) common associated injury
3) signs and sx
4) dx
5) cystogram findings and rx of extraperitoneal bladder rupture
6) cystogram findings and rx of intraperitoneal bladder rupture

A

1) hematuria
2) >95% have associated pelvic fx
3) meatal blood, sacral or scrotal hematoma
4) cystogram
5) cysto shows starbursts, foley for 7-14d
6) cysto shows leak (more likely in kids) . rx- operate and repair defect followed by foley drainage

117
Q

Ureteral trauma
1) best diagnostic studies
2) best repair if > 2cm of ureteral segment missing and can’t reanastamose
a- if injury in upper and middle 2/3 of ureter (above pelvic brim that won’t reach bladder
b- lower 1/3 injuries
3) repair if small ureteral segment
a- upepr and middle 1/3 injuries
b-lower 1/3 injuries
4) does a one-shot IVP evaluate the ureters sufficiently?
5) where is blood supply in relation to the ureter
6) what can be used to check for leaks

A

1) IVP and retrograde urethrogram (RUG)
2) a- temporize with perc nephrostomy and tie off both ends of ureter, later do ileal interposition or transureteroureterostomy
b- reimblant in bladder, may need bladder hitch procedure
3) a-mobilize ends of ureter and perform primary repair over stent
b- re-implant in bladder
*leave drains for all injuries
4) no
5) blood supply is medial in upper 2/3 of ureter and lateral in lower ureter
6) IV indigo carmine or IV methylene blue

118
Q

urethral trauma

1) best signs
2) T/F: place a foley to allow for healing
3) best study to dx and area most at risk for transection
4) rx of significant tears
5) rx of small, partial tears
6) rx of genital trauma (fx in erectile bodies from vigorous sex
7) testicular trauma- first study to get

A

1) hematuria, blood at meatus are best. also free-floating prostate gland suggests, usually associated with pelvic trauma
2) false- DON’T place foley for urethral trauma
3) retrograde urethrogram (RUG); membranous portion is most at risk for transection
4) suprapubic cystostomy and repiar in 2-3 months (early repair can lead to stricture and impotence)
5) may get away with just bridging urethral catheter across tear area and repairing in 2-3mo
6) repair the tunica and Buck’s fascia
7) get US to see if tunica albuginea is violated. if it is-> repair

119
Q

Pediatric trauma

1) T/F: blood pressure is a good indicator of blood loss in kids
2) what are the best indicators of shock in children
3) T/F: Kids have same risk of hypothermia as adults
4) T/F: Kids have increased risk of head injury
5) normal vital signs for kids 10yo

A

1) false, last resort
2) HR, RR, mental status, clinical exam
3) false, kids have increased risk bc increased BSA compared with weight
4) True
5) Infant (10yo: HR 120, SBP 100, RR 20

120
Q

Trauma during pregnancy

1) ethics: who to save? mother or child
2) T/F: pregnant pts can have up to a 1/3 total blood volume loss without signs
3) how to estimate pregnancy week
4) Can you get a CT scan in early prgnancy?
5) what special physical exam findings should you look for
6) lab tests to determine fetal maturity

A

1) mother at all costs
2) True
3) based on fundal height. 20 cm=20wk=umbilicus. place fetal monitor
4) try to avoid unless life-threatening and needed
5) vaginal discharge- blood, amnion. check for effacement, dilation, fetal station
6) lecithin: sphingomyelin (LS) ratio >2:1 and positive phosphatidylcholine in amniotic fluid

121
Q

Placental abruption

1) signs
2) causes
3) tests
4) prognosis for fetus

A

1) uterine tenderness, contractions, fetal HR sign of placental abruption
4) >50% result in fetal demise

122
Q

Uterine rupture

1) MC location of rupture
2) rx

A

1) posterior fundus
2) if after delivery of child, aggressive resuscitation even in the face of shock. eventually uterus will clamp down after delivery

123
Q

Indications for C-section during trauma ex-lap

A
  • persistent maternal shock or severe injuries and pregnancy near term (>34wks)
  • pregnancy a threat to mothers life (hemorrhage, DIC)
  • mechanical limitation to life-threatening vessel injury
  • risk of fetal distress exceeds risk of immaturity
  • direct intra-uterine trauma
124
Q
Management of hematomas:
1) what size is considered significant?
2)Management of hematoma following penetrating/blunt injury in the
a- pelvis
b-paraduodenal
c- portal triad
d-retrohepatic
e- midline supramesocolic
f- midline inframesocolic
g- pericolonic
h- perirenal
A

1) >/= 2 cm
2) a-open/leave
b-open for both
c- open for both
d- leave for both if stable
e, f, g- open for both
h- open unless CT/IVP shows no injury/ leave unless preop CT/IVP shows injury

125
Q

1) what injuries should you leave drains in for

A

pancreatic, liver, biliary, urinary and duodenal injuries

126
Q

Snake bites

1) symptoms
2) rx

A

1) (depend on species)-> shock, bradycardia, arrhythmia

2) stabilize pt, anti-venin, tetanus shot

127
Q

Zones of the peritoneum and associated injuries

1) Zone 1
2) Zone 2
3) Zone 3
- and hematoma management for each

A

1) central retroperitoneum- pancreaticoduodenal injuries or major vascilar injury (usually open hematomas in these areas)
2) flank or periphephric- GU and colon injuries (often penetrating trauma, usually open hematomas in these areas)
3) pelvis- pelvic fractures- usually leave hematomas in these areas

128
Q

Cardiovascular System: Normal Values

1) Cardiac output (CO) L/min
2) Cardiac index (CI) L/min
3) Systemic vascular resistance (SVR)
4) Pulmonar Capillary wedge pressure (PCWP)
5) Central venous pressure (PAP)
6) mixed venous oxygen saturation

A

1) 4-8
2) 2.5-4
3) 800-1400
4) 11 +/- 4
5) 25/10 +/- 5
6) 75 +/- 5

129
Q

MAP=

A

SVR x CO

130
Q

C.I.=

A

CO/BSA

131
Q

1) what % of C.O. does kidney get
2) what % of C.O. does brain get
3) what % of C.O. does heart get

A

1) 25%
2) 15%
3) 5%

132
Q

relation of left ventricular end-diastolic length to left ventricular end-diastolic volume and filling pressure

A

linear relationship

133
Q

explain the relation of preload to stroke volume seen in the starling curve

A

as preload increase, the increase in stroke volume for equivalent increases in preload is less. At the far left (steep) part of the curve a small increase in preload will sig increase stroke volume. At the right (flat) portion of the curve, the same increase in preload will only create a slight increase in stroke volume

134
Q

What are the following a measure of:

1) Afterload
2) stroke volume (3 things that determine SV)
3) ejection fraction
4) end-diastolic volume (EDV)
5) end-systolic volume (ESV)
6) effect of HR on C.O.

A

1) resistance against the ventricle contracting (SVR)
2) determined by left ventricular end diastolic volume, contractility and afterload
SV= LVEDV - LVESV
3) stroke volume/LVEDV
4) determined by preload and distensibility of the ventricle
5) determined by contractility and afterload
6) C.O. increases with HR up to 120-150bpm then starts to go down bc of decreased diastolic filling time

135
Q

1) how much of LVEDV does the atrial kick account for
2) Anrep effect
3) Bowditch effect

A

1) 20%
2) automatic increase in CONTRACTILITY 2/2 inc afterload
3) auromatic increase in contractility 2/2 inc HR

136
Q

Equation for arterial O2 content

CaO2=

A

Hgb x 1.34 x O2 sat x (Po2x0.003)

137
Q

Equation for O2 delivery=

A

COx arterial O2 content (CaO2) x 10

138
Q

Equation for O2 consumption (VO2)=

A

CO x (CaO2-CvO2); where CvO2= venous O2 content

139
Q

1) What is the normal O2 delivery to consumption ratio and how is it kept constant
2) does consumtion change with O2 supply

A

1) 5:1. CO2 increases to keep this ratio constant

2) O2 consumption usually supply independent (doesn’t change until low levels of delivery are reached)

140
Q

Causes of right shift on oxygen- Hgb dissociation curve

A

inc CO2, dec pH, inc temperature, inc ATP production, inc 2,3-DPG production all lead to O2 unloading

141
Q

1) What is normal p50 (O2 at which 50% of O2 receptors are saturated)
2) normal SvO2

A

1) 27 mmHg

2) 75% +/- 5%

142
Q

1) what causes SvO2 to increase

2) to decrease

A

1) occurs with inc shunting of blood or dec O2 extraction (ie- sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hypothermia, paralysis, coma, sedation)
2) occurs with inc O2 extraction or dec O2 delivery (ie- dec O2 saturation, dec C.O., malignant hyperthermia)

143
Q

what can throw off the pulmonary wedge pressure

A

pulmonary HTN, aortic regurg, mitral stenosis or regurg, high PEEP, poor LV compliance

144
Q

Swan-Ganz catheter
1) Where to place
2) management of hemoptysis after flushing swan-ganz catheter
3) relative contraindications to placing
4) distances for placing swan-ganz catheter to wedge from
a- R SCV, b- R IJ, c- L SCV, d- L IJ
5) what pulmonary value can only be measured w Swan Ganz catheter
6) when should wedge pressure measurements be taken

A

1) Zone III, lower lung
2) increase the PEEP->taponade of pulmonary artery bleed. Then mainstem intubate the non-affected side (can try to place fogarty balloon down non-effected side)
3) previous pneumonectomy, L bundle branch block
4) a-45cm, b-50cm, c-55cm, d-60cm
5) PVR pulmonary vascular resistance (ECHO does not meausre)
6) at end-expiration for both ventilated and non-vent

145
Q

1) what are primary determinants of myocardial O2 consumption
2) why is LV blood 5mm Hg lower PO2 than pulmonary capillaries
3) what is a notmal alveolar-arterial gradient in nonventilated pt
4) what blood has the lowest venous saturation

A

1) increased ventricular wall tension (#1) and heart rate
2) unsaturated bronchial blood empties into pulmonary veins-> LV blood 5mmHG lower
3) 10-15mmHg
4) coronary sinus blood (30% saturated)

146
Q

1) definition of shock
2) Change in CVP&PCWP/CO/SVR in
a-hemorrhagic shock
b- septic (hyperdynamic shock)- early
c- septic shock late
d-cardiogenic shock
e- neurogenic shock
f- adrenal insufficiency

A

1) inadequate tissue oxygenation
2) a-D/D/I
b-D (or nml)/I/D
c-D/D/I
d-I/D/I
e-D (or nml)/D/D
f-D (or nml)/D/D

147
Q

Adrenal insufficiency

1) MCC
2) sx of acute insuf
3) rx of acute insuf
4) steroid potency bw cortisonek, hydrocortisone, prednisone, prednisolone, methylprednisolone, dexamethasone

A

1) withdrawl of exogenous steroids
2) cardiovascular collapse, typically unresponsive to fluids and pressors, N/V, abd pain, fever, lethargy, hypoglycemia
3) Dexamethasone
4) 1x= cortisone, hydrocortisone
3x=prednisone, prednisolone, methylprednisolone
5x= dexamethasone

148
Q

Neurogenic shock

1) associated injury
2) vitals, skin temp
3) rx

A

1) spinal or head injury
2) dec HR and BP, warm skin
3) volume 1st then phenylephrine after resuscitation

149
Q

1) initial alteration in hemmorhagic shock

A

1) increased diastolic pressure

150
Q

Cardiac tamponade

1) mech of cardiogenic shock
2) Beck’s triad
3) Echo findings
4) does pericardiocentesis blood form clot
5) rx

A

1) decreased ventricular filling due to fluid in the pericardial sac around the heart
2) hypotension, JVD, muffled heart sounds
3) impaired diastolic filling of right atrium initially (1st sign of tamponade)
4) no
5) fluid resuscitation to temporize the situation. need pericardial window or pericardiocentesis

151
Q

1) Early Sepsis triad
2) insulin and glucose levels in
a- early GN sepsis
b- late GN sepsis
3) what is a typical lab finding in a pt just before they become clinically septic

A

1) hyperventilation, confusion, hypotension
2) decreased insulin, increased glucose (impaired utilization)
3) increased insulin and glucose (2/2 to insulin resistance)
4) hyperglycemia

152
Q

Neurohormonal response to hypovolemia

1) rapid response
2) sustained response

A

1) epinephrine and norepi release (adrenergic release) -> vasoconstriction and inc cardiac contractility
2) renin released from kidney-> renin-angiotensin pathway activated resulting in vasoconstriction and water resorption
- ADH released from pituitary-> water reabsorption
- ACTH release from pituitary-> inc cortisol

153
Q
Emboli
1) Fat emboli- 
a- sx
b-MC cause
c- special stain that can show fat in sputum and urine in pt with fat emboli
2) PE
a- where do most arise from
b- sx, Po2, Pco2, HR and  RR, pH abnormality
c- rx
3) Air emboli rx
A

1)a-petechia, hypoxia, confusion
b-LE (hip, femur) fx/ortho procedures
c-sudan red stain
2) a-ileofemoral resion
b- CP and dyspnea, dec Po2 and Pco2, respiratory alkalosis, inc HR and RR, hypotension and shock if massive
c- heparin, coumadin. open or percutaneous suction catheter embolectomy if pt is in shock despite massive pressors and ionotropes
3) place pt head down and roll to left (keeps air in RV and RA), then aspirate air out with central line of PA catheter to RA/RV.

154
Q

Intra-aortic balloon pump (IABP)

1) when does it inflate?
2) deflate?
3) what is a contraindication
4) where to place
5) effect on afterload, BP and coronary perfusion

A

1) diastole (T wave)
2) P wave (systole)
3) aortic regurg
4) tip of catheter just distal to left subclavian (1-2 cm above the top of the arch)
5) decreases afterload (deflation during ventricular systole), improves diastolic BP (inflation during ventricular diastole), improves diastolic coronary perfusion

155
Q

Cardiovascular receptors- actions of each

1) alpha-1
2) alpha-2
3) beta-1
4) beta-2
5) dopamine receptors

A

1) vascular smooth muscle constriction, gluconeogenesis and glycogenolysis
2) venous smooth muscle constriction
3) myocardial contraction and rate
4) relaxes bronchial smooth muscle, relaxes vascular smooth muscle, increases insulin, glucagon and renin
5) relax renal and splanchnic smooth muscle

156
Q

CV drugs- what receptors do they act on, dose and effects

1) Dopamine (include actions at each dose)

A

1) start at 2-5ug/kg/min initially= renal dose (dopamine receptors)
6-10ug/kg/min= beta adrenergic= heart contractility
>10ug/kg/min=alpha-adrenergic (vasoconstriction and inc BP)

157
Q

CV drugs- what receptors do they act on, dose and effects

2) Dobutamine

A

3ug/kg/min initially. Beta-1=inc contractility, tachycardia with higher doses

158
Q

CV drugs- what receptors do they act on, dose and effects

3) Milrinone (and secondary effects)

A

Phosphodiesteras inhibitor-> inc cAMP–> inc Ca flux and myocardial contractility
- also causes vascular smooth muscle relaxation and pulmonary vasodilation

159
Q

CV drugs- what receptors do they act on, dose and effects

4) Phenylephrine
5) Norepinephrine
6) Epinephrine

A

4) 10ug/min. alpha-1-> vasoconstriction
5) 5ug/min. low dose- beta-1-> inc contractility.
-high dose- alpha-1 and alpha-2->vasoconstriction (potent slanchnic vasoconstrictor
6) 1-2ug/min to start.
low dose- beta 1 and 2 (inc contractility and vasodilation)-> can lower BP at low doses
high dose- alpha-1 and alpha-2 (vasoconstriction)-> inc cardiac ectopic pacer activity and myocardial O2 demand

160
Q

CV drugs- what receptors do they act on, dose and effects

7) Isoproterenol (and s/e)

A

1-2ug/min initially.
Beta 1 and 2-> inc HR and contractility, vasodilates
S/E- arrhythmogenic, inc heart metabolic demand (rarely used), may actually dec BP

161
Q

CV drugs- what receptors do they act on, dose and effects

8) Vasopressin

A

V1 receptor-> vasoconstriction
V2 (intrarenal)-> water reabsorption at collecting ducts
V2 (extrarenal)-> release for factor VIII and vWF

162
Q

CV drugs- what receptors do they act on, dose and effects
9) Nipride
( and s/e- what should you check for)

A

arterial vasodilator

s/e- cyanide toxicity at doses >3ug/kg/min for 72 hours. check thiocyanate levels and signs of metabolic acidosis

163
Q

Cyanide toxicity treatment

A

amyl nitrite, then sodium nitrite

164
Q

CV drugs- what receptors do they act on, dose and effects

10) Nitroglycerin

A

venodilation with dec myocardial wall tension from decreased preload.
*moderate coronary vasodilator

165
Q

CV drugs- what receptors do they act on, dose and effects

11) hydralazine

A

alpha-blocker- lowers BP but can cause rebound hypertension

166
Q

Pulmonary system:

1) equation for compliance
2) what does a high compliance equate to
3) in pts with ARDS, fibrotic lung diseases, reperfusion injury, pulmonary edema, atelectasis is compliance increased or decreased

A

1) change in volume/ change in pressure
2) easy to ventilate
3) decreased

167
Q

Aging

1) how does aging effect FEV1
2) vital capacity
3) functional residual capacity

A

1) decreased FEV1
2) decreased vital capacity
3) increased functional residual capacity

168
Q

V/Q ratio

1) where is it highest
2) where is it lowest

A

ventilation/perfusion ratio

1) highest in upper lobes
2) lowest in lower lobes

169
Q

Ventilator

1) how to improve oxygenation
2) how to decreased CO2
3) purpose of pressure support
4) what FiO2 should you keep it to prevent O2 radical toxicity
5) at what plateau and peak is barotrauma of concern and what should you do to prevent
6) how does PEEP work
7) complications from excessive PEEP
8) when to use high-frequency ventilation

A

1) inc FiO2 or inc PEEP (alveoli recruitment->improves FRC)
2) inc rate or volume
3) decreases the work of breathing (inspiratory pressure is held constant untill minimum volume is reached
4) 30 and peak >50–> need to decrease TV and consider pressure control ventilation
6) improves FRC and compliance by keeping alveoli open-> best way to improve oxygenation
7) dec RA filling, dec CO, dec renal blood flow, dec UOP, inc pulm vascular resistance
8) used a lot in kids, tracheoesophageal fistula, bronchopleural fistula

170
Q

Pulmonary function measurements

1) total lung capacity
2) Forced vital capacity
3) Residual volume
4) Tidal Volume
5) functional residual capacity
6) effect of surgery, sepsis and trauma on FRC and why
7) expiratory reserve volume

A

1) lung volume after maximal inspiration (TLC=FVC +RV)
2) maximal exhalation after inhalation
3) lung volume after maximal expiration (20% TLC)
4) volume of air with normal inspiration and expir
5) lung volume after nl expiration (FRC=ERV+RV)
6) all decrease FRC. Surgery (atelectasis), sepsis (ARDS), trauma (contusion, atelectasis, ARDS)
7) volume of air that can be forcefully expired

171
Q

Pulmonary function measurements
8) Inspiratory capacity
9) FEV1
10) minute ventilation (how to calculate)
Describe changes in TLC, RV, FVC, and FEV1 in
11) Restrictive lung disease
12) Obstructive lung disease

A

8) maximum air breathed in from FRC
9) volume of air that can be forcefully expired in 1 second after max inhalation
10) TV x RR= minute ventilation
11) dec TLC, RV and FVC. nl or inc FEV1
12) inc TLC and RV. dec FEV1. FVC can be nl or dec

172
Q

1) dead space- what is it and where is it
2) do the following increase or decrease dead space: drop in C.O., PE, pulm HTN, ARDS, excessive PEEP
3) why is work of breathing increased in COPD

A

1) area of lung that is ventilated but not perfused
2) increases with all. can lead to high CO2 buildup (hypercapnia)
3) prolonged expiratory phase

173
Q

ARDS

1) primary mediating cell type
2) MC cause and other causes
3) effect on lungs
4) Criteria for diagnosing ARDS

A

1) PMNs
2) MC- pneumonia. Other- sepsis, multi-trauma, severe burns, pancreatitis, aspiration, DIC
3) inc proteinaceous material, inc A-a gradient, inc pulmonary shunt
4) acute onset, bilateral pulmonary infiltrates, PaO2/FiO2 <18)

174
Q

Aspiration

1) what pH and volume is associated with inc degree of damage
2) What is Mendelson’s syndrome
3) MC site of aspiration pneumo

A

1) pH0.4cc/kg
2) chemical pneumonitis from aspiration of gastric secretions
3) Right Lower Lobe

175
Q

Atelectasis

1) what is it
2) MC cause
3) symptoms
4) what comorbidities increase risk
5) rx

A

1) collapse of alveoli resulting in reduced oxygenation
2) poor inspiration post-op (MC cause of fever in 1st 48hr)
3) fever, tachycardia, hypoxia
4) COPD, upper abd surgery, obesity
5) IS, pain control, ambulation

176
Q

what can throw off a pulse ox

A

nail polish, dark skin, low-flow states, ambient light, anemia, vital dyes

177
Q

effect on lung vasculature of

1) PGE1, prostacyclin (PGI2), Nitric oxide and bradykinin
2) hypoxia, histamine, serotonin, TXA2
3) Alkalosis
4) Acidosis
5) Nitroprusside, nitroglycerin and nifedipine

A

1) pulm vasodilation
2) pulm vasoconstrict
3) pulm vasodilator
4) pulm vasoconstrictor
5) pulmonary shunting

178
Q

Renal system

1) MC of postop renal failure
2) how many nephrons need to be damaged for renal dysfnc to occur
3) what is best test for azotemia
4) how to calculate and what the results mean

A

1) hypotension
2) 70%
3) FeNa
4) FeNa= (urine Na/Cr)/(plasma Na/Cr). 3%=parenchymal

179
Q

Prerenal/parenchymal (renal)

1) Urine osmolarity (mOsm)
2) U/P osmolality
3) U/P creatinine
4) Urine Na
5) FeNa

A

1) >500/ 250-350
2) >1.5/ 20/ 40
5) 3%

180
Q

Management steps for Oliguria

A

1st- make sure pt is volume loaded (CVP 11-15)
2nd- do diuretic (lasix) trial
3rd- dialysis if needed

181
Q

Indications for dialysis

A

fluid overload, hyperkalemia, metabolic acidosis, uremic encephalopathy, uremic coagulopathy, poisoning

182
Q

1) Difference bw hemodialysis and CVVHD

2) how much does hct increase for each liter taken off with dialysis

A
  1. HD- rapid, can cause large volume shifts
    CVVH- sloer, good for ill pts who cannot tolerate the volume shifts (ie- septic shock).
    2) 5-8
183
Q
Renin
1) what causes release and by what cells
2) action
Angiotensin Converting enzyme
3) where is it
4) effect
Aldosterone
5) what causes release and where from
6) effect
7) effect of angiotensin II
A

1) decreased pressure sensed by juxtaglomerular apparatus or increased Na concentration sensed by macula densa
- beta-adrenergic stimulation and hyperkalemia also cause release
2) converts angiotensinogen (synth in liver) to angiotensin I
3) lung
4) converts angiotensin I to angiotensin II
5) adrenal cortex releases in response to angiotensin II
6) acts at distal convoluted tubule to reabsorb water by up-regulating the Na/K ATPase on the membrane (Na reabsorbed, K secreted)
7) vasoconstricts and inc HR, Contractility, glycogenolysis and gluconeogenesis. Inhibits renin release

184
Q

Atrial natriuretic peptide (or factor)

1) where is it released from
2) actions

A

1) atrial wall 2/2 atrial distension

2) inhibits Na and water resorption in the collecting ducts and vasodilates

185
Q

which limb of kidney controls GFR

A

efferent limb

186
Q

renal toxic drugs, how they cause injury

1) NSAIDS
2) Aminoglycosides
3) Myoglobin and rx
4) contrast dyes and prevention/rx

A

1) inhibit prostaglandin synthesis-> renal arteriole vasoconstriction
2) direct tubular injury
3) direct tubular injury (rx- alkalinize urine)
4) direct tubular injury. rx- pre-hydrate before contrast exposure is best. otherwise- HCO3- or N-acetylcysteine

187
Q

SIRS

1) causes
2) what is most potent stimulus and what is released as a consequence
3) mechanism behind it
4) diff bw sepsis and SIRS

A

1) shock, infection, burns, multi-trauma, pancreatitis, severe inflammatory responses
2) endotoxin (lipopolycaccharide-lipid A) is the most potent stimulus for SIRS-> TNF release
3) TNF-alpha and IL-1-> inflam response-> shock and multiorgan dysfnc 2/2 capillary leakage, microvascular thrombi and hypotension
4) sepsis= SIRS + infectious source

188
Q

Definition of

1) SIRS
2) Shock
3) Multisystem Organ Dysfunction

A

1) T>38 or 90bpm, RR>20 or PaCO212,000 or <4,000
2) above + arterial hypotension despite adequate volume resuscitation (inadequate tissue oxygenation)
3) above + progressive but reversible dysfnc of 2+ organs 2/2 acute disruption in hemostasis

189
Q

Diagnositic criteria for sig organ dysfnc

1) pulmonary
2) CV
3) Renal
4) Liver
5) Nutrition
6) CNS
7) Coagulation
8) Host defenses

A

1) need for mech. ventilation, PaO2:FiO2 ration < 2.5 L/min/m^2
3) Cr>2xbaseline on 2 consecutive days or need for dialysis
4) bili >3mg/dl on 2 consec days or PT>1.5
5) >10% reduction in lean body mass; albumin<1000 or invasive infection including bacteremia

190
Q

Brain death

1) what Temperature, BP, drugs and metabolic derangements preclude diagnosis
2) what physical exam findings must the pt exhibit and for how long
3) EEG findings
4) MRA findings
5) T/F: you cannot have deep tendon reflexes with brain death

A

1) T

191
Q

Apnea test for brain death

1) what is it
2) what is a positive test result
3) what are negative results

A

1) pt pre-oxygenated via catheter delivering O2 at 8L/min at carina and CO2 nl before start of test
- then disconnect from ventilator for 10 min to determine if brain death
2) CO2>60 or increase in CO2 by 20mmHg at end of test is positive (meets criteria for brain death)
3) BP drops ( put back on vent

192
Q

Carbon Monoxide poisoning

1) effect on O2 sat
2) how it works and sx
3) how to diagnose
4) rx

A

1) can falsely elevate O2 sat on pulse ox
2) binds Hgb directly-> carboxyhemoglobin-> can’t bind O2-> sx- Nausea, HA, confusion, coma, death
3) carboxyhemoglobin level >10% or >20% in smokers
4) 100% O2 on ventilator. Displaces carbon monoxide. rarely need hyperbaric O2

193
Q

Methemoglobinemia

1) Cause
2) mechanism
3) effect on O2 sat
4) rx

A

1) from nitrites such as Hurricaine spray
2) nitrites bind Hgb
3) O2 sat reads 85%
4) rx- methylene blue

194
Q

What is critical illness polyneuropathy and effect on ventilation

A

motor>sensory neuropathy with sepsis. Can lead to failure to wean from vent

195
Q

Reperfusion injury

1) Cause
2) other role for the cause
3) Most important cell mediator

A

1) Xanthine Oxidase in endothelial cells forms toxic oxygen radicals
2) Xanthine oxidase also involved in metabolism of proteins to uric acid
3) PMNs

196
Q

DKA

1) sx and labs
2) rx

A

1) N/V, thirst, polyuria, inc glucose and ketones, dec Na, inc K
2) NS and insulin

197
Q

ETOH withdrawal

1) sx
2) rx

A

1) HTN, tachycardia, delirium, seizures after 48hrs

2) thiamine, folate, B12, Mg, K, prn lorazepam (Ativan)

198
Q

ICU psychosis

1) when do you see it
2) what other causes must you r/o

A

1) after POD3

2) r/o metabolic (hypoglycemia, DKA, hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes

199
Q

Burn classification- symptoms/depth

1) 1st degree
2) 2nd degree
3) 3rd degree
4) 4th degree

A

1) Sunburn (epidermis only) superficial
2) superficial dermis (papillary)- painful to touch, blebs and blisters, hair follicles intact, blanches (don’t need skin graft
deep dermis (reticular)- decreased sensation, loss of hair follicules (need skin graft)
3) down to subcutaneous fat- leathery (charred parchment)
4) Down to bone, into adjacent adipose or muscle tissue

200
Q

1) which burns heal by epithelialization (and where does epithelialization begin)
2) which burns can cause rhabdomyolysis with myoglobinuria
3) what is rx of rhabdo

A

1) 1st and superficial 2nd degree burns. epithelialization is primarily from the hair follicles
2) extremely deep burns, electrical burns or compartment syndrome
3) IVF, alkalinize urine (diuretics)

201
Q

Admission criteria for burns- what burns should you admit

A

1) 2nd or 3rd degree burns if
* >20% for all ages or >10% if age 50
* to significant portions of hands, face, feet, genitalia, perineum, or skin overlying major joints
2) 3rd degree burns >5% any age
3) electrical and chemical burns
4) inhalation injury, mechanical trauma, preexisting medical conditions
5) suspect of child abuse or neglect
6) injuries in pts with special social, emotional or long-term rehabilitation needs

202
Q

Burns

1) what age groups is death highest in
2) MC type of burn
3) most likely type to come to hospital and be admitted

A

1) children and elderly (hardest to get away)
2) scald
3) flame burns

203
Q

Assessing percentage of body surface burned (rule of 9’s. How many percent for each in adults and kids:

1) head
2) arms
3) chest
4) back
5) legs
6) perineum
7) palm

A

1) 9% in adult, 18% in kids
2) 9% each arm (18% total)
3) 18% anterior,
4) 18% posterior
5) 18% each leg in adult, 14% each leg in kids
6) 1%
7) 1% each
* can also use pt palm to estimate injury (palm=1%)

204
Q

Parkland formula

1) what % burn can it be used for
2) calculation
3) what type of fluid to use
4) best measure of resucitation
5) in what pts canparkland grossly underestimate volume requirements
6) at what point can you use colloid

A

1) >/=20%
2) 4cc/kg x %burn in first 24 hours (give 1/2 of volume in first 8hr)
3) LR in first 24 hr
4) UOP (0.5-1.0 cc/kg in adults, 2-4cc/kg in children

205
Q

Indications for Escharotomy

1) how soon do you need to perform
2) when should you perform it
3) when to do fasciotomy

A

1) within 4-6hr
2) circumferential deep burns, low temp, weak pulse, dec capillary refill, dec pain sensation or dec neuro fnc in extremity, prbms ventilating pt with significant chest/torso burns
3) if compartment syndrome suspected after escharotomy

206
Q

risk factors for burn

A

v. old or young, ETOH or drug use, smoking, low socioeconomic status, violence, epilepsy

207
Q

Child abuse

1) accounts for what % of burns
2) what history elements should make you suspect
3) physical exam elements

A

1) 15%
2) delayed presentation for care, conflicting hx’s, previous injury
3) sharply demarcated margins, uniform depth, absence of splash marks, dorsal location on hands, very deep localized contact injury

208
Q

lung injury in Burn

1) cause
2) risk factors for airway injury
3) signs/sx on physical exam
4) indications for intubation
5) MC infection and cause of death in pts with >30%BSA burns

A

1) carbonaceous materials and smoke (NOT heat)
2) ETOH, trauma, closed space, rapid combustion, extremes of age, delayed extrication
3) facial burns, wheezing, carbonaceous sputum
4) upper airway stridor or obstruction, worsening hypoxemia (massive volume resuscitation can worsen sx)
5) pneumonia

209
Q
Unusual Burns
1) Acid and alkali burns
a- rx
b- which causes deeper burns and type of necrosis associated with each
2) rx for hydrofluoric acid burns
3) rx for powder burns
4) tar burn rx
5) electical burn complications
6) lightening complications
A

1) a- copious water irrigation
b- alkalis produce deeper burns 2/2 liquefaction necrosis. Acid burns produce coagulation necrosis
2) spread Calcium over wound
3) wipe away before irrigation
4) cool, then wipe away with a lipophilic solvent (adhesive remover)
5) rhabdomyolysis, compartment syndrome, polyneuritis, quadriplegia, transverse myelitis, cataracts, liver necrosis, intestinal or gallbladder pref, pancreatic necrosis
6) Cardiopulmonary arrest 2/2 electrical paralysis of brainstem

210
Q

1st week of burn care

1) when to excise burn wounds and for what burns
2) how much blood loss, skin excision and OR time is maximum for each burn wound excision
3) caloric need in 1st week
4) protein need
5) best non-protein source of calories in burn pts

A

1)

211
Q

Grafts

1) when are skin grafts C/I in burn
2) what type of skin graft is best
3) Split thickness or full thickness skin grafts-
- a) advantages
- b) where is donor skin site regenerated from on STSG
- c) what is blood supply to skin graft for days 0-3
- d) when does neovascularization occur
- e) what areas are unlikely to support the graft
4) thickness of STSG and parts of skin that comprise it

A

1) cx + for beta-hemolytic strep or bacteria >10^5
2) Autograft (STSG or FTSG)
3) a-dec infection, dessication, protein loss, pain, water loss, heat loss and RBC loss compared to dermal substitutes
- b) from hair follicles and skin edges
- c) imbibition (osmotic)
- d)around day 3
- e) poorly vascularized beds including tendon, bone without periosteum and XRT areas
4) 12-15 mm (includes epidermis and part of dermis)

212
Q
1) Homografts
a-give examples
b- when to use and how long they last
2)Xenografts
a- when to use
-why aren't they as good as homografts
3) what is last resort
A
1) a-allografts, cadaveric skin
b- vascularize but are eventually rejected, last 2-4 wks. good temporizing material
2) ie- Porcine
a- last 2 weeks
-don't vascularize
3) Dermal substitutes
213
Q

Grafts

1) when to use meshed grafts
2) reasons to delay autografting
3) MC reason for skin graft loss
4) when to use STSG and advantages and disadvantages
5) when to use FTSG and advantages and disadvantages

A

1) use for back, flank, trunk, arms, legs
2) infection, not enoug skin donor sites, pt septic or unstable, don’t want any more donor sites with concomitant blood loss
3) hematoma or seroma under graft
- apply pressure dressing (cotton balls) to the graft to prevent fluid build up underneath
4) more likely to survive bc easier for imbibition and subsequent revascularization
5) less wound contraction- good for areas such as palms and back of hands

214
Q

what type of graft can improve burn scar hypopigmentation and irregularities

A

dermabrasion thin split thickness grafts

215
Q

Specialized Burn Care

1) Rx of face burns
2) Hand burn rx (superficial and deep)
3) Palms
4) Genitals

A

1)topical abx for 1st week, FTSG for unhealed areas (nonmeshed)
2)superficial- ROM exercises, splint in extension if too much edema
deep- immobilize in extension for 7 days after skin graft (need FTSG), then PT. may need wire fixation of joints if unstable or open
3)try to preserve specialized palmar attachments. splint hand in extension for 7days after FTSG
4) can use meshed STSG

216
Q

Burn wound infection rx

1) role of ppx abx
2) what to apply immediately after burn
3) MC infecting organisms (top 4)
4) what burns are more likely to become infected
5) T/F: Topical agents have decreased incidence of burn wound bacterial infections
6) what has increased in incidence 2/2 topical abx

A

1) none
2) bacitracin or neosporin
3) Pseudomonas> Staph> E. Coli and Enterobacter
4) >30%BSA
5) True
6) candida

217
Q

1) How is immunity impaired in burn pts

A

granulocyte chemotaxis and cell-mediated immunity are impaired

218
Q

Slivadene (Silver Sulfadiazine)

1) side effects
2) what allergy in pts in C/I to use
3) what is it ineffective for
4) what is it effective for
5) penetration and effect on epithelialization

A

1) neutropenia and thrombocytopenia
2) sulfa
3) some Pseudomonas
4) Candida
5) limited eschar penetration, can inhibit epithelialization

219
Q

SIlver Nitrate

1) S/E and what pts is it C/I in
2) penetration
3) what is it ineffective for

A

1) -electrolyte imbalances (hyponatremia, hypochoremia, hypocalcemia, hypokalemia)
- discoloration
- methemoglobinemia (C/I in pts with G6PD def)
2) limited eschar penetration
3) some pseudomonal species and GPC

220
Q

Sulfamylon (mafenide sodium)

1) S/E
2) penetration
3) coverage compared to other burn abx

A

1) metabolic acidosis 2/2 carbonic anhydrase inhibition (-> dec renal conversion of H2CO3 to H2O and CO2)
2) good eschar penetration-> good for burns overlying cartilage
3) broadest spectrum against pseudomonas and GNRs

221
Q

which of the burn abx have painful application

A

sulfamylon

222
Q

Mupirocin

1) good for what type of infection
2) drawback of use

A

1) MRSA

2) expensive

223
Q

WHAT are the following a sign of in burn: peripheral edema, 2nd to 3rd degree burn conversion, hemorrhage into scar, erythema gangrenosum, green fat, black skin around wound, rapid eschar separation, focal discoloration

A

burn wound infection

224
Q

1) MCC of burn wound sepsis
2) MC viral infection in burns
3) amount of bacteria that is cutoff for burn wound infection
4) best way to detect burn wound infection/differentiate from colonization

A

1) pseudomonas
2) HSV
3)

225
Q

Complications after burns- why do the following occur

1) Seizures
2) peripheral neuropathy
3) ectopia and rx
4) eye injury- how to dx and rx
5) symblepharon- what is it and rx
6) heterotopic ossification of tendons rx
7) fractures- rx
8) curling’s ucler- what is it
9) Marjolin’s ulcer- what is it
10) rx of corneal abrasion

A

1) usually iatrogenic 2/2 [Na]
2) 2/2 small vessel injury and demyelination
3) from contraction of burned adnexa (rx- eyelid release)
4) dx- fluorescein staining to find injury, rx- topical flouroquinolone or gentamicin
5) eyelid stuck to conjuctiva. rx-release with glass rod
6) PT, may need OR
7) often need external fixation while burn treatment
8) gastric ulcer 2/2 burn
9) highly malignant sqamous cell CA that arises in chronic non-healing burn wounds or unstable scars
10) topical abx

226
Q

Hypertrophic scar

1) when does it occur
2) what burn injuries is it more common in
3) rx

A

1) 3-4 mo after injury 2/2 inc neovascularization
2) more likely to be deep thermal injuries that take >3wk to heal, heal by contraction and epithelial spread, or heal across flexor surfaces
3) steroid injection into lesion (best), silicone, compression, wait 1-2 yr before scar modification surgery

227
Q

Erythema multiforme and variants

1) list the variants in order from least severe to most severe and how to dx
2) underlying disease in all
3) causes
4) rx
5) T/F- give steroids to these pts

A

1) Erythema Multiforme- least severe (self-limited, target lesions)
Stevens-Johnson syndrome- more serious (

228
Q

Skin- composition of each layer

1) Epidermis
2) Dermis

A

1) primarily cellular (keratinocytes and melanocytes)

2) primarily structural proteins (collagen) for the epidermis

229
Q
1) keratinocytes
a-skin layer
b-where it originates from
c- purpose
2) melanocytes
a-origin
b) skin layer
c) how is melanin transferred bw melanocytes
d) differences in melanocytes bw races
A

1) a) epidermis
b) basal layer
c) provides mechanical barrier
2) a) neuroectodermal (neural crest) cells in basal layer of epidermis
b) basal layer of epidermis
c) have dendritic processes that transfer melanin to neighboring keratinocytes via melanosomes
d) same density of melanocytes. Difference is in melanin production

230
Q

1) Langerhans cells
a- function
b- where they originate from
c- what type of hypersensitivity reaction do they have a role in

A
1)a-dendritic cells (Antigen-presenting cells MHC class II) of skin and mucosa
b- bone marrow
c- contact hypersensitivity reactions (type IV)
231
Q

Sensory nerves of the Skin- what do they sense:

1) pacinian corpuscles
2) Ruffini’s endings
3) Krause’s end-bulbs
4) Meissner’s corpuscles

A

1) pressure
2) warmth
3) cold
4) tactile sense

232
Q

1) role of eccrine sweat glands and type of sweat

2) role of apocrine sweat glands, type of sweat and where the highest concentration is

A

1) aqueous sweat (thermal regulation, usually hypotonic)

2) milky sweat (highest [] in palms and soles), most sweat is the result of sympathetic nervous system via acetylcholine

233
Q

1) t/F: lipid-soluble drugs have decreased skin absorption
2) what is predominant type of collagen in skin and role
3) what is tension and what creates it in skin
4) what is elasticity in skin and what is responsible for creating elasticity
5) what are cushing’s striae

A

1) false, increased absorption
2) Type I, gives tensile strength (70% of dermis)
3) resistance to stretching (Collagen)
4) ability to regain shape- created by branching proteins that can stretch to 2 x nl length
5) red stretch marks in cushing’s: caused by loss of tensile strength and elasticity

234
Q
FLAPS
1) MCC of pedicled or anastomosed free flap necrosis
2) how does tissue expansion occur
1) TRAM flabs:
a- what is it
b- what vessels does it rely on
c-what is most imp determinant of TRAM flap viability
d- potential complications
A

1) venous thrombosis
2) by local recruitment, thinning of the dermis and epidermis mitosis
3)a- Transverse rectus abdominis myocutaneous flap reconstruction
b-superior epigastric vessels
c- periumbilical perforators
d- flap necrosis, ventral hernia, bleeding, infection, abdominal wall weakness

235
Q

Pressure sores- describe the 4 stages and treatment for each

A

Stage I- erythema and pain, no skin loss- keep pressure off
Stage II- partial skin loss with yellow debris- local rx, keep pressure off
Stage III- full-thickness skin loss, subcutaneous fat exposure. rx- sharp debridement, likely need myocutaneous flap
Stage IV- involves boney cortex, muscle. rx- myocutaneous flap

236
Q

UV radiation

1) effect on skin
2) best factor for protecting skin from UV radiation
3) which type is responsible for chronic sun damage

A

1) damages DNA and repair mechanisms. Both a promoter and initiator.
2) melanin
3) UV-B

237
Q

Melanoma

1) % of skin cancers
2) % of skin cancer deaths
3) risk factors for melanoma
4) MC melanoma site in Men
5) in women

A

1) 5%
2) 65%
3) -displastic, atypical or large CONGENITAL nevi- 10% lifetime risk for melanoma
- familial BK mole syndrome- 100% lifetime risk
- Xeroderma pigmentosum
- fair complexion, easy sunburn, intermittent sunburns, previous skin CA, previous XRT
- 10% are familial
4) back
5) legs

238
Q

Melanoma
1) factors that worsen prognosis
2) signs of melanoma and what is most ominous sign
3) MC location for distant met
4) what cells does it originate from
5) how to dx and rx for
a-2cm lesion or cosmetically sensitive area

A

1) men, ulcerated lesions, ocular and mucosal lesions
2) ABCDE- asymmetry (angulation, indentation, notching, ulceration, bleeding), Borders irregular, Color change (darkening), diameter increase, evolving over time. Blue color is most ominous sign
3) lung
4) neural crest cells (melanocytes) in basal layer of epidermis
5)a- dx- excisional bx, rx- resection with margins
b-incisional bx/punch bx. rx- resect with margins

239
Q

What staging should you get for melanoma

A

CT chest/abd/pelvis, LFTs, LDH for all melanoma >/=1mm, examine all possible draining LNs

240
Q

Types of melanoma

1) which is most superficial and what kind of margins do you need for it
2) least aggressive type
3) most common type and where it originates from
4) most aggressive type
5) type MC in african americans
6) type MC on palms/soles

A

1) Melanoma in situ or thin lentigo maligna (hutchinson’s freckle)- just in spuerfical papillary dermis so 0.5-cm margins are ok
2) lentigo meligna melanoma- minimal invasion, radial growth first, elevated nodules
3) superficial spreading melanoma- intermediate malignancy, originates from nevus/sun-exposed areas
4) Nodular- most likely to have mets at time of dx with deepest growth. Verticle growth 1st, bluish-black with smooth borders. can occur anywhere on body
5) Acral lentiginous- v. aggressive
6) Acral lentiginous

241
Q
Management of melanoma
1) recommended surgical margins for tumor
a- in situ
b-2mm
2) management of nodes
a- if clinically positive nodes
b- if clinically negative nodes
3) management of mets
4) vaccines for systemic disease
A

1) a) 0.5-1cm
b) 1cm
c) 1-2cm
d) 2cm margins
2) involved nodes are usually NT, round, hard, 1-2cm
a) resect clinically positive nodes
b) sentinel LN bx if tumor >/=1mm deep
* if anterior head/neck melanoma >/=1mm deep need to include superficial parotidectomy (20% met rate to parotid)
3) resection if isolated and can be resected with low risk procedure
4) IL-2 and tumor vaccines

242
Q

Basal cell carcinoma

1) where does it originate from
2) pathology findings
3) what is the most aggressive type and what does it produce
4) treatment
5) MC location

A

1) epidermis- basal epithelial cells and hair follicles
2) peripheral palisading of nuclei and stromal retraction
3) Morpheaform type- has collagenase production
4) 0.3-0.5cm margins. XRT and chemo of limited benefit for inoperable disease, metastases or neuro/lymphatic/vessel invasion
5) 80% on head and neck

243
Q

Name the type of skin/soft tissue cancer

1) MC malignancy in the U.S.
2) overylying erythema, papulonodular with crust and ulceration, usually red-brown
3) pearly appearance, rolled borders, slow and indolent growth
4) MC soft tissue sarcoma
5) can develop in post-XRT areas or in old burn scars
6) actinic keratoses is a risk factor for
7) may have surrounding induration and satellite nodules

A

1) Basal cell CA (4x more common than squamous skin CA)
2) Squamous cell CA
3) basal cell CA
4) #1 malignant fibrous histiosarcoma, #2liposarcoma
5) squamous cell CA
6) squamous cell CA
7) squamous cell CA

244
Q

Squamous cell carcinoma

1) how common are mets compared to basal cell CA and melanoma
2) risk factors
3) risk factors for mets
4) rx

A

1)mets more frequent than basal cell but less frequent than melanoma
2) actinic keratoses, xeroderma pigmentosum, Bowen’s disease (SCC in situ), atrophic epidermis, arsenics, hydrocarbons (coal tar), chlorophenols, HPV, immunosuppresion, sun exposure, fair skin, previous XRT, previous skin CA
3) poorly differentiated, greater depth, recurrent lesions, immunosuppression
4) 0.5-1cm margins for low risk
high risk- can do Mohs (margin mapping using conservative slices, not for melanoma) when trying to minimize area of resection (ie-if on face)
*regional adenectomy for clinically positive nodes

245
Q

Soft Tissue Sarcoma

1) MC location and age group
2) tumor characteristics
3) what initial imaging do you need
4) dx
5) how does it spread
6) MC site for mets
7) how is it staged

A

1) 50% from extremities, 50% in children (arise from embryonic mesoderm)
2) large, rapid growth, painless
3) CXR to r/o lung mets; MRI before bx to r/o vascular, neuro or bone invasion
4) excisional bx if mass 4cm (need to eventually resect bx skin site if shows sarcoma)
5) hematogenous spread (LN mets rare)
6) lung
7) based on GRADE (not size)

246
Q

Sarcoma treatment

1) margins
2) adjuvant therapy (when to do XRT, type of chemo used and when to use)
3) rx of isolated mets
4) are drains used routinely?

A

1) at least 3-cm margins with at least 1 uninvolved fascial plane. try to perform limb-sparing op. Place clips to mark site of likely recurrence (will XRT these later
2) postop XRT for high-grade tumors, close margins or tumors >5cm
- chemo with doxorubicin-based. For tumors >10cm, may benefit from preop chemo-XRT to allow limb sparing resection
3) if no other evidence of systemic disease resect. Otherwise palliate with XRT
4) no

247
Q
Sarcoma
1) prognosis and why
2) Head and neck sarcomas
a- population they occur in
b- why is rx more difficult
c- MC type
3) visceral and retroperitoneal sarcomas
a-MC type
b-most imp prognostic factor
A

1) poor overall prog 2/2 delay in dx, difficulty with total resection, difficulty getting XRT to pelvic tumors, 40% 5-year survival rate with complete resection
2) a-peds pts
b-proximity to vital structures-> postop XRT for positive or close margins as neg margins may be impossible to obtain
c- rhabdomyosarcoma
3) leiomyosarcomas and liposarcomas

248
Q

Risk factors and associated CA

1) asbestos
2) PVC and arsenic
3) chronic lymphedema

A

1) mesothelioma
2) angiosarcoma
3) lymphangiosarcoma

249
Q

Kaposi’s sarcoma

1) type of sarcoma
2) MC sites and sx
3) MC malignancy in what pts
4) Rx

A

1) vascular sarcoma
2) oral and pharyngeal mucosa-> bleeding and dysphagia
3) AIDS pts
4) rarely a cause of death in AIDS pts. primary goal is palliation.
- AIDS tx (HAART) is best (shrinks tumor)
- consider XRT or intra-lesional vinblastine for local disease
- interferon-alpha for disseminated disease
- surgery for severe intestinal hemorrhage

250
Q

1) #1 soft tissue sarcoma in kids
a-where it occurs and which site has poorest prognosis
b- 2 subtypes (which is MC, which is worst Prog)
c-rx

A

1) Childhood rhabdomyosarcoma
a-head/neck, GU, extremities and trunk (poorest prog)
b- embryonal subtype is most common, Alveolar subtype-worst prognosis
c-surgery, doxorubicin-based chemo

251
Q
Bone sarcomas
1) T/F- rarely metastasize
2) Osteosarcoma
a-MC location
b- cell type it originates from
c-MC age group
A

1) False, most are metastatic at time of dx
2)a- increased incidence around knee
b-metaphyseal cells
c- children

252
Q

Genetic syndromes for soft tissue tumors: what tumors are seen in the following:

1) Neurofibromatosis
2) Li-fraumeni syndrome
3) hereditary retinoblastoma
4) Tuberous sclerosis
5) Gardners syndrome

A

1) CNS tumor, peripheral sheath tumor, pheo
2) childhood rhabdomyosarcoma and many others
3) other sarcomas
4) angiomyolipomas
5) familial adenomatous polyposis, and intra-abdominal desmoid tumors

253
Q

other skin conditions and rx

1) lip lacerations
2) Xanthoma- (and what cell type dose it contain)
3) Warts (verruca vulgaris)
4) growth associated with cafe-au-lait spots, axillary freckling, peripheral nerve and CNS tumors

A

1) align vermillion border
2) yellow, contains histiocytes. rx- excise
3) viral origin. initial rx- liquid nitrogen
4) Neuromas (neurofibromatosis and von Reckinghausen’s syndrome)

254
Q

Name the skin condition

1) keratoses- premalignant in sun-damaged areas, need excisional bx if suspicious
2) keratoses-not premalignant skin lesion on trunk on elderly, can be dark
3) keratoses-associated with squamous cell ca
4) neuroendocrine skin ca, very aggressive and malignant with early regional and systemic spread. has red to purple papulonodule or indurated plaque. Also name the components of the tumor
5) painful benign tumor composed of blood vessels and nerves, MC in terminal aspect of digit. What is rx?

A

1) Actinic Keratosis
2) Seborrheic keratosis
3) arsenical keratosis
4) Merkel cell CA- components are neuron specific enolase (NSE), cytokeratin, neurofilament protein
5) Glomus cell tumor. rx- tumor excision

255
Q

Desmoid tumors

1) where do they occur
2) when do they occur
3) prognosis
4) rx

A

1 and 2) occur in fascial planes

  • anterior abdominal wall (MC)- seen after pregnancy, trauma or surgery
  • intra-abdominal- associated with Gardner’s syndrome and retroperitoneal fibrosis (oten encases bowel making it hard to get en block resection)
    3) high risk of local recurrence, benign but v locally invasive, no distant spread
    4) surgery if possible, chemo (sulindac, tamoxifen) if vital structure involved or too much bowel would be taken
256
Q

Bowens Disease

1) associated CA
2) associated virus
3) rx
4) T/F- wide local excision is an good treatment

A

1) SCC in situ, 10% turn into invasive SCC
2) HPV
3) imiquimod, cautery ablation, topical 5-FU, regular bx to r/o CA
4) F- void wide local excision if possible (high recurrence rate with HPV)

257
Q

Keratoacanthoma

1) characteristics
2) benign or malignant
3) dx
4) rx

A

1) rapid growth, rolled edges, crater filled with keratin, involutes spontaneously over months. can be confused with SCC
2) benign
3) biopsy to be sure not SCC
4) excise if small; if large bx and observe

258
Q

Hyperhydrosis

1) what is it
2) rx

A

1) inc sweating, esp noticible in palms

2) thoracic sympathectomy if refractory to varient of antiperspirants

259
Q

Hydradenitis

1) what is it
2) MC organisms involved
3) rx

A

1) infection of the apocrine sweat glands, usually in axilla and groin regions
2) staph/strep are MC organisms
3) 1st- abx and improved hygeine. May need surgery to remove skin and associated sweat glands

260
Q

Benign cysts- name them

1) MC, completely mature epidermis with creamy keratin material
2) in scalp, no epidermis
3) over tendons, usually over wrist, filled with collagen material
4) midline, intra-abdominal and sacral lesions usual, need resection due to malignancy risk
5) congenital coccygeal sinus with ingrown hair, gets infected and needs to be excised

A

1) epidermal inclusion cyst
2) Trichilemmal cyst
3) Ganglion cyst
4) dermoid cyst
5) pilonidal cyst