trauma, inflammation, wound healing, burn, skin ICU Flashcards
(260 cards)
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
2
Q
role of macrophages in wound healing- what do they release
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dominant role, release PDGF (plt derived GF) and cytokines (IL-1 and TNF-alpha)
3
Q
Growth and activating factors in inflammation: role of the following1) 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 healing2, 3) Chemotactic, activates fibroblasts, angiogenesis, epithelialization4) generated by phospholipase in endothelium (a phospholipid) which is chemotactic for inflam cells and inc adhesion mlqs
4
Q
1) what are the chemotactic factors for inflammatory cells2) for fibroblasts3) angiogenesis factors4) epithelialization factors
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1) PDGF, IL-8, LTB-4, C5a and C3a, PAF2) PDGF, EGF, FGF3) PDGF, EGF, FGF, IL-8 and hypoxia4) PDGF, EGF, FGF
5
Q
1) How long do PMNs last in tissues and in blood2) how long do platelets last3) lymphocyte role in inflammation
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1) 1-2 days in tissues, 7 days in blood2) 7-10 days3) involved in chronic inflammation (T cells) and Ab production (B cells)
6
Q
Type 1 hypersensitivity rx:1) role of eosinophils2) what type of infections have increased eosinophils3) role of basophils, where aren’t they found4) Mast cells role5) role of histamine6) role of bradykinin7) what inactivates bradykinin and where is it found
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1) release major basic protien once bound to allergin-> stimulates basophils and mast cells to release histamine2) parasitic3) main source of histamine in blood (not in tissue)4) main source of histamine in tissues, primary cell in type 1 hypersensitivity5) vasodilation, tissue edema, postcapillary leakage; primary effector type in type I hypersensitivity rxs (allergic rxs)6) peripheral vasodilation, increased permeability, pain, pulm vasoconstriction7) Angiotensin-converting enzyme located in lung
7
Q
Nitric oxide1) what is its precursor2) what does it activate and end effect3) another name for it4) what has the opposite effect of NO
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1) Arginine2) guanulate cyclase-> inc cGMP-> vascular smooth muscle dilation3) endothelium-derived relaxing factor4) Endothelin-> vascular smooth muscle constriction
8
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cytokines1) main initial cytokine resonse to injury and infection is release of
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1) TNF-alpha and IL-1
9
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cytokines1) largest producer of TNF2) role of TNF-alpha3) what can high concentrations of TNF-a cause4) largest producer of IL-15) effects of IL-1 and what does it synergize with6) which cytokine causes cachexia in CA pts7) which cytokine is responsible for fever and how?8) how do NSAIDS reduce fever9) role of IL-6
A
1) Macrophages2) increases adhesion mlqs, procoagulant, activates neutrophils and macs-> more cytokine production and cell recruitment3) circulatory collapse and multisystem organ failure4) macs5) same as TNF-alpha, synergizes with TNF-alpha6) TNF-alpha7) IL-1 (how alveolar macs cause fever with atelectasis), PGE2 mediated in hypothalamus8) reduce PGE2 synthesis9) increases hepatic acute phase proteins (CRP, amyloid A -> activate complement), decreases albumin, pre-albumin and transferrin
10
Q
Interferons1) what are they released by2) what stimulates release3) effect of release
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1) lymphocytes2) viral infection or other stimulants3) activate macs, NK cells and cytotoxic T cells-> inhibit viral replication
11
Q
Cell adhesion mlqs- where are they located, what they bind and type of adhesion1)Selectins2) Beta-2 integrins (CD11/18 molecules)3) ICAM, VCAM, PECAM, ELAM
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1) L-selectins on leukocytes bind E- (endothelial) and P-(platelet) selectins-> rolling adhesion2) on leukocytes, bind ICAM etc-> anchoring adhesion3) on endothelial cells, bind beta-2 integrin mlqs located on leukocytes and platelets. Also involved in transendothelial migration
12
Q
Complement- what activates the following pathways and what factors are only in each one1) classic pathway2) alternative pathway3) what complement factor is common to both pathways4) what electrolyte is required for both pathways
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1) (IgG or IgM) Ag-Ab complex activates. Factors C1, C2, C42) endotoxin, bacteria, other stimuli activate. Factors B, D and P (properdin)3) C34) Mg
13
Q
Complement1) factors that are anaphylatoxins and actions2) membrane attack complex factors and actions3) opsonization factors and action4) factors involved in chemotaxis for inflammatory cells
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1) C3a, C4a, C5a. increase vascular permeability, bronchoconstriction and activate mast cells and basophils2) C5b-9b-> cell lysis (usually bacteria) by creating hole in the membrane3) C3b and C4b- targets Ag for immune response4) C3a and C5a
14
Q
Prostaglandins1) precursor2) LTC4, LTD4, and LTE4 actions3) LTB4 actions
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1) arachidonic precursors2) slow-reacting substances of anaphylaxis, bronchoconstriction, vasoconstriction followed by increased permeability3) chemotactic for inflammatory cells
15
Q
Catecholamines1) when after injury do they peak2) where is norepinephrine released?2) where is epinephrine released?
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1) 24-48hours2) sympathetic postganglionic neurons and adrenal medulla3) adrenal medulla (neural response to injury)
16
Q
T/F thyroid hormone plays a major role in injury/inflammation
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false
17
Q
neuroendocrine response to injury
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afferent nerves from site of injury stimulate CRF, ACTH, ADH, growth hormone, epi and norepi release
18
Q
CXC chemokines1) what are they2) what is their role3)what does CXC stand for
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1) IL-8 and platelet factor 42) chemotaxis, angiogenesis, wound healing3) C=cysteine, X= another amino acid
19
Q
1) what oxidants are generated in inflammation2) what are cellular defenses against oxidative species
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1) superoxide anion radical (NADPH oxidase), hydrogen peroxide (xanthine oxidase)2)superoxide anion radical- defense is superoxide dismutasehydrogen peroxide- defence is glutathione peroxidase, catalase
20
Q
primary mediator of reperfusion injury
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PMNs
21
Q
Chronic granulomatous disease:1) enzyme defect and result
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NADPH-oxidase system enzyme defect in PMNs-> decreased superoxide radical formation-> increased infection from bacteria and fungi
22
Q
stages of wound healing- cells involved, what happens during each and time frame1)Inflammation2)proliferation3) remodeling
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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 13)3wk to 1 year. decreased vascularity. net amount of collagen unchanged despite sig production and degradation
23
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rate of1) epithelialization2) peripheral nerve regeneration
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1)1-2 mm/day2) 1mm/day
24
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order of cell arrival in wound: PMNs, lymphoctes, macs, fibroblasts, platelets
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1) platelets2) PMNs3) Macrophages4) lymphocytes5) fibroblasts
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role of the following in wound healing1) macrophages2) fibronectin2) fibroblasts
1) release growth factors, cytokines, etc2) chemotactic for macs; anchors fibroblasts3) replace fibronectin-fibrin with collagen
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predominant cell type by day:1) day 0-22) days 3-43)days 5+
1)PMNs2)macrophages3)fibroblasts
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1) composition of the platelet plug2) composition of provisional matrix3) what wounds show accelerated wound healing
1) platelets and fibrin2) platelets, fibrin and fibronectin3)reopened wounds bc healing cells already present
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Open wounds1) most imp factor in healing open wounds2) where does epithelium migrate from
1) epithelial integrity2)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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closed wounds1)most imp factor in healing
tensile strength- depends on collagen eposition and cross-linking of collagen
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1) which layer of bowel provides the strength2) what is weakest time point for small bowel anastamosis
1) submucosa2) 3-5days
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myofibroblasts- what are they, how do they communicate and what part of wound healing are they involved in
smooth muscle cell fibroblast. communicate by gap junction. Involved in wound contraction and healing by secondary intention.
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t/F: perineum has better wound contraction than leg
true
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which type of collagen is:1)MC type, found in skin, bone and tendons. Primary collagen in healed wound2) widepread, particularly found in cornea3) increased in healing wound, also in blood vessels and skin4) basement membranes5) cartilage
1) type I2) type V3) type III4) type IV4) type II
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1) what aa improves wound tensile strength2) which of the following are not required for hydroxylation and subsequent cross-linking of proline residues: Alpha-ketoglutarate, Magnesium, Vitamin C, Oxygen and Iron
1) proline cross-linking. collagen has proline every 3rd aa.2) Magnesium
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cause of scurvy
Vit C deficiency
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1) max tensile strength of healed wound compared to pre-wound skin2) what is predominant collagen over days 1-23) collagen over days 3-44) at what point has all of the type of collagen in #2 been replaced by the collagen in #35)when does wound reach max tensile strength6) what inhibits collagen cross-linking
1) 80%2) III3) I4) 3 weeks5) 8 weeks6) d-Penicillamine
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optimal wound healing1) is dry or moist environment better2)how to inc O2 delivery3)effect of edema4) which vitamin counteracts the effects of steroids on wound healing5) what amount of bacteria impedes wound healing and why6) what drugs impair wound healing in 1st 14d after injury
1) moist2) optimize fluids, no smoking, pain control, supp O2, arterial revascularization3) avoid it by leg elevation4) vit A5) >10^5 2/2 dec O2 content, collagen lysis, prolonged inflammation6) cytotoxic drugs- 5FU, methotrexate, cyclosporin, FK-506
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1) how does DM contribute to poor wound healing2) what albumin level sig risk for poor wound healing3)mechanism via which steroids inhibit wound healing
1)impedes early-phase inflammation response (hyperglycemia causes poor leukocyte chemotaxis)2) dec tensile strength
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Diseases associated with abnormal wound healing- name the defect1) Osteogenesis Imperfecta2) Ehlers-Danlos syndrome3) Marfan's syndrome4) Epidermolysis bullosa and rx5) Scurvy6) what extraintestinal manifestation of IBD is associated with abnl wound healing
1) Type I collagen defect2) 10 types identifies, all collagen3) fibrillin defect (connective tissue protein)4) excessive fibroblasts. rx- phenytoin5) vit C def6) Pyoderma gangrenosum
40
Diabetic foot ulcers1) where they most commonly occur2) 2/2 what?3) cause of 90% of leg ulcers and rx
1) Charcot's joint (2nd MTP joint) MC, also on toes2)peripheral neuropathy (can't feel-> pressure from walking-> ischemia)3)venous insufficiency. rx- Unna boot (elastic wrap)
41
1) what are scars made of2) when to do scar revisions3) what pts heal with little to no scarring
1) proteoglycans, hyaluronic acid and water2) wait 1 year to allow for maturation, may improve with age3) infants
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1) how does cartilage get nutrients and oxygen2) does denervation effect wound healing3) does chemo affect wound healing
1) diffusion. Doesn't have blood vessels2)no3) no effect on healing after 14 days
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Keloids1) inheritance pattern2) difference bw them and hypertrophic scars3) rx4) rx hypertrophic scars5) when do hypertrophic scars occur
1) autosomal dominant, more common in dark skinned ppl2) in keloids collagen goes beyond original scar where as hypertrophic scar collagen is confined to original scar3) intra-lesion steroid injection, silicone, pressure garments, XRT4) steroid injection, silicone, pressure garments5) burns or wounds that take a long time to heal
44
Platelet granules:1) what are the alpha granules and what is their role2) dense granules3) platelet aggregation factors
1) platelet factor 4- aggregationbeta thrombomodulin- binds thrombinplatelet derived growth factor- chemoattractantTransforming growth factor beta (TGF-beta)- modulates above responses2) adenosine, serotonin and Ca3) TXA2, thrombin, platelet factor 4
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Trauma deaths by time after injury1) when does 1st peak occur and associated injuries2) when does 2nd peak occur and associated injuries3) when does 3rd peak occur and associated injuries
1) 0-30min- lac of heart, aorta, brain, brainstem, spinal cord. no hope to save2)30min-4hr-head injury (#1), hemorrhage (#2)- golden hour. pts can be saved with rapid assessment3)days to weeks-multi system organ failure and sepsis
46
1) what % of trauma is blunt injury and what is most commonly injured organ2) most commonly injured organ in penetrating injury3) biggest predictors of survival after fall4) what is the median lethal dose for fall (LD50)
1) 80%. Liver (although some texts say spleen)2) small bowel (some texts say liver3) age and body orientation4) 4 stories
47
kinetic energy calculation
1/2 MV^2; M=mass, V=velocity
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1) when will you see a change in BP with hemorrhage?2) resuscitation- when to switch to blood
1) >30% blood loss2) 2L LR then switch to blood
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MC cause of 1) death after reaching ER alive2) death long term3) upper airway obstruction
1) head injury2) infection3) tongue
50
1) injuries from seat belts2) best site for cutdown for venous access3) positive DPL- what makes it +4) what does DPL miss5) where to do DPL if pelvic fracture6) when might you get a false negative FAST
1) small bowel perf, lumbar spine fx, sternal fx2) saphenous vein at ankle3) >10cc blood, >100,000 RBCs/cc, food particles, bile, bacteria, >500WBC/cc4) retroperitoneal bleeds, contained hematomas5) supraumbilical6) free fluid
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1) where might pts with hypoTN and neg FAST be bleeding2) when do you need a CT scan following blunt trauma3) what might a CT scan miss in trauma4) 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
1) pelvic fx, chest, extremity2) abdominal pain, need for gen anesthesia, closed head injury, intoxicants on board, paraplegia, distracting injury, hematuria, negative DPL3) hollow viscus or diaphragm injury4) negative FAST
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1) abdominal injuries- when do you need to go to the OR2) first step after pt with penetrating anterior abd trauma, no obv peritonitis/eviscer and local wound exploration shows fascial violation or equivocal
1) any penetrating abd injury (GSW, evisceration), local wound exploration with fascial violation or equivocal. If no fascial violation can observe2) diagnostic laparoscopy. If peritoneal violation-> explore. if no peritoneal violation-> d/c after recovery
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Abdominal compartment syndrome1) when do you see it2) bladder pressure3) cause of decreased cardiac output4) result of low Cardiac output5) effect on ventilation/why?6) rx
1) after massive fluid resuscitation, trauma or abdominal surgery2) >25-303) IVC compression4) visceral and renal malperfusion-> dec UOP5) upward displacement of diaphragm affects ventilaton6) decompressive laparotomy
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1) when to use Pneumatic antishock garment2) when to do ER thoracotomy aftera-blunt traumab-penetrating tauma3) how to perform thoracotomy4) when should pt be transfered to OR after ED thoracotomy
1) pts with SBP70mmHg, if not situation is futile
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1) when do catecholamines peak after injury2) change in ADH, ACTH and glucagon after trauma3) type specific blood- why do ppl get reactions to it4)What should you do for all GCS
1) 24-48 hours2) fight or flight response-> increase ADH, etc3) blood is nonscreened, non cross-matched so can get effects from abs to HLA minor Ag in the donated blood4) Head CT5) Intubate6) ICP monitor
56
Epidural hematoma1) artery injured MC2) shape on head CT3) clinical picture4) when to operate
1) middle meningeal artery2) lenticular deformity3) LOC-> lucid interval-> sudden deterioration (vomiting, LOC, restlessness)4) significant neurologic degeneration or significant mass effect (shift >5 mm)
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subderal hematoma1) vessel injured2) shape on CT3) when to go to OR4) who gets chronic subdural hematomas
1) tearing of venous plexus (bridging veins bw dura and arachnoid)2) crescent-shaped3) sig neurologic degeneration or mass effect (>1cm shift)
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intracerebral hematoma-1) where does it usually occur2) when to operate3) type of injury with coup and countrecoup lesions
1) frontal or temporal2) significant mass effect3) cerebral contusion
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1) treatment for traumatic intraventricular hemorrhage2) how to dxs diffuse axonal injury, treatment and prognosis
1) ventriculostomy if causing hydrocephalus2)MRI better than CT. Tx- supportive, craniectomy if elevated ICP, very poor prognosis
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How to calculate Cerbral Perfusion Pressure (CPP)
CPP=MAP- ICP (intracranial pressure)
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When to use an ICP monitor
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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1) Normal ICP2) When to treat ICP3) where to keep CPP
1) 102) >203) >60
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How to increases Cerbral perfusion pressure? which of the following won't:sedation and paralysislower head of bedrelative hyperventilation (CO2 30-35)MannitolBarbituate comaventriculostomy with CSF drainagecraniotomy decompression
must RAISE the head of the bed to increase CPP
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1) which side is the temporal pressure increased in for a dilated pupil2)when does peak ICP occur3) what can be given prophylactically to prevent seizures with moderate to severe head injury4) how to dose mannitol5) what level to keep Na and serum Osm in head injury pts
1) same side (CNIII, oculomotor compression)2) 48-72hr after injury3) keppra and fosphenytoin4) 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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1) What do Racoon eyes signal?2) Battle's sign? and what is management3) Nerve injured in basal skull fracture4) nerves injured in temporal skull fx5) what kind of blows are associated with temporal skull fx6) when to operate for skull fx7) cause of coagulopthy in traumatic brain injury8) most common site of fascial nerve injury
1) per-orbital ecchymosis, anterior fossa fx2) 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 needed3) CN VII4) CNVII and VIII (vestibulocochlear nerve)5) orbital or lateral skull blows6) if signficantly depressed (>1cm), contaminated, or persistant CSF leak no responding to conservative therapy (lumbar CSF drainage)7) release of tissue factor8) geniculate ganglion
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Spine trauma1) Jefferson fracture- what level, cause, rx2) Hangman's fracture- level, cause, rx3)odontoid fx- level, 3 types and rx4) Facet fx/dislocation- how they occur and what else can be injured?
1) C1 burst 2/2 axial loading. Tx- rigid collar2) C2- caused by distraction and extension. rx- traction and halo3) 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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Thoracolumbar Spine1) what comprises the 3 columns of the thoracolumbar spine?2) when is thoracolumbar spine considered unstable3) what column is affected by compression (wedge) fx?4) what fx is unstable and rx5) what fx is stable
1) Anterior- anterior logitudinal ligament and anterior 1/2 of vertebral bodyMiddle- posterior 1/2 of vertebral body and posterior logitudinal ligamentPosterior- facet joints, lamina, spinous processes, interspinous ligament2) if >1 column disrupted3) anterior column only, stable4) Burst fractures (>1 column) require spinal fusion5) Compression (wedge) fx
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1) bones that are at risk for injury in upright fall2) when in spinal injury should you get an MRI?3) indications for emergent spinal decompression
1) calcaneous, lumbar, wrist/forearm2) neuro defects w/o bony injury to eval for ligamentous injury3) fracture/dislocation not reducible with distraction, open fx, soft tissue or bony compression of cord, progressive neuro dysfnc
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1) most common cause of facial nerve injury in trauma2) technique for repairing facial lacerations3) Le Fort Classification of Facial Fractures I-III. describe. what is the rx
1) temporal bone fx2) preserve skin and don't trim edges3) 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 ILe Fort III-lateral orbital walls (- -). rx-suspension wiring to stablize frontal bone, may need external fixation
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1) what type of facial fx have a 70% CSF leak and rx of CSF leak2) rx of nose bleeds
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 fail2) anterior- packingposterior- try balloon tamponade 1st. May need angioembolization of internal maxillary artery or ethmoidal artery
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1) rx of orbital blowout fx and who needs repair2) Tripod fx- what is it and how to repair3) T/F: pts with maxillofacial fx are at high risk for cervical spine injuries
1) repair pts with upward gaze or diplopia with upward vision. rx- restoration of orbital floor with bone fragments or bone graft2) Zygomatic bone fx- ORIF for cosmesis3) True
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1) what is the #1 indicator of Mandibular injury2) how to diagnose mandibular injury3) rx
1) malocclusion2) fine0cut facial CT with reconstruction3) IMF (intramaxillary fixation- metal arch bars to upper and lower dental arches for 6-8wks) or ORIF
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Neck Trauma1) 3 neck zones of injury2) study to get in asymptomatic pt with blunt injury3) 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
1)ZOne I- clavical to cricoid cartilage. Zone II- Cricoid to angle of mandible. Zone III- angle of mandible to base of skull2) neck CT3) 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 lesionsZOne II-neck exploration in ORZone III-angiography and laryngoscopy. May need jaw subluxatin/digastric and SCM muscle release/mastoid sinus resection to reach vascular injuries in this location4) neck exploration in OR immediately
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Esophageal injury1) how to diagnose2) rx of contained injuries3) rx of non-contained injuries if:a- small injury, minimal contaminationb- extensive injury or contamination4) Approach to esophageal injuries in:a- the neckb- upper 2/3 of thoracic esophagusc- lower 1/3 of thoracic esophagus
1) hardest neck injury to find. Do esophagoscopy and esophagogram (finds 95% of injuries when combined)2) observe3) 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
75
Laryngeal fracture and tracheal injuries1) sx2) are these non-urgent, urgent or emergent?3) rx
1) stridor, crepitus, resp compramise2) emergent3) 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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1) rx of thyroid gland injury2) rx of recurrent laryngeal nerve injury3) management of shotgun injures to neck4) of vertebral artery bleeds5) common carotid bleeds and complication
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 evaluation4) embolize or ligate without any sequela5) ligation causes stroke in 20%
77
Chest trauma:1) when to go to OR for thoracotomy after CT placement2) how quickly do you need to drain blood in hemothorax and why3) management of unresolved hemothorax after 2 well-placed drains
1) >1500 cc after initial insertion in one side, >250cc/hr for 3 hours, >2500cc/24 hr or bleeding with instability2)
78
Sucking chest wound1) how big does it need to be to be clinically significant2) rx
1) >2/3 diameter of trachea2) cover wound with dressing that has tape on 3 sides to prevent tension pneumo
79
1) what should you think about if pt has worsening oxygenation after chest tube placement2) T/F Bronchus injuries are more common on the right3) dx of thracheobronchial injury4) rx- indications for repair and how to repair (type of incision)
1) tracheobronchial injury. one of the few indications to clamp NGT2) True3) bronchoscopy4) 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
80
Injuries of the diaphragm1) where are they more common?2) more common in blunt or penetrating trauma?3) signs on CXR4) type of approach for repair
1) on left2) blunt trauma3) air-fluid level in chest from stomach herniation4) transabdominal if 1wk bc will have to take down adhesions in the chest. May need mesh
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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
1) aortic transection
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1) where is aortic transection most common2) how good is CXR at diagnosing?3) when should you do aortic evaluation if nl CXR4) Dx of aortic transection5) operative approach6) if pt has aortic transection and + DPL twhat should be addressed first
1) ligamentum arteriosum (just distal to subclavian takeoff) is MC. also seen near ortic valve and where aorta traverses diaphragm2) nl in 5%3) significant mechanism (head on car crash >45 mph, fall >15ft)4) CT angio chest5) 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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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
aortic transection
84
Aortic transection1) MC place for tear and other places2) How good is CXR at detecting3) Diagnostic study4) operative approach5) T/F: you can not defer treatment to treat other life-threatening injuries or positive DPL first
1) ligamentum arteriosum just distal to subclavian takeoff (MC). Also, near aortic valve where aorta traverses diaphragm2) misses 5%, need evaluation of aorta for pts with sig mech (head on car crash >45mph or fall >15ft3) CT angio chest4) 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
85
what operative approach should you use for the following injuries:1) ascending aorta, innominate artery, proximal right subclavian artery, inominate vein, proximal left common carotid2) left subclavian artery, descending aorta3) distal right subclavian artery
1) median sternotomy2) left thoracotomy3) midclavicular incision with removal of medial clavical
86
Myocardial contusion1) what is MC cause of death2) MC arrhythmia seen3) how long to monitor and when is risk highest
1) v-tach and v-fib2) SVT3) risk highest in 1st 24 hours, monitor for 24-48hrs
87
1) flail chest ddefinition and rx and biggest pulm impairment2) T/F: aspiration produces immediate CXR findings
1) 2+ consecutive rib fx with 2+ break sites. rx- occlusive dressing taped at 3 sides. can result in underlying pulm contusion2) false- may not be immediate
88
Penetrating Chest injuries1) first imaging study in stable pts2) penetrating "box" injuries- location and studies to do to dx injuries3) penetrating chest wound outside box w/o pneumo or hemothorax- what to do4) what to do if find blood on doing pericardial window?5) when do you need to go to OR for laparoscopy or laparotomy
1) CXR (if pneumothorax or hemothorax place a chest tube)2) borders are clavicles, xiphoid process, nipples-do pericardial window, bronchoscopy, esophagoschopy, barium swallow3) need chest tube if pt req intubation otherwise just follow serial CXR4) median sternotomy to fix possible injury to heart or great vessels, place pericardial drain5) penetrating injuries anterior-medial to midaxillary line below the nipples (may also need penetrating box injury eval)
89
1) traumatic causes of cardiogenic shock2) tension pneumo: what do you see for BP, airway pressures, breath sounds, neck veins, trachea3) cause of cardiac compromise in tension pneumo4) pts with what type of fx are at high risk for cardiac contusion5) what fx put pt at high risk for aortic transection
1) tension pneumo, cardiac tamponade, cardiac contusion2) hypotension, inc airway pressures, dec breath sounds, bulging neck veins, tracheal shift3) 2/2 ICV/SVC compression-> dec venous return4) sternal5) 1st and 2nd rib fx
90
Pelvic trauma1) what to do with hemodynamically unstable with pelvic fx and negative DPL, CXR and not other signs of blood loss or reason for shock2) what other structures may be injured3) 3 types of fx, mortality and bld loss
1) stabilize pelvis (C-clamp, external fixator, sheet) and go to angio for embolization2) genitourinary and abdominal injuries3) Type I- crush, unstable, mortality 20-30%, blood loss >10unitsType II- verticle incision completely transecting, unstable, mortality 8-12%, blood loss 2-10uType III- fx in rami, etc that doesn't transect entire pelvis. stable.
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Pelvic trauma1) can repair be delayed for other injuries2) Intra-op management of penetrating injury pelvic hematomas3) Intra-op management of blunt injury pelvic hematomas
1) yes2) 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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Duodenal Trauma1) MC cause of injury2) MC area injured3) MC rx4) for what section is segmental resection with primary end-to-end closure not possible5) mortality6) MC source of morbidity
1) blunt (crash or deceleration injury)2) 2nd portion (descending portion near ampulla of Vater)3) 80% get debridement and primary closure4) second portion of duodenum5) 25%6) fistulas
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1) rx of intra-op paraduodenal hematomas and where they are located with blunt injury2) presentation, dx and rx of paraduodenal hemotomas
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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1) what to do if at laparotomy and duodenal injury suspected
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
95
1) how to diagnoses suspected duodenal injury
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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1)Tx of duodenal trauma2) What to do if in 2nd portion of duodenum and can't do primary repair->
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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1) when to remove drains after duodenal injury repair1) rx of fistulas
1) when pt tol diet without increasing drainage2) bowel rest, TPN, octreotide, conservative management for 4-6wks.
98
Colon trauma1) MC type of injury2) repair for:a- right colonb- transverse colonc-left colond-paracolonic hematomas
1) penetrating injury2) a and b- perform primary repair/anastomosisc-primary repair/anastamosis, diverting ileostomyd-both blunt and penetrating need to be opened
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rectal trauma1) MC type of injury2) repair of high rectal injuries3) repair of low rectal injuries (<5cm)4) when to place diverting ileostomy
1) penetrating2) extraperitoneal- generally not repaired bc of inaccessibility. can do serial debridement or consider diverting ileostomyintraperitoneal- rx- repair defect, presacral drainage, consider diverting ileostomy3) repair transanally4) shock, gross contamination, extensive injury
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Liver trauma1) T/F- often need to do lobectomy2) 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
1) F2) yes- gastroduodenal artery has collaterals3)clamping portal triad. Does not stop bleeding from hepatic veins4) for retrohepatic IVC injury. Allows for control while performing repair5) explore
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Liver trauma cont1) ideal repair of common biled duct injury2) repair of portal vein injury and should you ligate portal vein3) when to use omental graft4) should you leave drains?
1) if 50% circumference or complex injury- do choledochojejunostomy. May need intraop cholangiogram to define injury. ALSO- place drains bc 10% of duct anastamoses leak2) 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% mortality3) place in liver lac to help with bleeding and prevent bile leaks.4) yes!
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Conservative management of blunt liver injuries1) activity level allowed for pt2) when should you go to the OR
1) bedrest for 5 days2) -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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spleen injury1) how long does it take spleen to fully heal2) when is postsplenectomy sepsis risk greatest3) T/F splenic salvage is associated with increased transfusions4) when to go to the OR/when has conservative management failed5) activity level with conservative management6) in what pts is threshold for splenectomy much higher7) what immunizations do you need after trauma splenectomy
1) 6 weeks2) greatest within 2 years of splenectomy3) true4) -pt unstable despite aggressive fluid resucitation (HR>120 or SBP2u needed to keep HCT>25)- if active blush on CT abd or pseudoaneurysm5) bedrest x 5days6) children7) Strept pneumo (pneumococcal), H flu (Hib), meningococcal
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Pancreatic Trauma1) MC injury type2) what type of injury can cause pancreatic duct fractures and typical orientation of fx3) what are CT signs of injury4)rx of pancreatic contusion5) rx of distal pancreatic duct injury6) rx of pancreatic head injury that is not reparable7) how do you decide bw a whipple vs distal pancreatectomy
1) penetrating accounts fo 80%2) bunt injury-> fx perpendicular to duct3) edema or necrosis of peripancreatic fat4) leave if stable, place drains if in OR5) distal pancreatectomy (can take up to 80% of the gland)6) place drains initially. delayed whipple or possible ERCP with stent may eventually be necessary7) based on duct injury in relation to SMV
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Pancreatic Trauma1) should you leave drains?2) what maneuver helps evaluate the pancreas operatively3) rx for pancreatic hematoma4) what lab value should make you suspect missed pancreatic injury5) when to use ERCP
1) YES!2) Kocher3) both blunt and penetrating need to be opened4) rising or persistent amylase5) good at finding ductal injuries and may be able to treat with temporary stent
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Vascular Trauma1) repair before or after ortho repair?2) when to go to the OR3) when to go to angio4) indications for saphenous vein graft5) what vein injuries need repair?6) what should you consider doing if ischemia>4-6hr
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 injuries5) vena cava, femoral, popliteal, brachiocephalic, subclavian and axillary6) fasciotomy
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1) rx for transection of single artery in the calf in otherwise healthy pt2) at what compartment pressure should you consider compartment syndrome3) clinical signs of compartment syndrome4) most common injuries leading to comp syndrome5) how to rx
1) ligate2) >20mmHg or clinical exam3) 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 4-6hr5) fasciotomy- incisions are anterolateral and posteromedial
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IVC injury1) how to best control bleeding, should you clamp it?2) how to repair
1) proximal and distal pressure- don't clamp bc can tear2) 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)
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Ortho trauma1) how much blood can be lost from femur fx2) 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 fx3) pt w femoral neck fx are at high risk for?4) rx of long bone fx or dislocation with loss of pulse or weak pulsea-first stepb- if pulse doesn't return->c- if pulse is weak ->4) rx monogram for knee dislocations5) fx associated with upright falls
1) >2L2) calcanear fx, unless associated with lumbar fx with neuro impairment3) avascular necrosis4) a- Immediate reduction and reassessment of pulseb- go to OR for vascular bypass or repair (may need OR angio to define injury)c-go to antio4) all knee dislocations go to angiogram unless pulse is absent in which case you go to OR5) lumbar, distal forearm (radial ulnar), calcaneous
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what is the concomitant nerve/artery injury UE1) Anterior shoulder disloc2) Posterior shoulder disloc3) Proximal humerus fx4) midshaft humerus fx (or spiral humerus fx)5) distal humerus fx (supracondylar6) Elbow dislocation7) Distal radius fx
1) axillary nerve2) axillary artery3) axillary nerve4) radial nerve5) brachial artery6) brachial artery7) median nerve
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what is the concomitant nerve/artery injury LE1) anterior hip disloc2) posterior hip disloc3) distal (supracondylar) femur fx4) posterior knee disloc5) fibula neck fx
1) femoral artery2) sciatic nerve3, 4) popliteal artery5) common peroneal nerve
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what is the concomitant nerve/artery/organ injury1) temoral or parietal bone fx2) maxillofacial fx3) sternal fx4) 1st or 2nd rib fx5) scapula fx6)Left ribs 8-12 fx7) Right ribs 8-12 fx8) pelvic fx
1) middle meningeal injury-> epidural hematoma2) cervical spine fx3) cardiac contusion4) aortic transection5) pulmonary contusion, aortic transection6) spleen lac7) liver lac8) bladder rupture, urethral transaction
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Renal trauma1) best indicator of kidney injury2) what imaging study should all pts with hematuria have3) 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
1) hematuria2) abd CT3) intravenous pyelogram
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Renal trauma1) T/F the left and right renal vein can be ligated near the IVC2) what are the renal hilum structures from anterior to posterior3) T/F- 95% of injuries are treated nonperatively4) T/F- all urine extravasation injuries require operation5) indications for operation in acute injury6) indications for OR after acute phase
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 collaterals2) VAP= vein artery pelvis3) True4) false5) ongoing hemorrhage with instability6)major collecting system dysruption, non-resolving urine extravasation, severe hematuria
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Renal Trauma1) with exploration in OR what should you try to get bleeding control of first2) should you place drains intra-op?3) how to check for leak at end of caseHow would you treat if at exploration for another blunt injury or penetrating trauma you find:4) blunt renal injury with hematoma5) Penetrating renal injury with hematomaHow do you rx:6) Trauma to flank and IVP shows no uptake in stable pt
1) vascular hilum control2) yes! especially if collecting system is injured3) methylene blue die4) leave unless pre-op CT/IVP shows no function or significant urine extravasation5) open unless pre-op CT/IVP shows good function without significant urine extravasaton6) angiogram (can stent if flap present)
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Bladder Trauma1) best indicator that the bladder is injured2) common associated injury3) signs and sx4) dx5) cystogram findings and rx of extraperitoneal bladder rupture6) cystogram findings and rx of intraperitoneal bladder rupture
1) hematuria2) >95% have associated pelvic fx3) meatal blood, sacral or scrotal hematoma4) cystogram5) cysto shows starbursts, foley for 7-14d6) cysto shows leak (more likely in kids) . rx- operate and repair defect followed by foley drainage
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Ureteral trauma1) best diagnostic studies2) best repair if > 2cm of ureteral segment missing and can't reanastamosea- if injury in upper and middle 2/3 of ureter (above pelvic brim that won't reach bladderb- lower 1/3 injuries3) repair if small ureteral segment a- upepr and middle 1/3 injuriesb-lower 1/3 injuries4) does a one-shot IVP evaluate the ureters sufficiently?5) where is blood supply in relation to the ureter6) what can be used to check for leaks
1) IVP and retrograde urethrogram (RUG)2) a- temporize with perc nephrostomy and tie off both ends of ureter, later do ileal interposition or transureteroureterostomyb- reimblant in bladder, may need bladder hitch procedure3) a-mobilize ends of ureter and perform primary repair over stentb- re-implant in bladder*leave drains for all injuries4) no5) blood supply is medial in upper 2/3 of ureter and lateral in lower ureter6) IV indigo carmine or IV methylene blue
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urethral trauma1) best signs2) T/F: place a foley to allow for healing3) best study to dx and area most at risk for transection4) rx of significant tears5) rx of small, partial tears6) rx of genital trauma (fx in erectile bodies from vigorous sex7) testicular trauma- first study to get
1) hematuria, blood at meatus are best. also free-floating prostate gland suggests, usually associated with pelvic trauma2) false- DON'T place foley for urethral trauma3) retrograde urethrogram (RUG); membranous portion is most at risk for transection4) 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 2-3mo6) repair the tunica and Buck's fascia7) get US to see if tunica albuginea is violated. if it is-> repair
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Pediatric trauma1) T/F: blood pressure is a good indicator of blood loss in kids2) what are the best indicators of shock in children3) T/F: Kids have same risk of hypothermia as adults4) T/F: Kids have increased risk of head injury5) normal vital signs for kids 10yo
1) false, last resort2) HR, RR, mental status, clinical exam3) false, kids have increased risk bc increased BSA compared with weight4) True5) Infant (10yo: HR 120, SBP 100, RR 20
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Trauma during pregnancy1) ethics: who to save? mother or child2) T/F: pregnant pts can have up to a 1/3 total blood volume loss without signs3) how to estimate pregnancy week4) Can you get a CT scan in early prgnancy?5) what special physical exam findings should you look for6) lab tests to determine fetal maturity
1) mother at all costs2) True3) based on fundal height. 20 cm=20wk=umbilicus. place fetal monitor4) try to avoid unless life-threatening and needed5) vaginal discharge- blood, amnion. check for effacement, dilation, fetal station6) lecithin: sphingomyelin (LS) ratio >2:1 and positive phosphatidylcholine in amniotic fluid
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Placental abruption1) signs2) causes3) tests4) prognosis for fetus
1) uterine tenderness, contractions, fetal HR sign of placental abruption4) >50% result in fetal demise
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Uterine rupture1) MC location of rupture2) rx
1) posterior fundus2) if after delivery of child, aggressive resuscitation even in the face of shock. eventually uterus will clamp down after delivery
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Indications for C-section during trauma ex-lap
-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
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Management of hematomas:1) what size is considered significant?2)Management of hematoma following penetrating/blunt injury in thea- pelvisb-paraduodenalc- portal triadd-retrohepatice- midline supramesocolicf- midline inframesocolicg- pericolonich- perirenal
1) >/= 2 cm2) a-open/leaveb-open for bothc- open for bothd- leave for both if stablee, f, g- open for bothh- open unless CT/IVP shows no injury/ leave unless preop CT/IVP shows injury
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1) what injuries should you leave drains in for
pancreatic, liver, biliary, urinary and duodenal injuries
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Snake bites1) symptoms2) rx
1) (depend on species)-> shock, bradycardia, arrhythmia2) stabilize pt, anti-venin, tetanus shot
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Zones of the peritoneum and associated injuries1) Zone 12) Zone 23) Zone 3- and hematoma management for each
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
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Cardiovascular System: Normal Values1) Cardiac output (CO) L/min2) Cardiac index (CI) L/min3) Systemic vascular resistance (SVR)4) Pulmonar Capillary wedge pressure (PCWP)5) Central venous pressure (PAP)6) mixed venous oxygen saturation
1) 4-82) 2.5-43) 800-14004) 11 +/- 45) 25/10 +/- 56) 75 +/- 5
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MAP=
SVR x CO
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C.I.=
CO/BSA
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1) what % of C.O. does kidney get2) what % of C.O. does brain get3) what % of C.O. does heart get
1) 25%2) 15%3) 5%
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relation of left ventricular end-diastolic length to left ventricular end-diastolic volume and filling pressure
linear relationship
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explain the relation of preload to stroke volume seen in the starling curve
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
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What are the following a measure of:1) Afterload2) stroke volume (3 things that determine SV)3) ejection fraction4) end-diastolic volume (EDV)5) end-systolic volume (ESV)6) effect of HR on C.O.
1) resistance against the ventricle contracting (SVR)2) determined by left ventricular end diastolic volume, contractility and afterloadSV= LVEDV - LVESV3) stroke volume/LVEDV4) determined by preload and distensibility of the ventricle5) determined by contractility and afterload6) C.O. increases with HR up to 120-150bpm then starts to go down bc of decreased diastolic filling time
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1) how much of LVEDV does the atrial kick account for2) Anrep effect3) Bowditch effect
1) 20%2) automatic increase in CONTRACTILITY 2/2 inc afterload3) auromatic increase in contractility 2/2 inc HR
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Equation for arterial O2 contentCaO2=
Hgb x 1.34 x O2 sat x (Po2x0.003)
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Equation for O2 delivery=
COx arterial O2 content (CaO2) x 10
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Equation for O2 consumption (VO2)=
CO x (CaO2-CvO2); where CvO2= venous O2 content
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1)What is the normal O2 delivery to consumption ratio and how is it kept constant2) does consumtion change with O2 supply
1) 5:1. CO2 increases to keep this ratio constant2) O2 consumption usually supply independent (doesn't change until low levels of delivery are reached)
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Causes of right shift on oxygen- Hgb dissociation curve
inc CO2, dec pH, inc temperature, inc ATP production, inc 2,3-DPG production all lead to O2 unloading
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1) What is normal p50 (O2 at which 50% of O2 receptors are saturated)2) normal SvO2
1)27 mmHg2)75% +/- 5%
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1) what causes SvO2 to increase2) to decrease
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)
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what can throw off the pulmonary wedge pressure
pulmonary HTN, aortic regurg, mitral stenosis or regurg, high PEEP, poor LV compliance
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Swan-Ganz catheter1) Where to place2) management of hemoptysis after flushing swan-ganz catheter3) relative contraindications to placing4) distances for placing swan-ganz catheter to wedge froma- R SCV, b- R IJ, c- L SCV, d- L IJ5) what pulmonary value can only be measured w Swan Ganz catheter6) when should wedge pressure measurements be taken
1) Zone III, lower lung2) 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 block4) a-45cm, b-50cm, c-55cm, d-60cm5) PVR pulmonary vascular resistance (ECHO does not meausre)6) at end-expiration for both ventilated and non-vent
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1) what are primary determinants of myocardial O2 consumption2) why is LV blood 5mm Hg lower PO2 than pulmonary capillaries3) what is a notmal alveolar-arterial gradient in nonventilated pt4) what blood has the lowest venous saturation
1) increased ventricular wall tension (#1) and heart rate2) unsaturated bronchial blood empties into pulmonary veins-> LV blood 5mmHG lower3) 10-15mmHg4) coronary sinus blood (30% saturated)
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1) definition of shock2) Change in CVP&PCWP/CO/SVR ina-hemorrhagic shockb- septic (hyperdynamic shock)- earlyc- septic shock lated-cardiogenic shocke- neurogenic shockf- adrenal insufficiency
1) inadequate tissue oxygenation2) a-D/D/Ib-D (or nml)/I/Dc-D/D/Id-I/D/Ie-D (or nml)/D/Df-D (or nml)/D/D
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Adrenal insufficiency1) MCC2) sx of acute insuf3) rx of acute insuf4) steroid potency bw cortisonek, hydrocortisone, prednisone, prednisolone, methylprednisolone, dexamethasone
1) withdrawl of exogenous steroids2) cardiovascular collapse, typically unresponsive to fluids and pressors, N/V, abd pain, fever, lethargy, hypoglycemia3) Dexamethasone4) 1x= cortisone, hydrocortisone3x=prednisone, prednisolone, methylprednisolone5x= dexamethasone
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Neurogenic shock1) associated injury2) vitals, skin temp3) rx
1) spinal or head injury2) dec HR and BP, warm skin3) volume 1st then phenylephrine after resuscitation
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1) initial alteration in hemmorhagic shock
1) increased diastolic pressure
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Cardiac tamponade1) mech of cardiogenic shock2) Beck's triad3) Echo findings4) does pericardiocentesis blood form clot5) rx
1) decreased ventricular filling due to fluid in the pericardial sac around the heart2) hypotension, JVD, muffled heart sounds3) impaired diastolic filling of right atrium initially (1st sign of tamponade)4) no5) fluid resuscitation to temporize the situation. need pericardial window or pericardiocentesis
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1) Early Sepsis triad2) insulin and glucose levels ina- early GN sepsisb- late GN sepsis3) what is a typical lab finding in a pt just before they become clinically septic
1) hyperventilation, confusion, hypotension2) decreased insulin, increased glucose (impaired utilization)3) increased insulin and glucose (2/2 to insulin resistance)4) hyperglycemia
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Neurohormonal response to hypovolemia1) rapid response2) sustained response
1) epinephrine and norepi release (adrenergic release) -> vasoconstriction and inc cardiac contractility2) 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
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Emboli1) Fat emboli- a- sxb-MC causec- special stain that can show fat in sputum and urine in pt with fat emboli2) PEa- where do most arise fromb- sx, Po2, Pco2, HR and RR, pH abnormalityc- rx3) Air emboli rx
1)a-petechia, hypoxia, confusionb-LE (hip, femur) fx/ortho proceduresc-sudan red stain2) a-ileofemoral resionb- CP and dyspnea, dec Po2 and Pco2, respiratory alkalosis, inc HR and RR, hypotension and shock if massivec- heparin, coumadin. open or percutaneous suction catheter embolectomy if pt is in shock despite massive pressors and ionotropes3) 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.
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Intra-aortic balloon pump (IABP)1) when does it inflate?2) deflate?3) what is a contraindication4) where to place5) effect on afterload, BP and coronary perfusion
1) diastole (T wave)2) P wave (systole)3) aortic regurg4) 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
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Cardiovascular receptors- actions of each1) alpha-12) alpha-23) beta-14) beta-25) dopamine receptors
1) vascular smooth muscle constriction, gluconeogenesis and glycogenolysis2) venous smooth muscle constriction3) myocardial contraction and rate4) relaxes bronchial smooth muscle, relaxes vascular smooth muscle, increases insulin, glucagon and renin5) relax renal and splanchnic smooth muscle
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CV drugs- what receptors do they act on, dose and effects1) Dopamine (include actions at each dose)
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)
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CV drugs- what receptors do they act on, dose and effects2) Dobutamine
3ug/kg/min initially. Beta-1=inc contractility, tachycardia with higher doses
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CV drugs- what receptors do they act on, dose and effects3) Milrinone (and secondary effects)
Phosphodiesteras inhibitor-> inc cAMP--> inc Ca flux and myocardial contractility- also causes vascular smooth muscle relaxation and pulmonary vasodilation
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CV drugs- what receptors do they act on, dose and effects4) Phenylephrine5) Norepinephrine6) Epinephrine
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 vasoconstrictor6) 1-2ug/min to start.low dose- beta 1 and 2 (inc contractility and vasodilation)-> can lower BP at low doseshigh dose- alpha-1 and alpha-2 (vasoconstriction)-> inc cardiac ectopic pacer activity and myocardial O2 demand
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CV drugs- what receptors do they act on, dose and effects7) Isoproterenol (and s/e)
1-2ug/min initially.Beta 1 and 2-> inc HR and contractility, vasodilatesS/E- arrhythmogenic, inc heart metabolic demand (rarely used), may actually dec BP
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CV drugs- what receptors do they act on, dose and effects8) Vasopressin
V1 receptor-> vasoconstrictionV2 (intrarenal)-> water reabsorption at collecting ductsV2 (extrarenal)-> release for factor VIII and vWF
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CV drugs- what receptors do they act on, dose and effects9) Nipride( and s/e- what should you check for)
arterial vasodilators/e- cyanide toxicity at doses >3ug/kg/min for 72 hours. check thiocyanate levels and signs of metabolic acidosis
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Cyanide toxicity treatment
amyl nitrite, then sodium nitrite
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CV drugs- what receptors do they act on, dose and effects10) Nitroglycerin
venodilation with dec myocardial wall tension from decreased preload.*moderate coronary vasodilator
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CV drugs- what receptors do they act on, dose and effects11) hydralazine
alpha-blocker- lowers BP but can cause rebound hypertension
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Pulmonary system:1) equation for compliance2) what does a high compliance equate to3) in pts with ARDS, fibrotic lung diseases, reperfusion injury, pulmonary edema, atelectasis is compliance increased or decreased
1) change in volume/ change in pressure2) easy to ventilate3) decreased
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Aging1) how does aging effect FEV12) vital capacity3) functional residual capacity
1) decreased FEV12) decreased vital capacity3) increased functional residual capacity
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V/Q ratio1) where is it highest2) where is it lowest
ventilation/perfusion ratio1) highest in upper lobes2) lowest in lower lobes
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Ventilator1) how to improve oxygenation2) how to decreased CO23) purpose of pressure support4) what FiO2 should you keep it to prevent O2 radical toxicity5) at what plateau and peak is barotrauma of concern and what should you do to prevent6) how does PEEP work7) complications from excessive PEEP8) when to use high-frequency ventilation
1) inc FiO2 or inc PEEP (alveoli recruitment->improves FRC)2) inc rate or volume3) decreases the work of breathing (inspiratory pressure is held constant untill minimum volume is reached4) 30 and peak >50--> need to decrease TV and consider pressure control ventilation6) improves FRC and compliance by keeping alveoli open-> best way to improve oxygenation7) dec RA filling, dec CO, dec renal blood flow, dec UOP, inc pulm vascular resistance8) used a lot in kids, tracheoesophageal fistula, bronchopleural fistula
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Pulmonary function measurements1) total lung capacity2) Forced vital capacity3) Residual volume4) Tidal Volume5) functional residual capacity6) effect of surgery, sepsis and trauma on FRC and why7) expiratory reserve volume
1) lung volume after maximal inspiration (TLC=FVC +RV)2) maximal exhalation after inhalation3) lung volume after maximal expiration (20% TLC)4) volume of air with normal inspiration and expir5) 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
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Pulmonary function measurements8) Inspiratory capacity9) FEV110) minute ventilation (how to calculate)Describe changes in TLC, RV, FVC, and FEV1 in11) Restrictive lung disease12) Obstructive lung disease
8) maximum air breathed in from FRC9) volume of air that can be forcefully expired in 1 second after max inhalation10) TV x RR= minute ventilation11) dec TLC, RV and FVC. nl or inc FEV112) inc TLC and RV. dec FEV1. FVC can be nl or dec
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1) dead space- what is it and where is it2) do the following increase or decrease dead space: drop in C.O., PE, pulm HTN, ARDS, excessive PEEP3) why is work of breathing increased in COPD
1) area of lung that is ventilated but not perfused2) increases with all. can lead to high CO2 buildup (hypercapnia)3) prolonged expiratory phase
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ARDS1) primary mediating cell type2)MC cause and other causes3) effect on lungs4) Criteria for diagnosing ARDS
1) PMNs2) MC- pneumonia. Other- sepsis, multi-trauma, severe burns, pancreatitis, aspiration, DIC3) inc proteinaceous material, inc A-a gradient, inc pulmonary shunt4) acute onset, bilateral pulmonary infiltrates, PaO2/FiO2 <18)
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Aspiration1) what pH and volume is associated with inc degree of damage2) What is Mendelson's syndrome3) MC site of aspiration pneumo
1) pH0.4cc/kg2) chemical pneumonitis from aspiration of gastric secretions3) Right Lower Lobe
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Atelectasis1) what is it2) MC cause3)symptoms4) what comorbidities increase risk5) rx
1) collapse of alveoli resulting in reduced oxygenation2) poor inspiration post-op (MC cause of fever in 1st 48hr)3) fever, tachycardia, hypoxia4) COPD, upper abd surgery, obesity5) IS, pain control, ambulation
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what can throw off a pulse ox
nail polish, dark skin, low-flow states, ambient light, anemia, vital dyes
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effect on lung vasculature of1) PGE1, prostacyclin (PGI2), Nitric oxide and bradykinin2) hypoxia, histamine, serotonin, TXA23) Alkalosis4) Acidosis5) Nitroprusside, nitroglycerin and nifedipine
1) pulm vasodilation2) pulm vasoconstrict3) pulm vasodilator4) pulm vasoconstrictor5) pulmonary shunting
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Renal system1) MC of postop renal failure2) how many nephrons need to be damaged for renal dysfnc to occur3) what is best test for azotemia4) how to calculate and what the results mean
1) hypotension2) 70%3) FeNa4) FeNa= (urine Na/Cr)/(plasma Na/Cr). 3%=parenchymal
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Prerenal/parenchymal (renal)1) Urine osmolarity (mOsm)2) U/P osmolality3) U/P creatinine4) Urine Na5) FeNa
1) >500/ 250-3502) >1.5/ 20/ 405) 3%
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Management steps for Oliguria
1st- make sure pt is volume loaded (CVP 11-15)2nd- do diuretic (lasix) trial3rd- dialysis if needed
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Indications for dialysis
fluid overload, hyperkalemia, metabolic acidosis, uremic encephalopathy, uremic coagulopathy, poisoning
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1) Difference bw hemodialysis and CVVHD2) how much does hct increase for each liter taken off with dialysis
1. HD- rapid, can cause large volume shiftsCVVH- sloer, good for ill pts who cannot tolerate the volume shifts (ie- septic shock).2) 5-8
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Renin1) what causes release and by what cells2) actionAngiotensin Converting enzyme3) where is it4) effectAldosterone5) what causes release and where from6) effect7) effect of angiotensin II
1) decreased pressure sensed by juxtaglomerular apparatus or increased Na concentration sensed by macula densa-beta-adrenergic stimulation and hyperkalemia also cause release2) converts angiotensinogen (synth in liver) to angiotensin I3) lung4) converts angiotensin I to angiotensin II5) adrenal cortex releases in response to angiotensin II6) 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
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Atrial natriuretic peptide (or factor)1) where is it released from 2) actions
1) atrial wall 2/2 atrial distension2) inhibits Na and water resorption in the collecting ducts and vasodilates
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which limb of kidney controls GFR
efferent limb
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renal toxic drugs, how they cause injury1) NSAIDS2) Aminoglycosides3) Myoglobin and rx4) contrast dyes and prevention/rx
1) inhibit prostaglandin synthesis-> renal arteriole vasoconstriction2) direct tubular injury3) direct tubular injury (rx- alkalinize urine)4) direct tubular injury. rx- pre-hydrate before contrast exposure is best. otherwise- HCO3- or N-acetylcysteine
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SIRS1) causes2) what is most potent stimulus and what is released as a consequence3) mechanism behind it4) diff bw sepsis and SIRS
1) shock, infection, burns, multi-trauma, pancreatitis, severe inflammatory responses2) endotoxin (lipopolycaccharide-lipid A) is the most potent stimulus for SIRS-> TNF release3) TNF-alpha and IL-1-> inflam response-> shock and multiorgan dysfnc 2/2 capillary leakage, microvascular thrombi and hypotension4) sepsis= SIRS + infectious source
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Definition of 1) SIRS2) Shock3) Multisystem Organ Dysfunction
1) T>38 or 90bpm, RR>20 or PaCO212,000 or <4,0002) 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
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Diagnositic criteria for sig organ dysfnc1) pulmonary2) CV3) Renal4) Liver5) Nutrition6) CNS7) Coagulation8) Host defenses
1) need for mech. ventilation, PaO2:FiO2 ration < 2.5 L/min/m^23) Cr>2xbaseline on 2 consecutive days or need for dialysis4) bili >3mg/dl on 2 consec days or PT>1.55) >10% reduction in lean body mass; albumin<1000 or invasive infection including bacteremia
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Brain death1) what Temperature, BP, drugs and metabolic derangements preclude diagnosis2) what physical exam findings must the pt exhibit and for how long3) EEG findings4) MRA findings5) T/F: you cannot have deep tendon reflexes with brain death
1) T
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Apnea test for brain death1) what is it2) what is a positive test result3) what are negative results
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 death2) 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
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Carbon Monoxide poisoning1) effect on O2 sat2) how it works and sx3) how to diagnose4) rx
1) can falsely elevate O2 sat on pulse ox2) binds Hgb directly-> carboxyhemoglobin-> can't bind O2-> sx- Nausea, HA, confusion, coma, death3) carboxyhemoglobin level >10% or >20% in smokers4) 100% O2 on ventilator. Displaces carbon monoxide. rarely need hyperbaric O2
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Methemoglobinemia1) Cause2) mechanism3) effect on O2 sat4)rx
1)from nitrites such as Hurricaine spray2) nitrites bind Hgb3) O2 sat reads 85%4) rx- methylene blue
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What is critical illness polyneuropathy and effect on ventilation
motor>sensory neuropathy with sepsis. Can lead to failure to wean from vent
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Reperfusion injury1) Cause2) other role for the cause3) Most important cell mediator
1) Xanthine Oxidase in endothelial cells forms toxic oxygen radicals2) Xanthine oxidase also involved in metabolism of proteins to uric acid3) PMNs
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DKA1) sx and labs2) rx
1) N/V, thirst, polyuria, inc glucose and ketones, dec Na, inc K2) NS and insulin
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ETOH withdrawal1) sx2) rx
1) HTN, tachycardia, delirium, seizures after 48hrs2) thiamine, folate, B12, Mg, K, prn lorazepam (Ativan)
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ICU psychosis1) when do you see it2) what other causes must you r/o
1) after POD32) r/o metabolic (hypoglycemia, DKA, hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes
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Burn classification- symptoms/depth1) 1st degree2) 2nd degree3) 3rd degree4) 4th degree
1) Sunburn (epidermis only) superficial2) superficial dermis (papillary)- painful to touch, blebs and blisters, hair follicles intact, blanches (don't need skin graftdeep 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
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1) which burns heal by epithelialization (and where does epithelialization begin)2) which burns can cause rhabdomyolysis with myoglobinuria3) what is rx of rhabdo
1) 1st and superficial 2nd degree burns. epithelialization is primarily from the hair follicles2) extremely deep burns, electrical burns or compartment syndrome3) IVF, alkalinize urine (diuretics)
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Admission criteria for burns- what burns should you admit
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 joints2) 3rd degree burns >5% any age3) electrical and chemical burns4) inhalation injury, mechanical trauma, preexisting medical conditions5) suspect of child abuse or neglect6) injuries in pts with special social, emotional or long-term rehabilitation needs
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Burns1) what age groups is death highest in2) MC type of burn3) most likely type to come to hospital and be admitted
1) children and elderly (hardest to get away)2) scald3) flame burns
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Assessing percentage of body surface burned (rule of 9's. How many percent for each in adults and kids:1) head2) arms3) chest4) back5) legs6) perineum7) palm
1) 9% in adult, 18% in kids2) 9% each arm (18% total)3) 18% anterior, 4) 18% posterior5) 18% each leg in adult, 14% each leg in kids6)1%7) 1% each* can also use pt palm to estimate injury (palm=1%)
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Parkland formula1) what % burn can it be used for2) calculation3) what type of fluid to use4) best measure of resucitation5) in what pts canparkland grossly underestimate volume requirements6) at what point can you use colloid
1) >/=20%2) 4cc/kg x %burn in first 24 hours (give 1/2 of volume in first 8hr)3) LR in first 24 hr4) UOP (0.5-1.0 cc/kg in adults, 2-4cc/kg in children
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Indications for Escharotomy1) how soon do you need to perform2) when should you perform it3) when to do fasciotomy
1) within 4-6hr2) 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 burns3) if compartment syndrome suspected after escharotomy
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risk factors for burn
v. old or young, ETOH or drug use, smoking, low socioeconomic status, violence, epilepsy
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Child abuse1) accounts for what % of burns2) what history elements should make you suspect3) physical exam elements
1) 15%2) delayed presentation for care, conflicting hx's, previous injury3) sharply demarcated margins, uniform depth, absence of splash marks, dorsal location on hands, very deep localized contact injury
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lung injury in Burn1) cause2) risk factors for airway injury3) signs/sx on physical exam4) indications for intubation5) MC infection and cause of death in pts with >30%BSA burns
1) carbonaceous materials and smoke (NOT heat)2) ETOH, trauma, closed space, rapid combustion, extremes of age, delayed extrication3) facial burns, wheezing, carbonaceous sputum4) upper airway stridor or obstruction, worsening hypoxemia (massive volume resuscitation can worsen sx)5) pneumonia
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Unusual Burns1) Acid and alkali burnsa- rxb- which causes deeper burns and type of necrosis associated with each2) rx for hydrofluoric acid burns3) rx for powder burns4) tar burn rx5) electical burn complications6) lightening complications
1) a- copious water irrigationb- alkalis produce deeper burns 2/2 liquefaction necrosis. Acid burns produce coagulation necrosis2) spread Calcium over wound3) wipe away before irrigation4) 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 necrosis6) Cardiopulmonary arrest 2/2 electrical paralysis of brainstem
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1st week of burn care1) when to excise burn wounds and for what burns2) how much blood loss, skin excision and OR time is maximum for each burn wound excision3) caloric need in 1st week4) protein need5) best non-protein source of calories in burn pts
1)
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Grafts1) when are skin grafts C/I in burn2) what type of skin graft is best3) 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 graft4) thickness of STSG and parts of skin that comprise it
1) cx + for beta-hemolytic strep or bacteria >10^52) 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 areas4) 12-15 mm (includes epidermis and part of dermis)
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1) Homograftsa-give examplesb- when to use and how long they last2)Xenograftsa- when to use-why aren't they as good as homografts3) what is last resort
1) a-allografts, cadaveric skinb- vascularize but are eventually rejected, last 2-4 wks. good temporizing material2) ie- Porcinea- last 2 weeks-don't vascularize3) Dermal substitutes
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Grafts1) when to use meshed grafts2) reasons to delay autografting3) MC reason for skin graft loss4) when to use STSG and advantages and disadvantages5) when to use FTSG and advantages and disadvantages
1)use for back, flank, trunk, arms, legs2) infection, not enoug skin donor sites, pt septic or unstable, don't want any more donor sites with concomitant blood loss3) hematoma or seroma under graft-apply pressure dressing (cotton balls) to the graft to prevent fluid build up underneath4) more likely to survive bc easier for imbibition and subsequent revascularization5) less wound contraction- good for areas such as palms and back of hands
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what type of graft can improve burn scar hypopigmentation and irregularities
dermabrasion thin split thickness grafts
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Specialized Burn Care1) Rx of face burns2) Hand burn rx (superficial and deep)3) Palms4) Genitals
1)topical abx for 1st week, FTSG for unhealed areas (nonmeshed)2)superficial- ROM exercises, splint in extension if too much edemadeep- immobilize in extension for 7 days after skin graft (need FTSG), then PT. may need wire fixation of joints if unstable or open3)try to preserve specialized palmar attachments. splint hand in extension for 7days after FTSG4) can use meshed STSG
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Burn wound infection rx1) role of ppx abx2) what to apply immediately after burn3) MC infecting organisms (top 4)4) what burns are more likely to become infected5) T/F: Topical agents have decreased incidence of burn wound bacterial infections6) what has increased in incidence 2/2 topical abx
1) none2) bacitracin or neosporin3) Pseudomonas> Staph> E. Coli and Enterobacter4) >30%BSA5) True6) candida
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1) How is immunity impaired in burn pts
granulocyte chemotaxis and cell-mediated immunity are impaired
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Slivadene (Silver Sulfadiazine)1) side effects2) what allergy in pts in C/I to use3) what is it ineffective for4) what is it effective for5) penetration and effect on epithelialization
1) neutropenia and thrombocytopenia2) sulfa3) some Pseudomonas4) Candida5) limited eschar penetration, can inhibit epithelialization
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SIlver Nitrate1) S/E and what pts is it C/I in2) penetration3) what is it ineffective for
1)-electrolyte imbalances (hyponatremia, hypochoremia, hypocalcemia, hypokalemia)-discoloration-methemoglobinemia (C/I in pts with G6PD def)2) limited eschar penetration3) some pseudomonal species and GPC
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Sulfamylon (mafenide sodium)1) S/E2) penetration3) coverage compared to other burn abx
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 cartilage3) broadest spectrum against pseudomonas and GNRs
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which of the burn abx have painful application
sulfamylon
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Mupirocin1) good for what type of infection2) drawback of use
1) MRSA2) expensive
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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
burn wound infection
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1)MCC of burn wound sepsis2) MC viral infection in burns3) amount of bacteria that is cutoff for burn wound infection4) best way to detect burn wound infection/differentiate from colonization
1) pseudomonas2) HSV3)
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Complications after burns- why do the following occur1) Seizures2) peripheral neuropathy3) ectopia and rx4) eye injury- how to dx and rx5) symblepharon- what is it and rx6) heterotopic ossification of tendons rx7)fractures- rx8) curling's ucler- what is it9) Marjolin's ulcer- what is it10) rx of corneal abrasion
1) usually iatrogenic 2/2 [Na]2) 2/2 small vessel injury and demyelination3) from contraction of burned adnexa (rx- eyelid release)4) dx- fluorescein staining to find injury, rx- topical flouroquinolone or gentamicin5) eyelid stuck to conjuctiva. rx-release with glass rod6) PT, may need OR7) often need external fixation while burn treatment8) gastric ulcer 2/2 burn9) highly malignant sqamous cell CA that arises in chronic non-healing burn wounds or unstable scars10) topical abx
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Hypertrophic scar1) when does it occur2) what burn injuries is it more common in3) rx
1) 3-4 mo after injury 2/2 inc neovascularization2) more likely to be deep thermal injuries that take >3wk to heal, heal by contraction and epithelial spread, or heal across flexor surfaces3) steroid injection into lesion (best), silicone, compression, wait 1-2 yr before scar modification surgery
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Erythema multiforme and variants1) list the variants in order from least severe to most severe and how to dx2) underlying disease in all3) causes4) rx5) T/F- give steroids to these pts
1) Erythema Multiforme- least severe (self-limited, target lesions)Stevens-Johnson syndrome- more serious (
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Skin- composition of each layer1) Epidermis2) Dermis
1) primarily cellular (keratinocytes and melanocytes)2) primarily structural proteins (collagen) for the epidermis
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1) keratinocytesa-skin layerb-where it originates fromc- purpose2) melanocytesa-originb) skin layerc) how is melanin transferred bw melanocytesd) differences in melanocytes bw races
1) a) epidermisb) basal layerc) provides mechanical barrier2) a) neuroectodermal (neural crest) cells in basal layer of epidermisb) basal layer of epidermisc) have dendritic processes that transfer melanin to neighboring keratinocytes via melanosomesd) same density of melanocytes. Difference is in melanin production
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1) Langerhans cellsa- functionb- where they originate fromc- what type of hypersensitivity reaction do they have a role in
1)a-dendritic cells (Antigen-presenting cells MHC class II) of skin and mucosab- bone marrowc- contact hypersensitivity reactions (type IV)
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Sensory nerves of the Skin- what do they sense:1) pacinian corpuscles2) Ruffini's endings3) Krause's end-bulbs4) Meissner's corpuscles
1) pressure2) warmth3) cold4) tactile sense
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1) role of eccrine sweat glands and type of sweat2) role of apocrine sweat glands, type of sweat and where the highest concentration is
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
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1) t/F: lipid-soluble drugs have decreased skin absorption2) what is predominant type of collagen in skin and role3) what is tension and what creates it in skin4) what is elasticity in skin and what is responsible for creating elasticity5) what are cushing's striae
1) false, increased absorption2) 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 length5) red stretch marks in cushing's: caused by loss of tensile strength and elasticity
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FLAPS1) MCC of pedicled or anastomosed free flap necrosis2) how does tissue expansion occur1) TRAM flabs:a- what is itb- what vessels does it rely onc-what is most imp determinant of TRAM flap viabilityd- potential complications
1) venous thrombosis2) by local recruitment, thinning of the dermis and epidermis mitosis3)a- Transverse rectus abdominis myocutaneous flap reconstructionb-superior epigastric vesselsc- periumbilical perforatorsd- flap necrosis, ventral hernia, bleeding, infection, abdominal wall weakness
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Pressure sores- describe the 4 stages and treatment for each
Stage I- erythema and pain, no skin loss- keep pressure offStage II- partial skin loss with yellow debris- local rx, keep pressure offStage III- full-thickness skin loss, subcutaneous fat exposure. rx- sharp debridement, likely need myocutaneous flapStage IV- involves boney cortex, muscle. rx- myocutaneous flap
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UV radiation1) effect on skin2) best factor for protecting skin from UV radiation3) which type is responsible for chronic sun damage
1) damages DNA and repair mechanisms. Both a promoter and initiator.2) melanin3) UV-B
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Melanoma1) % of skin cancers2) % of skin cancer deaths3) risk factors for melanoma4) MC melanoma site in Men5) in women
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 familial4) back5) legs
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Melanoma1) factors that worsen prognosis2) signs of melanoma and what is most ominous sign3) MC location for distant met4) what cells does it originate from5) how to dx and rx for a-2cm lesion or cosmetically sensitive area
1) men, ulcerated lesions, ocular and mucosal lesions2) ABCDE- asymmetry (angulation, indentation, notching, ulceration, bleeding), Borders irregular, Color change (darkening), diameter increase, evolving over time. Blue color is most ominous sign3) lung4) neural crest cells (melanocytes) in basal layer of epidermis5)a- dx- excisional bx, rx- resection with marginsb-incisional bx/punch bx. rx- resect with margins
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What staging should you get for melanoma
CT chest/abd/pelvis, LFTs, LDH for all melanoma >/=1mm, examine all possible draining LNs
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Types of melanoma1) which is most superficial and what kind of margins do you need for it2) least aggressive type3) most common type and where it originates from4) most aggressive type5) type MC in african americans6) type MC on palms/soles
1) Melanoma in situ or thin lentigo maligna (hutchinson's freckle)- just in spuerfical papillary dermis so 0.5-cm margins are ok2) lentigo meligna melanoma- minimal invasion, radial growth first, elevated nodules3) superficial spreading melanoma- intermediate malignancy, originates from nevus/sun-exposed areas4) 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 body5) Acral lentiginous- v. aggressive6) Acral lentiginous
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Management of melanoma1) recommended surgical margins for tumora- in situb-2mm2) management of nodesa- if clinically positive nodesb- if clinically negative nodes3) management of mets4) vaccines for systemic disease
1) a) 0.5-1cmb) 1cmc) 1-2cmd) 2cm margins2) involved nodes are usually NT, round, hard, 1-2cma) resect clinically positive nodesb) 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 procedure4) IL-2 and tumor vaccines
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Basal cell carcinoma1) where does it originate from2) pathology findings3) what is the most aggressive type and what does it produce4) treatment5) MC location
1) epidermis- basal epithelial cells and hair follicles2) peripheral palisading of nuclei and stromal retraction3) Morpheaform type- has collagenase production4) 0.3-0.5cm margins. XRT and chemo of limited benefit for inoperable disease, metastases or neuro/lymphatic/vessel invasion5) 80% on head and neck
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Name the type of skin/soft tissue cancer1)MC malignancy in the U.S.2) overylying erythema, papulonodular with crust and ulceration, usually red-brown3) pearly appearance, rolled borders, slow and indolent growth4) MC soft tissue sarcoma5) can develop in post-XRT areas or in old burn scars6) actinic keratoses is a risk factor for7) may have surrounding induration and satellite nodules
1) Basal cell CA (4x more common than squamous skin CA)2) Squamous cell CA3) basal cell CA4) #1 malignant fibrous histiosarcoma, #2liposarcoma5) squamous cell CA6) squamous cell CA7) squamous cell CA
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Squamous cell carcinoma1) how common are mets compared to basal cell CA and melanoma2) risk factors3) risk factors for mets4) rx
1)mets more frequent than basal cell but less frequent than melanoma2) 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 CA3) poorly differentiated, greater depth, recurrent lesions, immunosuppression4) 0.5-1cm margins for low riskhigh 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
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Soft Tissue Sarcoma1) MC location and age group2) tumor characteristics3) what initial imaging do you need4) dx5) how does it spread6) MC site for mets7) how is it staged
1) 50% from extremities, 50% in children (arise from embryonic mesoderm)2) large, rapid growth, painless3) CXR to r/o lung mets; MRI before bx to r/o vascular, neuro or bone invasion4) excisional bx if mass 4cm (need to eventually resect bx skin site if shows sarcoma)5) hematogenous spread (LN mets rare)6) lung7) based on GRADE (not size)
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Sarcoma treatment1) margins2) adjuvant therapy (when to do XRT, type of chemo used and when to use)3) rx of isolated mets4) are drains used routinely?
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 later2) 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 resection3) if no other evidence of systemic disease resect. Otherwise palliate with XRT4) no
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Sarcoma1) prognosis and why2) Head and neck sarcomasa- population they occur inb- why is rx more difficultc- MC type3) visceral and retroperitoneal sarcomasa-MC typeb-most imp prognostic factor
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 resection2) a-peds ptsb-proximity to vital structures-> postop XRT for positive or close margins as neg margins may be impossible to obtainc- rhabdomyosarcoma3) leiomyosarcomas and liposarcomas
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Risk factors and associated CA1) asbestos2) PVC and arsenic3) chronic lymphedema
1) mesothelioma2) angiosarcoma3) lymphangiosarcoma
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Kaposi's sarcoma1) type of sarcoma2) MC sites and sx3) MC malignancy in what pts4) Rx
1) vascular sarcoma2) oral and pharyngeal mucosa-> bleeding and dysphagia3) AIDS pts4) 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
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1) #1 soft tissue sarcoma in kidsa-where it occurs and which site has poorest prognosisb- 2 subtypes (which is MC, which is worst Prog)c-rx
1) Childhood rhabdomyosarcomaa-head/neck, GU, extremities and trunk (poorest prog)b- embryonal subtype is most common, Alveolar subtype-worst prognosisc-surgery, doxorubicin-based chemo
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Bone sarcomas1) T/F- rarely metastasize2) Osteosarcomaa-MC locationb- cell type it originates fromc-MC age group
1) False, most are metastatic at time of dx2)a- increased incidence around kneeb-metaphyseal cellsc- children
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Genetic syndromes for soft tissue tumors: what tumors are seen in the following:1) Neurofibromatosis2) Li-fraumeni syndrome3) hereditary retinoblastoma4) Tuberous sclerosis5) Gardners syndrome
1) CNS tumor, peripheral sheath tumor, pheo2) childhood rhabdomyosarcoma and many others3) other sarcomas4) angiomyolipomas5) familial adenomatous polyposis, and intra-abdominal desmoid tumors
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other skin conditions and rx1) lip lacerations2) 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
1) align vermillion border2) yellow, contains histiocytes. rx- excise3) viral origin. initial rx- liquid nitrogen4) Neuromas (neurofibromatosis and von Reckinghausen's syndrome)
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Name the skin condition1)keratoses- premalignant in sun-damaged areas, need excisional bx if suspicious2) keratoses-not premalignant skin lesion on trunk on elderly, can be dark3) keratoses-associated with squamous cell ca4) 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 tumor5) painful benign tumor composed of blood vessels and nerves, MC in terminal aspect of digit. What is rx?
1) Actinic Keratosis2) Seborrheic keratosis3) arsenical keratosis4) Merkel cell CA- components are neuron specific enolase (NSE), cytokeratin, neurofilament protein5) Glomus cell tumor. rx- tumor excision
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Desmoid tumors1) where do they occur2) when do they occur3) prognosis4) rx
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 spread4) surgery if possible, chemo (sulindac, tamoxifen) if vital structure involved or too much bowel would be taken
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Bowens Disease1) associated CA2) associated virus3) rx4) T/F- wide local excision is an good treatment
1) SCC in situ, 10% turn into invasive SCC2) HPV3) *imiquimod*, cautery ablation, topical 5-FU, regular bx to r/o CA4) F- void wide local excision if possible (high recurrence rate with HPV)
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Keratoacanthoma1) characteristics2) benign or malignant3) dx4) rx
1) rapid growth, rolled edges, crater filled with keratin, involutes spontaneously over months. can be confused with SCC2) benign3) biopsy to be sure not SCC4) excise if small; if large bx and observe
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Hyperhydrosis1) what is it2) rx
1) inc sweating, esp noticible in palms2) thoracic sympathectomy if refractory to varient of antiperspirants
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Hydradenitis1) what is it2) MC organisms involved3) rx
1)infection of the apocrine sweat glands, usually in axilla and groin regions2) staph/strep are MC organisms3) 1st- abx and improved hygeine. May need surgery to remove skin and associated sweat glands
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Benign cysts- name them1) MC, completely mature epidermis with creamy keratin material2) in scalp, no epidermis3) over tendons, usually over wrist, filled with collagen material4) midline, intra-abdominal and sacral lesions usual, need resection due to malignancy risk5) congenital coccygeal sinus with ingrown hair, gets infected and needs to be excised
1) epidermal inclusion cyst2) Trichilemmal cyst3) Ganglion cyst4) dermoid cyst5) pilonidal cyst
