Midterm exam Flashcards
1
Q
Acute Wound
A
- sudden loss anatomical structure in tissue following transfer of kinetic, chemical, thermal energy
- in recently uninjured, normal tissue
- acute wound healing within 6-12 weeks
- surgical wounds
2
Q
Chronic Wound
A
- fail of wound healing
* prolonged tissue repair
3
Q
When does healing arrest most commonly occur?
A
Inflammatory phase
4
Q
failed epithelialization due to repeated trauma or desiccation may result in?
A
Chronic partial thickness wound
5
Q
Primary healing
A
- tissue cleanly incised
- anatomically reapproximated
- healing by primary intention
- no complications, minimal scarring
6
Q
Secondary Healing
A
- wounds left open through formation of granulation tissue, coverage by migration of epithelial cells
- healing by secondary intention
- infected wounds and burns
7
Q
Delayed primary closure
A
- wound left open to heal under carfeully maintained, moist healing environment for abt 5 days
- closed primarily
- less likely to become infected → bacterial balance achieved, O₂ requirements optimized through granulation tissue
- third intention
8
Q
Granulation tissue
A
- red, moist, granular tissue
* collagen, new blood vessels, fibroblasts, inflammatory cells, scar tissue
9
Q
Mechanism of Wound Healing
A
• from coagulationa nd inflammation through fibroplasia, matrix deposition, angiogenesis, epithelialization, collagen maturation, wound contraction
10
Q
What do wound healing signals include
A
peptide growth factors, complement, cytokine inflammatory mediators, metabolic signals (hypoxia & accumulated lactate)
11
Q
What is redundant and pleiotropic in Wound healing
A
Cellular signaling pathways
12
Q
What is the first step of Wound Healing Mechanism and until when does it last
A
- Hemostasis and Inflammation
* 0-5th day after injury
13
Q
What happens in the first step of Wound Healing: Homeostasis and Inflammation
A
- stops bleeding
- immediately, coagulation products fibrin, fibrinopeptides, thrombin split products and complement components attract inflam. cells
- inflam cells increase metabolic demand
- local microvasc damaged → local energy ↓ , PaO₂ ↓ , Co₂ ↑
- oxidative stres triggers tissue repair
- Macrophages synthesize wound healing molecules, release lactate
- lactate stimulates angiogenesis and collagen deposition
- if not infected wound _> granulocyte population diminishes
- fibroblasts and new blood vessels
14
Q
What factors are released by Platelets activated (by thrombin) in the 1st step of wound healing?
A
• insulinlike growth factor (IGF-1), transforming growth factor α (TGF- α), transforming growth factor β (TGF-β), platelet derived growth factor (PDGF)
15
Q
What do IGF-1, TGF- α, TGF-β, PDGF attract to the wound?
A
leukocytes, macrophages, fibroblasts
16
Q
what complement products are involved in the signal cascade which damaged endothelial cells respond to?
A
C5a, tumor necrosis factor α (TNF- α), interleukin-1 (IL-1), interleukin 8 (IL-8)
17
Q
What happens in the second step of healing: Proliferation (Fibroplasia and Matrix Synthesis) 4-14d
A
- Fibroplasia, localize near wound edge → active tissue repair environment with tissue oxygen tension of 40mmHg, optimal for fibroblast replication
- smooth muscle cells progenitors of fibroblasts
- lipocytes, pericytes, stem cells may differentiate into fibroblasts
- Extracellular matrix depostion
- fibroblasts secrete collagen and proteoglycans
- extracelullar molecule sof matrix become physical basis of wound strength
- growth factors & metabolic products (lactate) regulate and stimulate synthesis of collagen
- collagen gene expression controlled by stress corticoids, TGF_β signaling pathway, retinoids
18
Q
What is Fibroplasia stimulated by?
A
PDGF, IGF-1, TGF- β, later by peptide growth fsctor release
19
Q
What stimulates fibroplasia?
A
• growth factors and cytokines: → fibroblast growth factor FGF → IGF-1 → vascular endothelial growth factor VEGF → IL-1, IL-2, IL-8 → PDGF →TGF- α, TGF- β → TNF- α
20
Q
What do growth factors regulate regardless of collagen gene expression?
A
- glycosaminoglycans
* tissue inhibitors of metalloproteinase (TIMP), fibronectin synthesis
21
Q
What happens in Angiogenesis?
A
- 2nd to 4th day after injury
- earlier than 4 days when new capillaries sprout from preexisting venules and grow towards injury in response to chemoattractants
- budding vessels soon meet and fuse with counterparts
- blood flow establishment across wound
- in left open wounds, new capillaries connect with adjacent capillaries in same direction → granulation tissue
22
Q
Where are the dominant angiogenic stimulants in wounds derived from?
A
- platelets in response to coagulation
* then from macrophages in response to hypoxia or ↑ lactate, fibrin
23
Q
What growth factors are involved in Angiogenesis?
A
PDGF, FGF, TNF α, TGF β, VEGF
24
Q
What happens in Epithelization
A
- starts from wound edges
- new migrate to unhealed area, anchor to first unepithelialized matrix encountered
- PaO₂ low under cell at anchor point → further mitosis
- epidermal mesenchymal communication continues until wound closed
25
What regulates epithelial cell replication?/ are potent epithelial mitogens
* TGF α, keratinocyte growth factor (KGF)
| * TGF- β which blocks epithelial cells from differentiating and therefore is a potent mitogen
26
What triggers TGF- β production from squamous epithelial cells?
low PaO₂
27
When does Squamous epithelialization and differentiation proceed maximally
* when surface of wound kept moist
| * e.g exudates froma cute uninfected wounds also contains growth factors and lactate
28
What impairs process of epithelialization and differentiation
drying of wound
29
What happens in Maturation and Remodeling?
* 8d to months
* fibroblasts replace fibrin matrix with collagen monomers
* extracellular enzymes, some PaO₂ dependent, polymerize monomers, collagen fibrils and cross link them to collagen fibers
* random pattern, predispose early aournd joints → disabling
30
What might prevent disabling wound contractures?
Skin grafts, especially thick ones, dynamic splints
31
What are wounds vulnerable to during rapid turnover?
contraction and stretching
32
What do wound myofibroblasts express which also contributes force to fibroblast-mediated wound contraction?
express intracellular actin filaments
33
Which part of the GI is least reliably and more likely to leak compared to the stomach or small intestine anastomoses with rare leakage
colon, esophageal
34
Does Intestinal anastomoses or skin wounds regain strength rapidly?
intestinal anastomoses
35
what part of GI lacks serosal mesothelial lining (source of repair cells) which might contribute to failed wound healing?
esophagus, retroperitoneal colon
36
When is danger of leakage the greatest?
4th to 7th day, when tensile strength could be impeded by impaired collagen deposition or ↑ lysis
37
From where does Injury (fracture) cause hematoma formation?
damaged blood vessels of periosteum, endosteum, surrounding tissue
38
What do monocytes and granulocytes debride and digest on fracture surface?
necrotic tissue and debris including bone
39
What is callus?
* thickened and hardened part of skin or soft tissue, especially in area of friction
* composed of fibroblasts, endothelial cells, bone-forming cells (chondroblasts, osteoblasts)
40
What is endochondral bone formation?
•osteocytes (fibroblasts) deposit collagenous matrix, chondroblasts deposit proteoglycans
41
What is the most frequent cause of healing failure?
* impaired perfusion
| * inadequate oxygenation
42
Which factors lead to failure to heal
* anti-inflammatory corticosteroids, immune suppressants, cancer chemotherapeutic agents that inhibit inflam. cells
* malnutrition
* weight loss
* protein depletion
43
Where is upregulation of fibroblast growth factor like TGF-β implicated?
hypertrophic & keloid scar formation
44
The PaO₂ of wound fluid in human incision is about...?
30-40 mmHg
45
critical collagen oxygenases involved have Km values for oxygen of...?
20 mmHg → 200mmHg
46
What are the most common acute wound complications?
• pain, infection, mechanical dehiscence, hypertrophic scar
47
How do venous ulcers occur?
* largely of lower leg
* reflect poor perfusion & perivascular leakage of plasma into tissue (stimulates inflammation)
* most heal of venous congestion and edema relived by leg elevation, compression stockings, surgical procedures
48
Arterial or ischemic ulcers?
* lateral ankle or foot
* treated by revascularization
* hyperbaric oxygen expensive treatment of O₂ delivery
49
Diabetic ulcers
* ischemic disease (with neuropathy or not): at risk for gangrene
* neuropathy if trauma
* amputation if revascularisation not possible, protection of ulcer
50
Wat are pyoderma gangrenosum, granulomatous inflammation excess cytokine release leads to? what are these ulcers associated with?
* cause skin necrosis
| * associated with inflammatory bowel disease
51
Decubitus ulcer
* immobilization
* prolonged pressure, reduces tissue supply, irritative or contaminated injections, prolonged contact with moisture, urine, feces
* poorly nourished patients, immobile elderly, ICU patients
* greater trochanter, sacrum, heels, head
* treated with drainage of infected space, excision of necrotic tissue, musculocutaneous flap
52
What is the treatment of chronic wounds and ulcer
* control infection with antibiotics
* treat underlying circulatory disease
* moist
* debridement of unhealthy tissue
* reduce autonomic vasoconstriction
53
Peritoneal scarring (adhesions)
* bands of scar tissue connecting organs
* fibrin, fibroblasts, collagen = filmy adhesions
* fibrinolysis within 1 week
* migration of capillaries, nerves, connective tissue = solid adhesions
54
silk suture
* soft tissue
* is an animal protein, inert in human
* loses strengt over period of time
* unsuitable for arteries, insertion prosthetic cardiac valves
* multifilament
* provide immune barriers for bacteria
55
synthetic non absorbable sutures
* inert polymers → strength
* knotted at least 4 times
* incr amount of retained foreign material
* may become infected
* no harbour of bacteria
* nylon extremely unreactive, but hard to tie
56
synthetic absorbable sutures
* strong, predictable loss of strength
* minimal inflammation
* useful in contaminated GI, urologic, gynecologic operations
57
stainless steel wire
* inert, maintains strenght for long time
* difficult to tie
* painful
* no harbour of bacteria
* can be left in granulating wounds
58
Staples
* steel-tantalum alloys
* min tissue reaction
* skin closure
59
surgical glues, tissue adhesive
* safe and effective for repair of small skin incisions
* cryanoacrylate based glues
* seal serves as wound dressing
60
What is the goal in surgical technique/incisions/operations
* anatomic tissue approximation achieved but optimum tissue perfusion preserved
* fine instruments!!
* proteCt tissue from drying and contamination!
61
What is the optimal suture length to wound length ratio in laparotomy closure?
4:1
62
What happens, when wound closure is excessively tight?
* strangulates tissue
* impair wound perfusion & oxygen delivery
* hernia formation or infection
63
delayed primary closure
* wound left open 4-5 days
| * angiogenesis and fibroplasia start, bacteria cleared from wound
64
What are examples of wounds that should be left open for secondary closure?
• fibrin-covered or inflamed wounds
65
What level of β-hemolytic streptococcal wound infection predicts delayed wound healing
any level
66
What do highly incompatible material like wood splinters elicit
• acute inflammatory process, massive release of proteolytic enzymes
67
What influence has Negative Pressure Wound Therapy on Wounds
* stabilizes distractive forces of an open wound and supports healing
* distractive forces keep wound open with force vectors opposing wound contraction, impair healing
68
What treatment is done when chronic infection and significant tissue loss are combined?
Musculocutaneous flaps
69
What are pros and cons of Adhesive tapes?
+ rapid, simple, no risk of needle injury
- needs dry skin, poor adherence, poor hemostasis, accidental removal
70
What are pros and cons of skin glue
+ rapid, simple, reduced pain, good aesthetic result
- poor approximation of deep layer, poor hemostasis
71
Pros and cons of Surgical skin staples
+ fast closure of large wounds, less reaction than sutures
- poor hemostasis
72
example cutting instrument
* scalpels
| * scissors for sutures or tissues
73
examples grasping instruments
* tissue forceps
* ratcheted tissue forceps
* needle-holder
74
example retracting instruments
* hand-held retractors
* self- retaining retractors
* large (complex) self-retaining retractors
75
Surgical staplers
* skin stapler
* linear stapler
* GI anastomosis stapler
* circular stapler
76
Local anesthetics mechanism
• nerve conduction relies on cell membrane depolarisation (Na⁺ inflow) and repolarization (K⁺ outflow)
→ local anesthetics inhibit electrical conduction along neurones
• transient blocking of Na⁺ transport channels → blocking depolarization
→ sensory neurons more sensitive than motor neurons
77
Examples Local Anesthetics
* Lidocaine (Xylocaine 2%-20mg/ml) with or without adrenaline
* Bupivacine (Marcaine 0.5%-5mg/dl)
* Ropivacaine (Naropaine 0.75%-7.5 mg/ml)
```
onset = 5-10 min
duration = 1-6 hours
```
78
Method local anesthetics: Topical
* lipid soluble cream
| * skin and mucosa up to few mm deep
79
Method local anesthetics: Local infiltration
* injected into tissue
| * local nerves
80
Method local anesthetics: Nerve block
* injected around nerve or plexus
| * distribution of nerve blocked
81
Method local anesthetics: Intravenous block
* IV injection in arterial turniqueted limp
| * nerve tissues within limb
82
Method local anesthetics: centrineural block
* epidural or spinal injection
| * multiple dermotomes
83
Method local anesthetics: Cavity administration
* intrapleural or intraperitoneal administration
| * local nerves in cavity
84
What are side effects of local anesthesia toxicity
* mouth and tongue numbness
* anxiety
* tremor
* drowsiness
* tachypnea
* hypotension
* nausea & vomiting
* allergy
85
Lidocaine
* onset 5-10min
| * max dose 300mg for 70kg person
86
Name the total body water distribution
• 30-40% intracellular
• 15-20% extracellular
→ 80% (12-16% of TBM) in interstitial compartment, 20% (3-4%) in intravascular(1/4 proximal to arterioles, 3/4 distal to arterioles)
87
what is the main intracellular cation?
potassium ion K⁺
88
what is the main extracellular cation?
sodium ion Na⁺
89
what are intracellular cations electrically balanced by?
polyatomic ion phosphate (PO₄³⁻ ) and negatively charged proteins
90
what are extracelullar cations balanced by?
chloride ion (Cl⁻)
91
what is the main cause for high colloid pressure in serum, which in turn is chief regulator of fluid distribution between 2 extracellular compartments?
albumin, protein in intravascular fluid
92
What does the relationship between colloid osmotic pressure and hydrostatic pressure govern?
movement of water across capillary membrane
93
how is the body's voluem status and electrolyte composition dtermined by kidneys?
• maintain constant volume and osmolality by modulating amount of free water and Na⁺ being reabsorbed from renal filtrate
94
What is the chief regulator of osmolality?
Antidiuretic hormone, or arginine vasopressin
95
Is following true:
| collecting duct is permeable to water leading to water accumulation and production of dilute urine
NO
impermeable to water, leading to water loss and prod of dilute urine
96
at high levels ADH(antidiuretic hormone) has what effect on arterioles
vasoconstriction
97
where is most filitered Na⁺ reabsorbed into? (60-70%)
proximal tubule
20-30 into thick ascending limb LOH
5-10% reabsorbed by distal tubule
98
what is osmolality
* total solute concentration
| * 290-310 mOsm/Kg
99
Hypovolemia
• surgical patients
• loss of isotonic fluids in setting of hemorrhage, GI losses, sequestration of fluids in gut lumen, burns, excessive diuretic therapy
• in poor settings: sweat as well
• loss of Na⁺ and water without affecting osmolality of extracellular fluid, little shift of water
• stimulation aldosterone secretion from zona glomerulosa (adrenal cortex)
→ ↑ reabsorption of Na⁺ and water from renal filtrate, excretion of low vol of hypertonic urine (oliguria)
100
Clinical Presentation of Hypovolemia & laboratory
* longitudinal furrows on tongue, dry oral and nasal mucous membranes
* ↑ capillary refill time, unclear speach, upper & lower extremity wekaness, dry axilla, postural hypotension
* elevated blood urea nitrogen (BUN)
* disproportionate rise in BUN compared to creatinine (Cr)
101
what is 91-100% sensitive clinical finding for severe Hypovolemia
postural incr in heart rate of at least 30 beats per min with postural dizziness
102
Treatment hypovolemia?
isotonic fluid
103
Metabolism of what is decreased by liver disease
• circulating aldosterone and ADH
104
Hypervolemia
* surgical patients
* after treatment of shock with colloid and crytalloid fluids
* postoperative period when ADH secreted, disrupting role in regulation of osmolality
* high ADH → vasoconstrictive
105
Clinical presentation and treatment of hypervolemia
• hypertension, decreased arterial oxygen saturation, basilar crackles, jugular venous distention, soft tissue edema, gallop rythmus, rapid weight gain
* edema = diuretics, if extreme: hemodialysis
* mechanical ventilation
106
Sodium
* predominant in extracellular fluid
* c influences fluid osmolality
* changes Na⁺ inversely proportional to TBW
* serum Na⁺ = 135-145 mEq/L
107
Serum Sodium?
135-145 mEq/L
108
Hyponatremia
* < 135 mEq/L
| * caused by dilution as result of excess H₂O or ↑Na loss
109
What are causes of Hyponatremia
* Dilution: iatrogenic, polydipsia, severe hyperglycemia, secretion of ADH, drugs
* Depletion: low sodium diet, GI losses, renal losses
110
clinical observation of severe hyponatremia
• < 120 mEq/L
→ CNS (mental obtundation, seizures, coma, incr intracranial pressure)
• musculoskeletal (weakness, fatigue, cramps)
111
What can lead to osmotic demyelination syndrome (central pontine and extrapontine myelinolysis) in Hyponatremia?
• rapid correction with hypertonic saline
SLOW CORRECTION
112
what does extrarenal loss indicate in reference to the amount of Na⁺ urine concentration
it's low
113
what does renal losses indicate in reference to the amount of Na⁺ urine concentration
it's high
114
Hypernatremia & its causes
* > 145 mEq/L, Urine specific gravity (SG) > 1.030 if nonrenal water loss
* loss of free water
* caused by high vol due to gain of Na⁺ in excess of water (iatrogenic), hyperaldosteronism, Cushing syndrome
* normal or low vol due to loss of free water via renal, GI, diabetes insipidus)
115
What is induced hypernatremia a treatment for?
• in patients with traumatic brain injury to reduce cerebral edema, decrease intracranial pressure, increase cerebral perfusion pressure
116
What are clinical observations of Hypernatremia?
• thirst
• if Na⁺ > 160mEq/L
→ cellular dehydration (extracellular water shifting)
→ CNS symptoms (restlessness, irritability, seizures, coma)
→ musculoskeletal (weakness)
• of hypovolemic hypernatremia
→ tachycardia
→ orthostatic hypotension
117
Potassium
* major intracellular cation
* 2% extracellular, 98 % intracellular (1/50)
* critical to cardiac and neuromuscular function
* serum: 3.5-5 mEq/L
118
What is the K⁺ concentration determined by?
• acid-base homeostasis
→ H⁺ and K⁺ exchanged between intra and extracellular spaces, disturbances influence K⁺
• size of total body K⁺ pool
→ intracellular stores of K⁺ large, exhausted when prolonged ketoacidosis
119
Hypokalemia
* < 3.5 mEq/L
* either decreased GI losses, excessive diuretic admin., prolonged malnutrition (alcoholics), prolonged alkalosis (intracellular K⁺ shifting
120
Clinical presentation of Hypokalemia
• decreased muscle contractibility
→ diaphragmatic paralysis, fatigue, weakness, decr reflexes
• GI (ileus, constipation)
• Cardiovascular
→ flattened or inverted T wave, prominent U wave
→ cardiac arrhythmias
→ PEA, asystole
121
Hyperkalemia
• > 5 mEq/L
• catabolism inducing events, cell destruction
→ crush injuries, burns, hemolysis, rhabdomyolysis
• renal insufficiency
• adrenal insufficiency
• excessive K⁺ admin.
• impaired K⁺ secretion
→ pottassium sparing diuretics, renal insuffciency
• K⁺ extracellular shifting
→ acidosis
122
Clinical presentation Hyperkalemia
```
• GI
→ nausea, vomiting, colic, diarrhea
• Neuromuscular
→ weakness, paralysis, cramps, muscle twitches, paresthesia
• low BP
• Cardiovascular
→ flattened P wave, peaked T wave, later alarming finding of widened QRS → ventricular fibrillation
→ arrest!!!
```
123
Where do we find the Chvostek's sign and Trousseau's sign?
Hypokalemia, hypocalcemie (chvostek)
124
Where is Magnesium needed?
* ATP must be bound to Mg²⁺ to be active
| * required for DNA transcription and translation , nerve conduction, ion transport, Ca²⁺ channel activity
125
Magnesium
* predom intracellular
* 1/3 albumin bound
* 50-60% in bone
* serum: 1.5-2.5 mg/dL
* absorbed by gut, excess excreted by kidneys, if insufficient, kidney retains it
126
Hypomagnesemia
* malnutrition (alcoholism)
* GI losses (diarrhea)
* diuretic or aminoglyceride use (renal excretion)
* acidosis
* hypo or hypercalcemia, hypophosphatemia
127
Clinical presentation Hypomagnesemia
* hypokalemia refractory to parenteral K⁺ admin
* canc ause sedation, muscle paralysis, tetany, seizures, coma
* Cardiovascular ECG alterations → torsade de pointes(tachycardia), arrest
* can cause hykpokalemia
128
Calcium
* half of serum bound to albumin
* unboudn fraction active
* homeostasis influenced by Vit D, parathyroid hormone, calcitonin, acid-base balance, PO₄³⁻ homeostasis
129
Hypocalcemia
• hypothyroidism, hypoparathyroidism, pancreatitis, renal insufficiency, crush injuries, severe soft tissue infections, necrotizing infections
130
Clinical presentation Hypocalcemia
• neuromuscular dysfunction
→ hyperactive deep tendon refelxes
Chvostek sign, muscle cramps, abd pain, tetany, cardiac arrythmias
131
Hypercalcemia
• primary or tertiary hyperparathyroidism, hyperthyroidism, bony cancer metastases, paraneoplastic syndromes, thiazide diuretic use
132
Clinical presentation Hypercalcemia
• anorexia, nausea, vomiting, polydipsia, polyuria, depression, confusion, memory loss, stupor, coma, psychosis, cardiac arrythmias, constipattion, acute pancreatitis, nephrolithiasis, osteoporosis, osteomalacia,...
133
Phosphorus P⁻³
* primarily a constituent of bone
* predom intracellular anion HPO₄³⁻
* high in metabolic active cells = high energy phosphate products ATP
* controlled by urinary secretion
* 2.5-4.5 mg/dL
134
Phosphate PO₄³⁻
* in skeleton
* intracellular
* energy metabolism
135
Hyophosphatemia
* < 2.5 mg/dL
* malnutrition, alcoholic
* consumption large amount antacids following liver resection → binding of P in bowel
* refeeding syndrome (caloric for 5 days eats again)
* hyperparathyroidism
136
Clinical presentation of Hypophosphatemia
```
• muscular and neurological dysfunction
→ muscle wekness, diplopia, depressed cardiac output, respiratory depression due to diaphragmatic weakness, confusion, coma, death, delirium
• rhabdomyolysis
• osteomalakia (chronic depletion)
• severe = < 1mg/dL
```
137
Hyperphosphatemia
* severe renal disease
* after trauma
* incr intake (phosphorus rich laxatives
* incr production due to cell destruction
* > 4.5 mg/dL
138
Clinical Presentation Hyperphosphatemia
* asymptomatic
| * may cause hypocalcemia → ↑ calcium phosphate product deposited in tissue → calcifications
139
What does Acid-Base Balance involve
* dietary intake, renal clearance
* extracellular and intracellular buffer systems
* respiratory, renal excretion
140
Acid-Base Balance
* daily metabolism produces 1 mEq/kg of H⁺
| * CO₂ → H₂CO₃
141
What Buffer Systems are included in Acid-Base balance
* intracellular proteins (hemoglobin)
* extracelullar bicarbonate/ carbonic acid
H⁺ + HCO₃⁻ H₂CO₄ H₂O + CO₂
142
What does the concentration of H⁺ determine in a solution?
its acidity
143
Henderson Hasselbach equation?
* strength of acid determined by degree of dissociation into H⁺ and corresponding base
* pH = pK x log [A−]/[HA]
K = dissociation constant, [A−] = concentration of acid, [HA] = concentration of base. Stronger acids have a higher K than weaker acids.
144
what is the main buffer in human blood?
carbonic acid/ bicarbonate system (H₂CO₃/ HCO₃⁻)
pH = pK xlog[HCO₃⁻]/[H₂CO₃ ]
145
What is the reaction of carbonic acid to CO₂ catalyzed by?
carbonic anhydrase
146
How is Acid-base homeostasis maintained
is maintained by pulmonary excretion of CO2
147
What is PCO₂ regulated by
pulmonary ventilation
148
What is HCO₃⁻ regulated by
kidney
* HCO₃⁻ reabsorption
* secretion of H⁺
* secretion of NH₄⁺
149
What is the normal pH
7-34-7.45
150
Acidemia
pH < 7.35
151
Alkalemia
pH > 7.45
152
Normal value HCO₃⁻
22-26 mmol/L
153
PCO₂ normal value
35-45 mmHg
154
Anion Gap
• represents difference between primary measured serum cation Na⁺ and primary measured serum anions CL⁻ and HCO₃⁻
AG = Na+ − (Cl− + HCO3−) = UA- UC
• normally 3-11 mEq/L
155
Incr acid production causes an ↑ or ↓ in Anion Gap?
↑
156
Respiratory acidosis
* increased PCO₂ causes decreased pH
* PCO₂ above 45 mmHg
* ventilation inadequate, CO₂ accumulates in blood, carbonic anyhdrase converts to H₂CO₃ → acidosis
* respiratory arrest,a cute airway obstruction, pulmonary edema, pneumonia, saddle pulmonary embolus, aspiration of intraoral contents, acute respiratory distress syndrome
* excess ethanol ingestion
* head trauma
157
Acute Respiratory acidosis
* acute respiratory failrue (obstruction, aspiration)
* high PCO₂
* HCO₃⁻ stable
* pH decreased (acidemia)
158
Chronic Respiratory acidosis
* chronid resp failure
* high PCO₂
* high bicarbonate → renal excretion of ammonium as compensation
* pH normal
159
Where can Hypoventilation occur?
• postoperatively oversedated (narcotics, benzodiazepines) or recovery from general anesthesia
160
Treatment respiratory acidosis
* restoration ventilation
* aggr4essive chest physical therapy, pulmonary toilet
* diuretic if edema
* neumonia, antibiosis
* naloxone or flumazenil if narcotic or benzodiazepine overdfose
161
Respiratory alkalosis
* PCO₂ < 35 mmHg
* Hyperventilation (sepsis, psychogenic) decreases PCO₂
* seizures, tachycardia, low or normal BP, confusion, nausea
162
Acute Respiratory alkalosis
* acute hyperventilation
* PCO₂ decreases
* HCO₃⁻ stable
* pH increases
163
Chronic Respiratory alkalosis
* PCO₂ decreases
* HCO₃⁻ decreases
* pH normal
164
Compensation to Respiratory Alkalosis
* 80% of acidosis buffered by bodys tissue and intracellular hemoglobin
* rest buffered by HCO₃⁻ in blood, kidney claims and reabsorbs
• renal compensation slower than respiratory
165
Compensation Respiratory Alkalosis
* decreased reabsorption of filtered HCO₃⁻, increaed urinary HCP₃⁻ excretion
* while bicarbonate decreases, CL⁻ increases, since reabsorbed with Na⁺
166
Metabolic acidosis
• HCO₃⁻ < 22 mmol/L
• excessice lost HCO₃⁻, increased H⁺
• diarrhea diuretics
• Cl⁻ increased
• trauma, ill postoperative patients, shock
.* excessive acid production (lactic acid, acetoacetate, b-hydroxybutyrate)
→ anion gap increased more than 12 mEq/L
167
Metabolic Alkalosis
* HCO₃⁻ > 26 mmol/L
* loss of H* → high HCO₃⁻
* vomiting, nasogastric suction
* impaired renal excretion of HCO₃⁻
* hypochloremia
* vol depletion
168
Name types of replacement fluids
• crystaloids
→ solution of water with electrolytes (Na⁺,Cl⁻)
→ solution of water with glucose (dextrose)
• colloids
→ solution of high molecular weight macromolecules
169
What are the replacement fluid guidelines
* 30-40 ml/kg/day → maintenance fluid
* replace all losses vol for vol
* isotonic vs hypotonic vs hypertonic
* no K⁺ for early potsoperative period
170
What is the infused fluids distribution of glucose, Na⁺, colloids?
Glucose: 2/3 intracellular, 1/3 extracellular
Na⁺: 1/4 intravascular, 3/4 interstitial
Colloids: intravascular space
171
Immediate postoperative period
```
• postanesthetic phase
• postanesthesia care unit (PACU)
→ monitoring 1-3 hours after surgery
→ discharge when normalized functions
• discharge with written orders to ward, ICU and high dependency unit HDU
```
172
What are Postoperative orders?
* monitoring
* respiratory care
* position in bed and mobilization
* diet
* fluids & electrolytes
* meds
* lab and imaging exams
173
What are disease of thoracic wall
```
• thoracic wall infections
• osteomyelitis after e.g sternotomy
• Mondor's disease
→ thrombophlebitis of sup thoracic v
→ after mastectomy or breast augmentation
• Tietze syndrome
→ painful non supportive costtochondritis
→ probably seroneg rheumatic disease
```
174
Thoracic wall tumors
• 25% asymptomatic, 60% malignant
• soft tisse tumor
→ Benign: Lipoma, Neurogenic tumors (neurofibromas)
→ Malignant: Fibrosarcomas, Liposarcomas
• skeletal tumors
→ benign: Chondromas, osteochondromas, myxochondromas
→ Malignant: Osteosarcomas, Chondrosarcomas, Myelomas
175
Diseases of the Pleura
• Pleural effusion
→ Hydrothorax (transudate in pleural cavity)
→ empyema (gathering of pus in existent cavity)
→ hemothorax (blood in pleural cavity)
→ chylothorax (lymphatic fluid from major thoraci duct in pleural cavity)
176
Mechanism of pleural fluid accumulation
* increase pulmonary hydrostatic pressure
* decreased vascular colloidal osmotic pressure
* increased capillary permeability due to inflammation
* decrease intrapleural pressure
* decrease lymphatic drainage
* transdiaphragmatic movement of abdominal fluid
* rupture of vascular structure
177
What is the difference between Transudate and Exudate
Transudate: fluid created as a result of hydrostatic pressure
Exudate: fluid ccreated as a result of inflammation
178
Transudate components
* Protein < 3g/dL
* protein fluid/ serum ratio < 0.5
* LDH < 200 U/dL
* LDH fluid/serum ratio < 0.6
* SG < 1.016
179
In which diseases do we find Hydrothorax
Malignancy of 25%
* Cardiovascular disease
* renal disease
* pancreatitis
* cirrhosis
* thromboembolism
180
Diagnosis of pleural effusion
* Chest X Ray
| * Pleural fluid analysis
181
Treatment of Pleural effusion
Drainage, Pleurodesis
182
Pneumothorax
* collapsed lung
* air leaks between lung and chest wall
* Simple pneumothorax
* Open Pneumothorax (air between chest wall and lung due to open wound or physical defect)
* Tension Pneumothorax (accumulation under pressure, decreasing venous return to heart and compressing the lung
* Spontaneous → rupture of apical bullae, Marfan's syndrome
* Secondary → traumatic, barotrauma
183
Localized fibrous tumor of pleura
* from fibroblasts
* asymptomatic
* benign 70%
184
Diffuse malignant pleural mesothelioma
* asbestos exposure (after 15-50 years)
* dyspnea, chest wall discomfort, fever, malaise, weight loss
* radiology (xray.CT): pleural thickening, effusion 75%
* median survival of 7-16 months
185
Acute mediastinitis
• caused by esophageal perforation (90%)
• manifestation: chills, fever, shock, subcutaneous emphysema/ pneumomediastinum
• Diagnosis: contrast x-ray, CT
• treatment: surgical exploration
→ early less than 24 h = primary closure
→ late more than 48h = drainage, late reconstruction
• mortality 30-60%
186
thymoma
• 30% myasthenia gravis
→ ↓ acetylcholine receptors
→ anti Ach receptor antibody
→ weakness
→ fatigability of voluntary muscle
• paraneoplastic syndromes: cytopenia, aplasia, hypogammaglobulinemia, autoimmune disorders
• diagnosis: tensilon test = short acting acticholinesterase = improvement of symptoms
• treatment: anicholinesterases, corticoids, total thmectomy
187
Name congenital diseases of the lung
* tracheobronchial atresia (absence trachea)
* Bronchogenic cysts (abnormal growth of tissue filled with fluid or mucous)
* Bronchopulmonary dysplasia (alveoli do not function, always O₂ supply)
* Pulmonary sequestrations (cystic piece of abnormal lung tissue, does not function as lung)
188
Lung Diseases
```
• Lung abscess
• Bronchiectasis
• Cystic fibrosis & Mucoid impaction
• Lung tuberculosis
• Fungal infections
→ histoplasma capsulatum, coccidioides immitis, blastomyces dermatidis, cryptococcus neoformans, aspergillus spp, mucormucosis, pneumocytosis carinii
• Sarcoidosis
→ granulomatosus disease
→ blacks / whites = 15/1
→ erythema nodosum, weight loss, fatigue, wekaness, malaise, peripheral lymph node enlargement
→ diagnosis by exclusion
```
189
Primary lung cancer
* 1st cause of cancer related death
* 85% due to smoking, asbestos, uranium, exposure
* pathology
Non small cell carcinoma
→ squamous cell carcinoma (2/3) near hilum
→adenocarcinoma (80% peripheral)
→ large cell carcinoma
Small cell carcinoma
→ occur centrally
→ early metastases
→ worse prognosis
190
Clinical presentation of primary lung cancer
* central tumors: cough, hemoptysis, respiratory difficulties, pain, pneumonia
* peripheral tumors: cough, chest wall pain, pleural effusion, pulmonary abscess, Horner's syndrome (ipsilateral myosis, ptosis, anhidrosis), Pancoast syndrome (ipsilateral shoulder and arm pain C8-T1)
* disease spread to recurrent laryngeal nerve, phrenic nerve, esophagus, superior vena cava
* paraneoplastic syndromes
191
Diagnosis of Primary Lung Cancer
* chest xray
* CT scan of chest, abdomen, brain
* PET (FDG)
* bronchoscopy with biopsy
* CT guided FNA
* thoracocentecis (removal of fluid)/ thoracoscopy
* serum ALP
192
Treatment of Primary Lung Cancer
• small cell carcinoma
→ chemotherapy + radiation
→ surgical resection for localized early disease
• non-small cell carcinoma
→ early stage (I/II): surgery +/- adjuvant chemotherapy
→ Stage III: Multimodality treatment (chemotherapy, radiation, surgery)
→ Stage IV: Chemotherapy or Palliative treatment
193
Prognosis Lung Cancer
```
• Non small cell carcinoma 5 year survival
→ Stage I: 50%
→Stage II: 30%
→Stage III: 10%
→Stage IV: < 2%
```
• small cell carcinoma median survival
→ 12-16 months
194
Solitary pulmonary nodule
• solitary nodule = coin lesion
• incidence cancer of 10%
• differential diagnosis
→ cancer, tuberculosis, histoplasmosis, echincoccosis, rheumatoid arthritis, Wegener's granulomatosis, congenital anomalies, benign neoplasms
• suspicipus characteristics
→ large, rapid growth with no calcifications
→ smokers under 50 and negative skin test (TB,..)
• Diagnosis
→ CT, FNA; SURGICAL EXCISIONAL BIOPSY
195
Metastatic lung cancer
* 30% of patients with metastases
* from testicular, head-neck cancers, sarcomas, renal cell carcinomas, colon carcinoma, melanoma
* from hematogenous spread
* asymptomatic
* medically fit patients with controlled disease that have isolated lung metastases may be resected
196
Cardiopulmonary bypass
• cardiac surgery in bloodless, motionless field
• blood drained from heart and lungs, returned oxygenated to cannulated arterial system using a pump and artificial lung (gas- exchanger)
• ascending aorta cross clamped above coronary ostia
• myocardial protection
→ diastolic electromechanical arrest with drugs
→ K⁺ rich solutions
→ Hypothermia (25-32°)
• effects of CPB: SIRS, disturbance in fibrinolysis
197
Postoperative management
```
• controlled mechanical ventilation for 12-24h
• drainage catheters in mediastinum
• monitoring of ECG, SpO₂, BP,ABG
• antibioprophylaxis
• complications
→ bleeding (2-5% reoperation)
→ arrythmias
→postoperative pulmonary hypertensive crisis
```
198
Congenital heart disease
* duplex ultrasound to diagnose
* cardiac catherization useful because it gives information abt blood flow and resistance
* most require surgical treatment with cardiopulmonary bypass
199
Coarctation of aorta?
birth defect in which part of aorta is narrower
200
Atrial septal defect
hole in eseptum, blood flows from left atrium to right atrium
201
Atrioventricular canal defect
hole between two heart chambers, mixed blood
202
Patent Ductus Arteriosus
ductus arteriosus fails to close after birth, mixing of blood
203
Tetralogy of Fallot
* ventricular septal defect (hole in ventricles, mix of blood)
* pulmonary stenosis (pulmonary valve to small ,narrow stiff)
* overriding of aorta (arises above both ventricle sinstead of just left one)
* right ventricular hypertrophy (thickening walls of right ventricle)
204
Acquired heart disease
* 1st cause of death
* account for 40% of death
* ischemic heart disease 25% of death in developed world
205
Ischemic heart disease
```
• right coronary artery
-Y post descending branch
• left coronary artery
→ left ant descending
→ left circumflex coronary artery
```
206
Angina pectoris
• retrosternal chest pain (angina pectoris)
I no symptoms
II symptoms with severe exertion
III symptoms with mild exertion
VI chest pain at rest
• chest pain due to coronary artery disease
207
Stable angina
heart works harder than usual,regular pattern. most common
208
Unstable angina
no regular pattern, doesnt go away with rest or medicine
209
Diagnosis of Coronary artery disease
• ECG, Cardiac enzymes, imaging studies (coronary arteriography, physiologic assessment (radionuclide exercise ventriculography, stress thalium scanning, exercise echocardiography
210
Treatment coronary artery disease
* medical treatment (nitroglycerin, β blocker, calcium channel blocker, antiplatelet drugs, heparin, glycoprotein IIB/IIA inhibitors, ACE inhibitors
* interventional treatment with percutaneos transluminal coronary angioplasty PTCA and stenting
* surgical treatment
211
Congenital heart disease
* duplex ultrasound to diagnose
* cardiac catherization useful because it gives information abt blood flow and resistance
* most require surgical treatment with cardiopulmonary bypass
212
Coarctation of aorta?
birth defect in which part of aorta is narrower
213
Symptoms of valvular heart disease
• dyspnea,, orthopnea
→ atrial fibrillattion → systemic emboli
→ mitral facies
→ accentuation of first heart sound, opening snap of mitral valve, diastolic murmur
• treatment
→ medical, percutaneous balloon valvotomy, surgical (open commisurotomy, valve replacement)
214
Atrioventricular canal defect
hole between two heart chambers, mixed blood
215
Patent Ductus Arteriosus
ductus arteriosus fails to close after birth, mixing of blood
216
Tetralogy of Fallot
* ventricular septal defect (hole in ventricles, mix of blood)
* pulmonary stenosis (pulmonary valve to small ,narrow stiff)
* overriding of aorta (arises above both ventricle sinstead of just left one)
* right ventricular hypertrophy (thickening walls of right ventricle)
217
Clinical findings and treatment of aortic stenosis
```
• clinical findings
→ angina pectoris
→ exertional syncope
→ congestive heart failure
→ harsh midsystolic murmur
```
• treatment
→ aortic valve replacement
218
Ischemic heart disease
```
• right coronary artery
-Y post descending branch
• left coronary artery
→ left ant descending
→ left circumflex coronary artery
```
219
Angina pectoris
• retrosternal chest pain (angina pectoris)
I no symptoms
II symptoms with severe exertion
III symptoms with mild exertion
VI chest pain at rest
• chest pain due to coronary artery disease
220
Stable angina
heart works harder than usual,regular pattern. most common
221
Unstable angina
no regular pattern, doesnt go away with rest or medicine
222
Diagnosis of Coronary artery disease
• ECG, Cardiac enzymes, imaging studies (coronary arteriography, physiologic assessment (radionuclide exercise ventriculography, stress thalium scanning, exercise echocardiography
223
Treatment coronary artery disease
* medical treatment (nitroglycerin, β blocker, calcium channel blocker, antiplatelet drugs, heparin, glycoprotein IIB/IIA inhibitors, ACE inhibitors
* interventional treatment with percutaneos transluminal coronary angioplasty PTCA and stenting
* surgical treatment
224
Surgical treatment of coronary artery disease
• coronary artery bypass surgery (CAB)
→ median sternotomy
→ cardiopulmonary bypass
→ saphenous vein or internal mammary artery graft
→ end to side internal mammary artery coronary anastomosis
• minimally invasive procedures
→ MIDCAB (minimally invasive coronary artery bypass)
→ OPCAB (off pump coronary artery bypass)
225
Valvular heart disease
• mitral stenosis
→ rheumatic fever (Group A Strept. pharyngitis)
→ congestion of pulmonary vessels → pulmonary hypertension
226
Symptoms of valvular heart disease
• dyspnea,, orthopnea
→ atrial fibrillattion → systemic emboli
→ mitral facies
227
Mitral regurgitation
• leakage of blood backward through mitral valve
• causes
→ rheumatic heart disease (40%)
→ idiopathic calcification
→ mitral valve prolapse (5%)
→ infective endocarditis
→ postinfarction papillary muscle rupture
228
Pathophysiology and treatment mitral regurgitation
• Pathophysiology
→ left atrial hypertension → pulmonary hypertension
→ chronic volume overload of left ventricle → myocardial failure
• Treatment
→ medical: diuretics (preload reduction), afterload reduction (ACE inhibitors)
→ surgical: mitral valve repair or replacement
229
Aortic stenosis
• narrowing of aortic valve
• causes
→ degenerative fibrosis & calcification, congenital, rheumatic
• resistance to left ventricular outflow
→ pressure overload left ventricle
→ concentric left ventricle hypertrophy (congestive heart failure)
→ increased myocardial oxygen consumption
230
Clinical findigns and treatment of aortic stenosis
```
• clinical findings
→ angina pectoris
→ exertional syncope
→ congestive heart failure
→ harsh midsystolic murmur
```
• treatment
231
Aortic insufficiency
• blood flow in reverse direction during ventricular diastole
• causes
→ rheumatic valvulitis, cystic medial necrosis, atherosclerosis, syphilitic degeneration, congenital bicuspid aortic valve
232
Clinical findings and treatment of Aorta insufficiency
• Clinical findings
→ poorly tolerated = severe pulmonary edema
→ high pitched diastolic murmur, 3 rd heart sound, diastolic rumble
→ widened pulse pressure and low diastolic pressure (Corrigan's pulse)
• Treatment
→ aortic valve replacement
233
Precutaneous valve replacement
* balloon valvuloplasty / valve replacement
* used in aortic valve stenosis, mitral valve stenosis, pulmonary valve stenosis
* for hish risk patients, absence of extensive calcifications
234
what are major determinants for choice of valve
* patients age
* expected longevity
* ability to take warfarin → wrong dosage could lead to bleed to death or clottage leading to death
* complexity of proceduure
* risk of valve thrombosis
235
Infective endocarditis
• bacterial infection of cardiac enndothelium
• pathophysiology
→ valve vegetations → leaflet destruction or embolism
→ microbes (skin): staph aureus, strept hemolyticus
• clinical findings
→ fever bacteremia, peripheral septic emboli
→ immunologic vascular phenomena (osler's nodules, roth's spots)
• diagnosis
→ blood cultures
-Y echocardiography
• treatment with antibiotics for 4-6 weeks, surgery
236
Thoracic aortic aneurysm
* causes: artherosclerosis, marfan's syndrome, trauma, infection
* clinical findings: local pressure, aortic regurgiation, sup vena cava obstruction
* imaging studies: chest xray, CT scan. MRI angiography
* treatment: control blood pressure, surgical treatment: aneurysms > 5,5 cm, growth rate >0.1 cm/year
237
hyperthyroidism
Serum TSH: decreased TSH
Primary: high free T4,T3 + low TSH
TSH mediated hyper: high TSH + high free T4
238
Hypothyroidism
Serum TSH: increased TSH
Primary: low free T4, high TSH
Central: low free T4, low TSH
free T3
239
Myxoedema
severe hypothyroidism
240
chronic lymphocytic Hashimoto thyroiditis
thyroid enlargement, variable clinical image, mild hyperthyroidism to hypothyroidism, high thyroid antibodies (anti TPO. anti TG) FNAC: lymphocytes
241
granulomatosus de Quervain's thyroiditis
* goiter, fever, head and chest pain, weakness, malaise
| * high ESR, high serum γ globulin, euthyroid or hyperthyroid
242
Riedel thyroiditis
* fibrosis with hard woody thyroid mass
* infiltrates muscle, tracheal compression
* hypothyroidism
243
Phaechromocytoma
• tumor of adrenal medulla or sympathetic ganglia
244
Follicular adenocarcinoma (10%)
* late life
* difficult to distinguish from normal thyroid
* metastases to lungs and bones
245
Medullary carcinoma
* solid hard nodule, contains amyloid, secretes calcitonin
* from parafollicular cells
* isolated or MEN2A, MEN2b, FMTC
246
Undifferentiated (anaplastic) carcinoma (1&)
* evolution of papillary or follicular neoplasm
* solid, quick enlarging, hard irregular mass
* infiltrates trachea, muscles and neurovascular structures
247
Physiology Cortex Adrenal Glands: Zona glomerulosa
• Aldosterone
→ Na⁺ retention
→ K⁺ excretion
248
Physiology Cortex Adrenal Glands: Zona fasciculata
```
• Cortisol
→ Glyconeogenesis
→ Lipolysis
→ decreased glucose utilization
→ decreased immunological response
• muscle catabolism
```
249
Physiology Cortex Adrenal Glands: Zona reticularis
• DHEA, DHEAS
250
Physiology Medulla Adrenal Glands:
```
• Adrenaline, Nor adrenaline, dopamine
• α & β adrenergic receptors
→ incr BP α1
→ incr HR and contractility β1
→ splanchnic vasoconstriction α1
→ skeletal muscle vasodil β2
→ bronchodilation β2
→ glyconeogenesis and lipolysis β2
```
251
Incidentaloma
adrenal mass detected incidentally by imaging studies
252
Cushing syndrome
* increased endogenous production of cortisol
| * ACTH dependent or independent
253
Conns syndrome
• hypersecrettion of aldosterone
→ hypertension
→ hypokalemia 88%
→ non specific symptoms
254
Adrenocortical carcinoma
• malignant cancer cells in outer layer adrenal cortex
255
Adrenal insufficiency
* Primary: loss of function adrenal cortex (addisons disease)
* secondary: deficiency of pituitary ACTH secretion
* Tertiary: deficiency of hypothalamus CRH secretion
256
Zollinger ellison syndrome
• tumor → stomach produce too much acid → ulcers
| 70% malignant
257
MEN1 syndrome
• Tumors:
→ anterior pituitary, parahyroid hyperplasia, phaechromocytomas
Mutation MEN1
258
MEN 2a syndrome
Tumors:
→ medullary thyroid carcinoma, parathyroid hyperplasia, phaechromocytomas
RET Mutation
259
MEN 2b syndrome
Tumors:
Medullary, thyroid carcinoma, phaechromocytoma, oral mucosal fibromas, intestinal ganglioneuromatosis, Marfanoid habittus
RET
260
Familial Medulary Thyroid carcinoma mutation?
RET, NTRK1
