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General Surgery > Midterm exam > Flashcards

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
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2
Q

Chronic Wound

A
  • fail of wound healing

* prolonged tissue repair

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3
Q

When does healing arrest most commonly occur?

A

Inflammatory phase

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4
Q

failed epithelialization due to repeated trauma or desiccation may result in?

A

Chronic partial thickness wound

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5
Q

Primary healing

A
  • tissue cleanly incised
  • anatomically reapproximated
  • healing by primary intention
  • no complications, minimal scarring
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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
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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
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8
Q

Granulation tissue

A
  • red, moist, granular tissue

* collagen, new blood vessels, fibroblasts, inflammatory cells, scar tissue

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9
Q

Mechanism of Wound Healing

A

• from coagulationa nd inflammation through fibroplasia, matrix deposition, angiogenesis, epithelialization, collagen maturation, wound contraction

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10
Q

What do wound healing signals include

A

peptide growth factors, complement, cytokine inflammatory mediators, metabolic signals (hypoxia & accumulated lactate)

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11
Q

What is redundant and pleiotropic in Wound healing

A

Cellular signaling pathways

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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

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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
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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)

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15
Q

What do IGF-1, TGF- α, TGF-β, PDGF attract to the wound?

A

leukocytes, macrophages, fibroblasts

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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)

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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
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18
Q

What is Fibroplasia stimulated by?

A

PDGF, IGF-1, TGF- β, later by peptide growth fsctor release

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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
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20
Q

What do growth factors regulate regardless of collagen gene expression?

A
  • glycosaminoglycans

* tissue inhibitors of metalloproteinase (TIMP), fibronectin synthesis

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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
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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

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23
Q

What growth factors are involved in Angiogenesis?

A

PDGF, FGF, TNF α, TGF β, VEGF

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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
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25
Q

What regulates epithelial cell replication?/ are potent epithelial mitogens

A
  • TGF α, keratinocyte growth factor (KGF)

* TGF- β which blocks epithelial cells from differentiating and therefore is a potent mitogen

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26
Q

What triggers TGF- β production from squamous epithelial cells?

A

low PaO₂

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27
Q

When does Squamous epithelialization and differentiation proceed maximally

A
  • when surface of wound kept moist

* e.g exudates froma cute uninfected wounds also contains growth factors and lactate

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28
Q

What impairs process of epithelialization and differentiation

A

drying of wound

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29
Q

What happens in Maturation and Remodeling?

A
  • 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
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30
Q

What might prevent disabling wound contractures?

A

Skin grafts, especially thick ones, dynamic splints

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31
Q

What are wounds vulnerable to during rapid turnover?

A

contraction and stretching

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32
Q

What do wound myofibroblasts express which also contributes force to fibroblast-mediated wound contraction?

A

express intracellular actin filaments

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33
Q

Which part of the GI is least reliably and more likely to leak compared to the stomach or small intestine anastomoses with rare leakage

A

colon, esophageal

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34
Q

Does Intestinal anastomoses or skin wounds regain strength rapidly?

A

intestinal anastomoses

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35
Q

what part of GI lacks serosal mesothelial lining (source of repair cells) which might contribute to failed wound healing?

A

esophagus, retroperitoneal colon

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36
Q

When is danger of leakage the greatest?

A

4th to 7th day, when tensile strength could be impeded by impaired collagen deposition or ↑ lysis

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37
Q

From where does Injury (fracture) cause hematoma formation?

A

damaged blood vessels of periosteum, endosteum, surrounding tissue

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38
Q

What do monocytes and granulocytes debride and digest on fracture surface?

A

necrotic tissue and debris including bone

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39
Q

What is callus?

A
  • thickened and hardened part of skin or soft tissue, especially in area of friction
  • composed of fibroblasts, endothelial cells, bone-forming cells (chondroblasts, osteoblasts)
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40
Q

What is endochondral bone formation?

A

•osteocytes (fibroblasts) deposit collagenous matrix, chondroblasts deposit proteoglycans

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41
Q

What is the most frequent cause of healing failure?

A
  • impaired perfusion

* inadequate oxygenation

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42
Q

Which factors lead to failure to heal

A
  • anti-inflammatory corticosteroids, immune suppressants, cancer chemotherapeutic agents that inhibit inflam. cells
  • malnutrition
  • weight loss
  • protein depletion
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43
Q

Where is upregulation of fibroblast growth factor like TGF-β implicated?

A

hypertrophic & keloid scar formation

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44
Q

The PaO₂ of wound fluid in human incision is about…?

A

30-40 mmHg

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45
Q

critical collagen oxygenases involved have Km values for oxygen of…?

A

20 mmHg → 200mmHg

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46
Q

What are the most common acute wound complications?

A

• pain, infection, mechanical dehiscence, hypertrophic scar

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47
Q

How do venous ulcers occur?

A
  • 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
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48
Q

Arterial or ischemic ulcers?

A
  • lateral ankle or foot
  • treated by revascularization
  • hyperbaric oxygen expensive treatment of O₂ delivery
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49
Q

Diabetic ulcers

A
  • ischemic disease (with neuropathy or not): at risk for gangrene
  • neuropathy if trauma
  • amputation if revascularisation not possible, protection of ulcer
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50
Q

Wat are pyoderma gangrenosum, granulomatous inflammation excess cytokine release leads to? what are these ulcers associated with?

A
  • cause skin necrosis

* associated with inflammatory bowel disease

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51
Q

Decubitus ulcer

A
  • 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
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52
Q

What is the treatment of chronic wounds and ulcer

A
  • control infection with antibiotics
  • treat underlying circulatory disease
  • moist
  • debridement of unhealthy tissue
  • reduce autonomic vasoconstriction
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53
Q

Peritoneal scarring (adhesions)

A
  • bands of scar tissue connecting organs
  • fibrin, fibroblasts, collagen = filmy adhesions
  • fibrinolysis within 1 week
  • migration of capillaries, nerves, connective tissue = solid adhesions
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54
Q

silk suture

A
  • 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
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55
Q

synthetic non absorbable sutures

A
  • 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
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56
Q

synthetic absorbable sutures

A
  • strong, predictable loss of strength
  • minimal inflammation
  • useful in contaminated GI, urologic, gynecologic operations
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57
Q

stainless steel wire

A
  • inert, maintains strenght for long time
  • difficult to tie
  • painful
  • no harbour of bacteria
  • can be left in granulating wounds
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58
Q

Staples

A
  • steel-tantalum alloys
  • min tissue reaction
  • skin closure
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59
Q

surgical glues, tissue adhesive

A
  • safe and effective for repair of small skin incisions
  • cryanoacrylate based glues
  • seal serves as wound dressing
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60
Q

What is the goal in surgical technique/incisions/operations

A
  • anatomic tissue approximation achieved but optimum tissue perfusion preserved
  • fine instruments!!
  • proteCt tissue from drying and contamination!
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61
Q

What is the optimal suture length to wound length ratio in laparotomy closure?

A

4:1

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62
Q

What happens, when wound closure is excessively tight?

A
  • strangulates tissue
  • impair wound perfusion & oxygen delivery
  • hernia formation or infection
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63
Q

delayed primary closure

A
  • wound left open 4-5 days

* angiogenesis and fibroplasia start, bacteria cleared from wound

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64
Q

What are examples of wounds that should be left open for secondary closure?

A

• fibrin-covered or inflamed wounds

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65
Q

What level of β-hemolytic streptococcal wound infection predicts delayed wound healing

A

any level

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66
Q

What do highly incompatible material like wood splinters elicit

A

• acute inflammatory process, massive release of proteolytic enzymes

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67
Q

What influence has Negative Pressure Wound Therapy on Wounds

A
  • stabilizes distractive forces of an open wound and supports healing
  • distractive forces keep wound open with force vectors opposing wound contraction, impair healing
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68
Q

What treatment is done when chronic infection and significant tissue loss are combined?

A

Musculocutaneous flaps

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69
Q

What are pros and cons of Adhesive tapes?

A

+ rapid, simple, no risk of needle injury

  • needs dry skin, poor adherence, poor hemostasis, accidental removal
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70
Q

What are pros and cons of skin glue

A

+ rapid, simple, reduced pain, good aesthetic result

  • poor approximation of deep layer, poor hemostasis
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71
Q

Pros and cons of Surgical skin staples

A

+ fast closure of large wounds, less reaction than sutures

  • poor hemostasis
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72
Q

example cutting instrument

A
  • scalpels

* scissors for sutures or tissues

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73
Q

examples grasping instruments

A
  • tissue forceps
  • ratcheted tissue forceps
  • needle-holder
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74
Q

example retracting instruments

A
  • hand-held retractors
  • self- retaining retractors
  • large (complex) self-retaining retractors
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75
Q

Surgical staplers

A
  • skin stapler
  • linear stapler
  • GI anastomosis stapler
  • circular stapler
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76
Q

Local anesthetics mechanism

A

• 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

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77
Q

Examples Local Anesthetics

A
  • 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
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78
Q

Method local anesthetics: Topical

A
  • lipid soluble cream

* skin and mucosa up to few mm deep

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79
Q

Method local anesthetics: Local infiltration

A
  • injected into tissue

* local nerves

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80
Q

Method local anesthetics: Nerve block

A
  • injected around nerve or plexus

* distribution of nerve blocked

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81
Q

Method local anesthetics: Intravenous block

A
  • IV injection in arterial turniqueted limp

* nerve tissues within limb

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82
Q

Method local anesthetics: centrineural block

A
  • epidural or spinal injection

* multiple dermotomes

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83
Q

Method local anesthetics: Cavity administration

A
  • intrapleural or intraperitoneal administration

* local nerves in cavity

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84
Q

What are side effects of local anesthesia toxicity

A
  • mouth and tongue numbness
  • anxiety
  • tremor
  • drowsiness
  • tachypnea
  • hypotension
  • nausea & vomiting
  • allergy
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85
Q

Lidocaine

A
  • onset 5-10min

* max dose 300mg for 70kg person

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86
Q

Name the total body water distribution

A

• 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)

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87
Q

what is the main intracellular cation?

A

potassium ion K⁺

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88
Q

what is the main extracellular cation?

A

sodium ion Na⁺

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89
Q

what are intracellular cations electrically balanced by?

A

polyatomic ion phosphate (PO₄³⁻ ) and negatively charged proteins

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90
Q

what are extracelullar cations balanced by?

A

chloride ion (Cl⁻)

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91
Q

what is the main cause for high colloid pressure in serum, which in turn is chief regulator of fluid distribution between 2 extracellular compartments?

A

albumin, protein in intravascular fluid

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92
Q

What does the relationship between colloid osmotic pressure and hydrostatic pressure govern?

A

movement of water across capillary membrane

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93
Q

how is the body’s voluem status and electrolyte composition dtermined by kidneys?

A

• maintain constant volume and osmolality by modulating amount of free water and Na⁺ being reabsorbed from renal filtrate

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94
Q

What is the chief regulator of osmolality?

A

Antidiuretic hormone, or arginine vasopressin

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95
Q

Is following true:

collecting duct is permeable to water leading to water accumulation and production of dilute urine

A

NO

impermeable to water, leading to water loss and prod of dilute urine

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96
Q

at high levels ADH(antidiuretic hormone) has what effect on arterioles

A

vasoconstriction

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97
Q

where is most filitered Na⁺ reabsorbed into? (60-70%)

A

proximal tubule

20-30 into thick ascending limb LOH

5-10% reabsorbed by distal tubule

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98
Q

what is osmolality

A
  • total solute concentration

* 290-310 mOsm/Kg

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99
Q

Hypovolemia

A

• 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)

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100
Q

Clinical Presentation of Hypovolemia & laboratory

A
  • 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)
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101
Q

what is 91-100% sensitive clinical finding for severe Hypovolemia

A

postural incr in heart rate of at least 30 beats per min with postural dizziness

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102
Q

Treatment hypovolemia?

A

isotonic fluid

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103
Q

Metabolism of what is decreased by liver disease

A

• circulating aldosterone and ADH

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104
Q

Hypervolemia

A
  • 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
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105
Q

Clinical presentation and treatment of hypervolemia

A

• 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
Q

Sodium

A
  • predominant in extracellular fluid
  • c influences fluid osmolality
  • changes Na⁺ inversely proportional to TBW
  • serum Na⁺ = 135-145 mEq/L
107
Q

Serum Sodium?

A

135-145 mEq/L

108
Q

Hyponatremia

A
  • < 135 mEq/L

* caused by dilution as result of excess H₂O or ↑Na loss

109
Q

What are causes of Hyponatremia

A
  • Dilution: iatrogenic, polydipsia, severe hyperglycemia, secretion of ADH, drugs
  • Depletion: low sodium diet, GI losses, renal losses
110
Q

clinical observation of severe hyponatremia

A

• < 120 mEq/L
→ CNS (mental obtundation, seizures, coma, incr intracranial pressure)
• musculoskeletal (weakness, fatigue, cramps)

111
Q

What can lead to osmotic demyelination syndrome (central pontine and extrapontine myelinolysis) in Hyponatremia?

A

• rapid correction with hypertonic saline

SLOW CORRECTION

112
Q

what does extrarenal loss indicate in reference to the amount of Na⁺ urine concentration

A

it’s low

113
Q

what does renal losses indicate in reference to the amount of Na⁺ urine concentration

A

it’s high

114
Q

Hypernatremia & its causes

A
  • > 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
Q

What is induced hypernatremia a treatment for?

A

• in patients with traumatic brain injury to reduce cerebral edema, decrease intracranial pressure, increase cerebral perfusion pressure

116
Q

What are clinical observations of Hypernatremia?

A

• 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
Q

Potassium

A
  • major intracellular cation
  • 2% extracellular, 98 % intracellular (1/50)
  • critical to cardiac and neuromuscular function
  • serum: 3.5-5 mEq/L
118
Q

What is the K⁺ concentration determined by?

A

• 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
Q

Hypokalemia

A
  • < 3.5 mEq/L
  • either decreased GI losses, excessive diuretic admin., prolonged malnutrition (alcoholics), prolonged alkalosis (intracellular K⁺ shifting
120
Q

Clinical presentation of Hypokalemia

A

• 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
Q

Hyperkalemia

A

• > 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
Q

Clinical presentation Hyperkalemia

A 
• 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
Q

Where do we find the Chvostek’s sign and Trousseau’s sign?

A

Hypokalemia, hypocalcemie (chvostek)

124
Q

Where is Magnesium needed?

A
  • ATP must be bound to Mg²⁺ to be active

* required for DNA transcription and translation , nerve conduction, ion transport, Ca²⁺ channel activity

125
Q

Magnesium

A
  • 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
Q

Hypomagnesemia

A
  • malnutrition (alcoholism)
  • GI losses (diarrhea)
  • diuretic or aminoglyceride use (renal excretion)
  • acidosis
  • hypo or hypercalcemia, hypophosphatemia
127
Q

Clinical presentation Hypomagnesemia

A
  • 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
Q

Calcium

A
  • half of serum bound to albumin
  • unboudn fraction active
  • homeostasis influenced by Vit D, parathyroid hormone, calcitonin, acid-base balance, PO₄³⁻ homeostasis
129
Q

Hypocalcemia

A

• hypothyroidism, hypoparathyroidism, pancreatitis, renal insufficiency, crush injuries, severe soft tissue infections, necrotizing infections

130
Q

Clinical presentation Hypocalcemia

A

• neuromuscular dysfunction
→ hyperactive deep tendon refelxes
Chvostek sign, muscle cramps, abd pain, tetany, cardiac arrythmias

131
Q

Hypercalcemia

A

• primary or tertiary hyperparathyroidism, hyperthyroidism, bony cancer metastases, paraneoplastic syndromes, thiazide diuretic use

132
Q

Clinical presentation Hypercalcemia

A

• anorexia, nausea, vomiting, polydipsia, polyuria, depression, confusion, memory loss, stupor, coma, psychosis, cardiac arrythmias, constipattion, acute pancreatitis, nephrolithiasis, osteoporosis, osteomalacia,…

133
Q

Phosphorus P⁻³

A
  • 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
Q

Phosphate PO₄³⁻

A
  • in skeleton
  • intracellular
  • energy metabolism
135
Q

Hyophosphatemia

A
  • < 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
Q

Clinical presentation of Hypophosphatemia

A 
• 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
Q

Hyperphosphatemia

A
  • severe renal disease
  • after trauma
  • incr intake (phosphorus rich laxatives
  • incr production due to cell destruction
  • > 4.5 mg/dL
138
Q

Clinical Presentation Hyperphosphatemia

A
  • asymptomatic

* may cause hypocalcemia → ↑ calcium phosphate product deposited in tissue → calcifications

139
Q

What does Acid-Base Balance involve

A
  • dietary intake, renal clearance
  • extracellular and intracellular buffer systems
  • respiratory, renal excretion
140
Q

Acid-Base Balance

A
  • daily metabolism produces 1 mEq/kg of H⁺

* CO₂ → H₂CO₃

141
Q

What Buffer Systems are included in Acid-Base balance

A
  • intracellular proteins (hemoglobin)
  • extracelullar bicarbonate/ carbonic acid

H⁺ + HCO₃⁻ H₂CO₄ H₂O + CO₂

142
Q

What does the concentration of H⁺ determine in a solution?

A

its acidity

143
Q

Henderson Hasselbach equation?

A
  • 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
Q

what is the main buffer in human blood?

A

carbonic acid/ bicarbonate system (H₂CO₃/ HCO₃⁻)

pH = pK xlog[HCO₃⁻]/[H₂CO₃ ]

145
Q

What is the reaction of carbonic acid to CO₂ catalyzed by?

A

carbonic anhydrase

146
Q

How is Acid-base homeostasis maintained

A

is maintained by pulmonary excretion of CO2

147
Q

What is PCO₂ regulated by

A

pulmonary ventilation

148
Q

What is HCO₃⁻ regulated by

A

kidney

  • HCO₃⁻ reabsorption
  • secretion of H⁺
  • secretion of NH₄⁺
149
Q

What is the normal pH

A

7-34-7.45

150
Q

Acidemia

A

pH < 7.35

151
Q

Alkalemia

A

pH > 7.45

152
Q

Normal value HCO₃⁻

A

22-26 mmol/L

153
Q

PCO₂ normal value

A

35-45 mmHg

154
Q

Anion Gap

A

• 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
Q

Incr acid production causes an ↑ or ↓ in Anion Gap?

A

↑

156
Q

Respiratory acidosis

A
  • 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
Q

Acute Respiratory acidosis

A
  • acute respiratory failrue (obstruction, aspiration)
  • high PCO₂
  • HCO₃⁻ stable
  • pH decreased (acidemia)
158
Q

Chronic Respiratory acidosis

A
  • chronid resp failure
  • high PCO₂
  • high bicarbonate → renal excretion of ammonium as compensation
  • pH normal
159
Q

Where can Hypoventilation occur?

A

• postoperatively oversedated (narcotics, benzodiazepines) or recovery from general anesthesia

160
Q

Treatment respiratory acidosis

A
  • restoration ventilation
  • aggr4essive chest physical therapy, pulmonary toilet
  • diuretic if edema
  • neumonia, antibiosis
  • naloxone or flumazenil if narcotic or benzodiazepine overdfose
161
Q

Respiratory alkalosis

A
  • PCO₂ < 35 mmHg
  • Hyperventilation (sepsis, psychogenic) decreases PCO₂
  • seizures, tachycardia, low or normal BP, confusion, nausea
162
Q

Acute Respiratory alkalosis

A
  • acute hyperventilation
  • PCO₂ decreases
  • HCO₃⁻ stable
  • pH increases
163
Q

Chronic Respiratory alkalosis

A
  • PCO₂ decreases
  • HCO₃⁻ decreases
  • pH normal
164
Q

Compensation to Respiratory Alkalosis

A
  • 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
Q

Compensation Respiratory Alkalosis

A
  • decreased reabsorption of filtered HCO₃⁻, increaed urinary HCP₃⁻ excretion
  • while bicarbonate decreases, CL⁻ increases, since reabsorbed with Na⁺
166
Q

Metabolic acidosis

A

• 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
Q

Metabolic Alkalosis

A
  • HCO₃⁻ > 26 mmol/L
  • loss of H* → high HCO₃⁻
  • vomiting, nasogastric suction
  • impaired renal excretion of HCO₃⁻
  • hypochloremia
  • vol depletion
168
Q

Name types of replacement fluids

A

• crystaloids
→ solution of water with electrolytes (Na⁺,Cl⁻)
→ solution of water with glucose (dextrose)

• colloids
→ solution of high molecular weight macromolecules

169
Q

What are the replacement fluid guidelines

A
  • 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
Q

What is the infused fluids distribution of glucose, Na⁺, colloids?

A

Glucose: 2/3 intracellular, 1/3 extracellular

Na⁺: 1/4 intravascular, 3/4 interstitial

Colloids: intravascular space

171
Q

Immediate postoperative period

A 
• 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
Q

What are Postoperative orders?

A
  • monitoring
  • respiratory care
  • position in bed and mobilization
  • diet
  • fluids & electrolytes
  • meds
  • lab and imaging exams
173
Q

What are disease of thoracic wall

A 
• 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
Q

Thoracic wall tumors

A

• 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
Q

Diseases of the Pleura

A

• 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
Q

Mechanism of pleural fluid accumulation

A
  • 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
Q

What is the difference between Transudate and Exudate

A

Transudate: fluid created as a result of hydrostatic pressure

Exudate: fluid ccreated as a result of inflammation

178
Q

Transudate components

A
  • Protein < 3g/dL
  • protein fluid/ serum ratio < 0.5
  • LDH < 200 U/dL
  • LDH fluid/serum ratio < 0.6
  • SG < 1.016
179
Q

In which diseases do we find Hydrothorax

A

Malignancy of 25%

  • Cardiovascular disease
  • renal disease
  • pancreatitis
  • cirrhosis
  • thromboembolism
180
Q

Diagnosis of pleural effusion

A
  • Chest X Ray

* Pleural fluid analysis

181
Q

Treatment of Pleural effusion

A

Drainage, Pleurodesis

182
Q

Pneumothorax

A
  • 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
Q

Localized fibrous tumor of pleura

A
  • from fibroblasts
  • asymptomatic
  • benign 70%
184
Q

Diffuse malignant pleural mesothelioma

A
  • 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
Q

Acute mediastinitis

A

• 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
Q

thymoma

A

• 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
Q

Name congenital diseases of the lung

A
  • 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
Q

Lung Diseases

A 
• Lung abscess
• Bronchiectasis
• Cystic fibrosis &amp; 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
Q

Primary lung cancer

A
  • 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
Q

Clinical presentation of primary lung cancer

A
  • 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
Q

Diagnosis of Primary Lung Cancer

A
  • chest xray
  • CT scan of chest, abdomen, brain
  • PET (FDG)
  • bronchoscopy with biopsy
  • CT guided FNA
  • thoracocentecis (removal of fluid)/ thoracoscopy
  • serum ALP
192
Q

Treatment of Primary Lung Cancer

A

• 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
Q

Prognosis Lung Cancer

A 
• 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
Q

Solitary pulmonary nodule

A

• 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
Q

Metastatic lung cancer

A
  • 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
Q

Cardiopulmonary bypass

A

• 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
Q

Postoperative management

A 
• 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
Q

Congenital heart disease

A
  • duplex ultrasound to diagnose
  • cardiac catherization useful because it gives information abt blood flow and resistance
  • most require surgical treatment with cardiopulmonary bypass
199
Q

Coarctation of aorta?

A

birth defect in which part of aorta is narrower

200
Q

Atrial septal defect

A

hole in eseptum, blood flows from left atrium to right atrium

201
Q

Atrioventricular canal defect

A

hole between two heart chambers, mixed blood

202
Q

Patent Ductus Arteriosus

A

ductus arteriosus fails to close after birth, mixing of blood

203
Q

Tetralogy of Fallot

A
  • 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
Q

Acquired heart disease

A
  • 1st cause of death
  • account for 40% of death
  • ischemic heart disease 25% of death in developed world
205
Q

Ischemic heart disease

A 
• right coronary artery
-Y post descending branch
• left coronary artery
→ left ant descending
→ left circumflex coronary artery
206
Q

Angina pectoris

A

• 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
Q

Stable angina

A

heart works harder than usual,regular pattern. most common

208
Q

Unstable angina

A

no regular pattern, doesnt go away with rest or medicine

209
Q

Diagnosis of Coronary artery disease

A

• ECG, Cardiac enzymes, imaging studies (coronary arteriography, physiologic assessment (radionuclide exercise ventriculography, stress thalium scanning, exercise echocardiography

210
Q

Treatment coronary artery disease

A
  • 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
Q

Congenital heart disease

A
  • duplex ultrasound to diagnose
  • cardiac catherization useful because it gives information abt blood flow and resistance
  • most require surgical treatment with cardiopulmonary bypass
212
Q

Coarctation of aorta?

A

birth defect in which part of aorta is narrower

213
Q

Symptoms of valvular heart disease

A

• 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
Q

Atrioventricular canal defect

A

hole between two heart chambers, mixed blood

215
Q

Patent Ductus Arteriosus

A

ductus arteriosus fails to close after birth, mixing of blood

216
Q

Tetralogy of Fallot

A
  • 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
Q

Clinical findings and treatment of aortic stenosis

A 
• clinical findings
→ angina pectoris
→ exertional syncope
→ congestive heart failure
→ harsh midsystolic murmur

• treatment
→ aortic valve replacement

218
Q

Ischemic heart disease

A 
• right coronary artery
-Y post descending branch
• left coronary artery
→ left ant descending
→ left circumflex coronary artery
219
Q

Angina pectoris

A

• 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
Q

Stable angina

A

heart works harder than usual,regular pattern. most common

221
Q

Unstable angina

A

no regular pattern, doesnt go away with rest or medicine

222
Q

Diagnosis of Coronary artery disease

A

• ECG, Cardiac enzymes, imaging studies (coronary arteriography, physiologic assessment (radionuclide exercise ventriculography, stress thalium scanning, exercise echocardiography

223
Q

Treatment coronary artery disease

A
  • 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
Q

Surgical treatment of coronary artery disease

A

• 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
Q

Valvular heart disease

A

• mitral stenosis
→ rheumatic fever (Group A Strept. pharyngitis)
→ congestion of pulmonary vessels → pulmonary hypertension

226
Q

Symptoms of valvular heart disease

A

• dyspnea,, orthopnea
→ atrial fibrillattion → systemic emboli
→ mitral facies

227
Q

Mitral regurgitation

A

• 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
Q

Pathophysiology and treatment mitral regurgitation

A

• 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
Q

Aortic stenosis

A

• 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
Q

Clinical findigns and treatment of aortic stenosis

A 
• clinical findings
→ angina pectoris
→ exertional syncope
→ congestive heart failure
→ harsh midsystolic murmur

• treatment

231
Q

Aortic insufficiency

A

• blood flow in reverse direction during ventricular diastole
• causes
→ rheumatic valvulitis, cystic medial necrosis, atherosclerosis, syphilitic degeneration, congenital bicuspid aortic valve

232
Q

Clinical findings and treatment of Aorta insufficiency

A

• 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
Q

Precutaneous valve replacement

A
  • balloon valvuloplasty / valve replacement
  • used in aortic valve stenosis, mitral valve stenosis, pulmonary valve stenosis
  • for hish risk patients, absence of extensive calcifications
234
Q

what are major determinants for choice of valve

A
  • 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
Q

Infective endocarditis

A

• 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
Q

Thoracic aortic aneurysm

A
  • 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
Q

hyperthyroidism

A

Serum TSH: decreased TSH
Primary: high free T4,T3 + low TSH
TSH mediated hyper: high TSH + high free T4

238
Q

Hypothyroidism

A

Serum TSH: increased TSH
Primary: low free T4, high TSH
Central: low free T4, low TSH
free T3

239
Q

Myxoedema

A

severe hypothyroidism

240
Q

chronic lymphocytic Hashimoto thyroiditis

A

thyroid enlargement, variable clinical image, mild hyperthyroidism to hypothyroidism, high thyroid antibodies (anti TPO. anti TG) FNAC: lymphocytes

241
Q

granulomatosus de Quervain’s thyroiditis

A
  • goiter, fever, head and chest pain, weakness, malaise

* high ESR, high serum γ globulin, euthyroid or hyperthyroid

242
Q

Riedel thyroiditis

A
  • fibrosis with hard woody thyroid mass
  • infiltrates muscle, tracheal compression
  • hypothyroidism
243
Q

Phaechromocytoma

A

• tumor of adrenal medulla or sympathetic ganglia

244
Q

Follicular adenocarcinoma (10%)

A
  • late life
  • difficult to distinguish from normal thyroid
  • metastases to lungs and bones
245
Q

Medullary carcinoma

A
  • solid hard nodule, contains amyloid, secretes calcitonin
  • from parafollicular cells
  • isolated or MEN2A, MEN2b, FMTC
246
Q

Undifferentiated (anaplastic) carcinoma (1&)

A
  • evolution of papillary or follicular neoplasm
  • solid, quick enlarging, hard irregular mass
  • infiltrates trachea, muscles and neurovascular structures
247
Q

Physiology Cortex Adrenal Glands: Zona glomerulosa

A

• Aldosterone
→ Na⁺ retention
→ K⁺ excretion

248
Q

Physiology Cortex Adrenal Glands: Zona fasciculata

A 
• Cortisol
→ Glyconeogenesis
→ Lipolysis
→ decreased glucose utilization 
→ decreased immunological response
• muscle catabolism
249
Q

Physiology Cortex Adrenal Glands: Zona reticularis

A

• DHEA, DHEAS

250
Q

Physiology Medulla Adrenal Glands:

A 
• Adrenaline, Nor adrenaline, dopamine
•  α &amp; 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
Q

Incidentaloma

A

adrenal mass detected incidentally by imaging studies

252
Q

Cushing syndrome

A
  • increased endogenous production of cortisol

* ACTH dependent or independent

253
Q

Conns syndrome

A

• hypersecrettion of aldosterone
→ hypertension
→ hypokalemia 88%
→ non specific symptoms

254
Q

Adrenocortical carcinoma

A

• malignant cancer cells in outer layer adrenal cortex

255
Q

Adrenal insufficiency

A
  • Primary: loss of function adrenal cortex (addisons disease)
  • secondary: deficiency of pituitary ACTH secretion
  • Tertiary: deficiency of hypothalamus CRH secretion
256
Q

Zollinger ellison syndrome

A

• tumor → stomach produce too much acid → ulcers

70% malignant

257
Q

MEN1 syndrome

A

• Tumors:
→ anterior pituitary, parahyroid hyperplasia, phaechromocytomas

Mutation MEN1

258
Q

MEN 2a syndrome

A

Tumors:
→ medullary thyroid carcinoma, parathyroid hyperplasia, phaechromocytomas

RET Mutation

259
Q

MEN 2b syndrome

A

Tumors:
Medullary, thyroid carcinoma, phaechromocytoma, oral mucosal fibromas, intestinal ganglioneuromatosis, Marfanoid habittus

RET

260
Q

Familial Medulary Thyroid carcinoma mutation?

A

RET, NTRK1

General Surgery (2 decks)

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