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Medicine year 2 semester 2 > Case 24- Pathology > Flashcards

Case 24- Pathology Flashcards

1
Q

Approach to a patient with a fracture

A
  • Mechanism of injury
  • High energy- ABCDE
  • Physiology of patient- extremes of age
  • Associated co-morbidities
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2
Q

Open fracture

A

The bone fragment communicates with the outside. You can have inside out or outside in. Inside out is when the bone pokes out of the skin. Outside in could be when there is gun powder around the bone
• Higher risk of contamination
• Generally high energy trauma
• More soft tissue injury
• Delayed healing or non-union due to loss of heamatoma
• Soft tissue cover required- otherwise infection will occur

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3
Q

Managing a patient with a fracture

A
  • Wound care
  • Pain management
  • Imaging- Generally plain Xrays
  • Fracture care- conservative or surgical
  • Reduction, immobilisation- most important
  • Conservative- Plaster/ splints
  • Operative- Fixation
  • Early movements
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4
Q

Clinical symptoms of a fracture

A
  • Pain
  • Deformity
  • Bone crepitus
  • Abnormal mobility
  • Associated soft tissue injury
  • Neurovascular comprimise
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5
Q

Fracture classification

A
  • Growth plate involvement- Skeletally mature/immature
  • Anatomy- location- proximal/distal, diaphysis, metaphysis, epiphysis
  • Extent- complete/ incomplete
  • Orientation- transverse/ oblique/ spiral
  • Displacement- Non displaced/ displaced, angulated
  • Fragmentation- comminuted/ segmental
  • Soft tissue- open/ closed
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6
Q

Direction of fracture- LARA

A

• Length- two parts of the bone move away from each
• Alignment- the two parts of the bone tilt away from each other
• Rotation
• Apposition- one part of the bone moves slightly to the side
Where is the fracture= Intra-articular and Extra-articular

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7
Q

Complication of bone fractures

A

• Neurovascular injuries
• Compartment syndrome
• Infection
• Long term- stiffness, arthritis, instability, growth disturbances, non-union, avascular necrosis, complex regional pain syndrome
• General- DVT/PE, Chest infection/ UTI/ Pressure sores
Growth arrest- the growth plates may fuse together

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8
Q

Anaesthesia

A
  • “Insensitivity to pain, especially as artificially induced by the administration of gases or the injection of drugs before surgical operations.”
  • Not the same as analgesia – typically used to refer to reduced sensitivity to pain
  • Local anaesthesia – insensitivity to pain in a specific area
  • General anaesthesia – insensitivity to pain everywhere; also involves loss of consciousness (or a dissociative state)
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9
Q

When is a single anaesthetic used

A

In simple, short surgical procedure

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10
Q

The variety of anaesthetics used during surgery

A
  • A sedative premedication (e.g. a benzodiazepine)
  • An intravenous anaesthetic for rapid induction (e.g. propofol)
  • A perioperative opioid analgesic (e.g. alfentanil or remifentanil)
  • An inhalation anaesthetic to maintain anaesthesia during surgery (e.g. nitrous oxide and isoflurane)
  • A neuromuscular blocking agent to produce adequate muscle relaxation (e.g. vecuronium)
  • An antiemetic agent (e.g. ondansetron)
  • A muscarinic antagonist to prevent or treat bradycardia or to reduce bronchial and salivary secretions (e.g. atropine or glycopyrrolate)
  • An anticholinesterase agent towards the end of the procedure (e.g. neostigmine) to reverse the neuromuscular blockade
  • An analgesic for postop pain relief (e.g. an opioid such as morphine and/or a NSAID)
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11
Q

Stage 1 of anaesthesia- Analgesia

A
  • Analgesia (depends on agent)
  • Amnesia
  • Euphoria
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12
Q

Stage II of Anaesthesia: Excitement

A

Excitement, Delirium and Combative behaviour

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13
Q

Stage III Anaesthesia: Surgical anaesthesia

A

Unconsciousness, Regular respiration, Decreasing eye movement

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14
Q

Stage IV of Anaesthesia: Medullary depression

A
  • Respiratory arrest
  • Cardiac depression and arrest
  • No eye movement
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15
Q

Stages of Anaesthesia- Danger

A
  • Stage 2 is the dangerous “excitement” stage.
  • Irregular respiration and heart rate, possible uncontrolled movements, vomiting and breath holding.
  • Since the combination of spastic movements, vomiting, and irregular respirations may lead to airway compromise, rapidly acting drugs are used to minimize time in this stage and reach stage 3 as fast as possible.
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16
Q

Mechanisms of general anaesthesia

A
  • Change in excitability- inhalational anaesthetics in particular tend to hyperpolarise neurons, generally through activation of K+ channels
  • Changes in synaptic signalling- both IV and volatile anaesthetics influence synaptic transmission; in general these effects are potentiation of GABA A and glycine signalling and inhibition of NMDA-R’s but reductions in presynaptic calcium signals are also seen
  • Changes in action potential firing- many anaesthetics have a modest effect on sodium channels
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17
Q

Intravenous anaesthetic

A
  • Parenteral anesthetics are the most common drugs used for anesthetic induction of adults
  • High lipophilicity, coupled with the relatively high perfusion of the brain and spinal cord, results in rapid onset and short duration after a single bolus dose.
  • These drugs ultimately accumulate in fatty tissue.
  • Each of these anesthetics has its own unique properties and side effects
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18
Q

Iv anaesthetic half lives are ‘context sensitive’

A
  • Drug t1/2 varies greatly from drug to drug, as might be predicted based on their differing hydrophobicities and metabolic clearances.
  • After a single bolus of thiopental, patients usually emerge from anesthesia in ~ 10 min; however, it may take more than a day to awaken from a prolonged thiopental infusion.
  • Most individual variability is due to PK factors, e.g., in patients with lower cardiac output, the relative perfusion of the brain and the fraction of anesthetic dose delivered to the brain are higher; so patients in septic shock or with cardiomyopathy usually require lower doses of parenteral anesthetics.
  • The elderly also typically require a smaller parenteral anesthetic dose, primarily because of a smaller initial volume of distribution.
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19
Q

Common parenteral general anaesthetics

A

Thiopental, Etomidate, Ketamine, Propofol

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20
Q

How do Propofol and etomidate act

A
  • Propofol and etomidate act (at least in part) through potentiation of GABA A receptors
  • Potentiating actions of the intravenous anaesthetics, propofol (PROP) and etomidate (ETOM) on α2β3γ2 GABAA receptors
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21
Q

How do Propofol and etomidate act

A
  • Propofol and etomidate act (at least in part) through potentiation of GABA A receptors
  • Potentiating actions of the intravenous anaesthetics, propofol (PROP) and etomidate (ETOM) on α2β3γ2 GABAA receptors
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22
Q

Propofol

A
  • Propofol is the most commonly used parenteral anesthetic
  • Formulation is an emulsion in soybean oil (possible allergen) and water.
  • MOA is believed to be primarily GABA-A, with different subunits mediating analgesia and sedation. Some effect also on nicotinic receptors and voltage gated sodium channels
  • Because of its fast induction and recovery time, propofol is also widely used for sedation of infants and children undergoing MRI. It is also often used in combination with ketamine as the two together have lower rates of side effects
  • One of propofol’s most frequent side effects is pain on injection, especially in smaller veins. This pain arises from activation of the pain receptor, TRPA1, found on sensory nerves and can be mitigated by pretreatment with lidocaine.
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23
Q

Etomidate

A
  • Etomidate is poorly soluble in water and is formulated as a 2-mg/mL solution in 35% propylene glycol
  • Etomidate is primarily used for anesthetic induction of patients at risk for hypotension.
  • Induction doses of etomidate are accompanied by a high incidence of pain at injection site and myoclonic movements – lidocaine effectively reduces pain, while myoclonic movements can be reduced by premedication with either benzodiazepines or opiates
  • Produces hypnosis but NOT analgesia – minimal effects on blood pressure and ICP
  • Etomidate produces increased EEG activity in epileptogenic foci and has been associated with seizures.
  • Milder respiratory depression than thiopental
  • Also inhibits adrenal biosynthetic enzymes required for the production of cortisol and some other steroids.
24
Q

Ketamine

A
  • Ketamine is a phencyclidine analogue and is associated with dreams and hallucinations in some patients. It is unusual because it stimulates the cardiovascular and respiratory systems and is useful in the field (eg combat) and for patients with shock.
  • Ketamine rapidly produces a hypnotic state quite distinct from that of other anesthetics. Patients have profound analgesia, unresponsiveness to commands, and amnesia, but may have open eyes, move their limbs involuntarily, and breathe spontaneously. This cataleptic state is termed dissociative anesthesia.
  • MOA: primarily NMDA-R and nAChR inhibition.
  • Since it suppresses breathing much less than most other anesthetics, it is the anesthetic of choice when reliable ventilation equipment is not available. Otherwise, it is usually an adjunct agent, due to the risk of hallucinations
  • Low doses of ketamine reduce morphine use and nausea and vomiting after surgery
25
Q

Volatile anaesthetics and MAC

A
  • The potency of inhalational anesthetics is defined by its MAC value (the Minimum Alveolar Concentration of an anesthetic agent required to produce lack of reflex response to skin incision in 50% of subjects). The MAC values for isoflurane = 1.1%, sevoflurane = 2.0%, desflurane = 6.3% and nitrous oxide = 105%.
  • In many cases, inhalation anesthetics are additive, eg 0.5 MAC isoflurane plus 0.5 MAC N2O will lead to anesthesia in half of all subjects.
  • Volatile anesthetics are often preferred for maintenance of anesthesia due to the easy control of levels, and rapid elimination (through exhalation) of the anesthetic at the end of surgery
26
Q

Volatile anaesthetics Pharmacokinetics

A
  • Inhalational anesthetics distribute between tissues (or between blood and gas) such that equilibrium is achieved when the partial pressure of anesthetic gas is equal in the two tissues. While the partial pressure (tension) of the anesthetic may be equal in all tissues, the concentration of anesthetic in each tissue will be different.
  • Anesthetic partition coefficients are defined as the ratio of anesthetic concentration in two tissues when the partial pressures of anesthetic are equal in the two tissues.
  • These partition coefficients show that inhalational anaesthetics are more soluble in some tissues (e.g., fat) than they are in others (e.g., blood). In clinical practice, equilibrium is achieved when the partial pressure in inspired gas is equal to the partial pressure in end-tidal (alveolar) gas.
  • The oil-gas partition coefficient measures solubility in fatty tissues – the higher this is, the more potent the anaesthetic
26
Q

Volatile anaesthetics Pharmacokinetics (DELETE)

A
  • Inhalational anesthetics distribute between tissues (or between blood and gas) such that equilibrium is achieved when the partial pressure of anesthetic gas is equal in the two tissues. While the partial pressure (tension) of the anesthetic may be equal in all tissues, the concentration of anesthetic in each tissue will be different.
  • Anesthetic partition coefficients are defined as the ratio of anesthetic concentration in two tissues when the partial pressures of anesthetic are equal in the two tissues.
  • These partition coefficients show that inhalational anaesthetics are more soluble in some tissues (e.g., fat) than they are in others (e.g., blood). In clinical practice, equilibrium is achieved when the partial pressure in inspired gas is equal to the partial pressure in end-tidal (alveolar) gas.
  • The oil-gas partition coefficient measures solubility in fatty tissues – the higher this is, the more potent the anaesthetic
27
Q

Uptake of inhalational general anaesthetics

A
  • Uptake of inhalational general anaesthetics. The rise in alveolar FA anesthetic concentration toward the inspired FI concentration is most rapid with the least-soluble anesthetics (nitrous oxide and desflurane) and slowest with the most soluble anesthetic, halothane.
  • Anaesthesia is produced when anaesthetic partial pressure in brain is equal to or greater than MAC. Because the brain is well perfused, anaesthetic partial pressure in brain becomes equal to the partial pressure in alveolar gas (and in blood) within minutes. Therefore, anaesthesia is achieved shortly after alveolar partial pressure reaches MAC
28
Q

Uptake and elimination of inhalational anaesthetics

A
  • For inhalational agents that are not very soluble in blood or other tissues, equilibrium is achieved quickly, (e.g. nitrous oxide).
  • Elimination of inhalational anesthetics is largely a reversal of uptake. For inhalational agents with high blood and tissue solubility, recovery will be a function of the duration of anesthetic administration, like IV anaesthetics.
  • Patients will be arousable when alveolar partial pressure reaches MACawake, a partial pressure somewhat lower than MAC
29
Q

Typical volatile anaesthetic mechanism- GABA plus

A
  • As potentiation of GABAA receptors containing β2 and β3 subunits is sufficient for anaesthesia (see IV anaesthetics), and many inhalational anaesthetics, such as halothane, isoflurane and sevoflurane, potentiate the same receptors, it seems reasonable that this will contribute to the anaesthesia caused by these agents.
  • However, the potentiation caused by volatile anaesthetics is usually smaller (typically half) than that caused by etomidate and propofol (at equi‐anaesthetic concentrations), so GABA-A receptors cannot be the only target.
  • Additionally, xenon and nitrous oxide show little activity at GABAA receptors.
30
Q

Other targets for volatile anaesthetics: Glycine receptors

A
  • Often colocalised with GABA A receptors, and of particular importance in lower brain centres and the spinal cord, glycine receptors are a major target for inhalational agents.
  • Glycine receptors are also ligand gated chloride conductances causing hyperpolarization (inhibition)
  • Glycine receptors present a much more homogeneous population of targets than GABAA receptors because there are only four α subunits and a single β subunit, mostly α1 and β in the adult.
  • Glycine receptors can exist as αβ heteromers or α homomers. Their plausibility as a target is particularly strong for the loss of response to a painful stimulus, which appears to be determined predominantly by actions in the spinal cord
31
Q

Other targets for volatile anaesthetics: Two pore potassium channels

A
  • Diverse family of channels that are characterized by having two pore‐forming domains in their primary sequences, while having only moderate sequence homologies outside these regions.
  • Two subfamilies, TREK and TASK, have members that are enhanced by volatile and gaseous anaesthetics.
  • Responsible for potassium leak current
32
Q

Diethyl ether

A
  • Depresses cardiac function and enhances bronchial secretion.
  • Ether was discontinued because (a) it is highly flammable, and (b) it causes post-anesthesia nausea and vomiting.
  • MOA is thought to be largely through GABA-A receptors, but is not well studied as it was replaced by Halothane in the 1950s (less severe nausea, milder smell, and non-flammable.
33
Q

Isoflurane- replaced Halothane in the 1960’s

A
  • Isoflurane has a low blood:gas partition coefficient and so induction and recovery from isoflurane are faster, as are changes in anesthetic depth. More than 99% of inhaled isoflurane is excreted unchanged by the lungs.
  • Isoflurane produces some relaxation of skeletal muscle by its central effects. It also enhances the effects of both depolarizing and non-depolarizing muscle relaxants.
  • MOA is complex: Isoflurane enhances GABA A receptors affinity for GABA, potentiates glycine receptor activity to decrease motor function, and inhibits certain subtypes of the NMDA-receptor. Isoflurane also reduces presynaptic release.
  • Sevoflurane is similar but smells better, is non irritating, and allows rapid induction and recovery (it can also burst into flame in contact with dessicated CO2 absorbants)
34
Q

Isoflurane- clinical use

A
  • Isoflurane is typically used for maintenance of anesthesia after induction with other agents because of its pungent odor.
  • Induction of anesthesia can be achieved in less than 10 min with an inhaled concentration of 1.5%–3% isoflurane in O2; this concentration is reduced to 1%–2% (~1–2 MAC) for maintenance of anesthesia. The use of adjunct agents such as opioids or nitrous oxide reduces the concentration of isoflurane required for surgical anesthesia.
  • Isoflurane has a low blood:gas partition coefficient and so induction are relatively fast.
  • More than 99% of inhaled isoflurane is excreted unchanged by the lungs.
35
Q

Isoflurane- ADR

A
  • Isoflurane produces a concentration-dependent decrease in BP due to decreased systemic vascular resistance – it produces vasodilation in most vascular beds, with pronounced effects in skin and muscle.
  • Concentration-dependent depression of ventilatory response to hypercapnia and hypoxia. Although a bronchodilator, it also is an airway irritant and can stimulate airway reflexes during induction of anesthesia, producing coughing and laryngospasm.
  • Like other halogenated inhalational anesthetics, isoflurane produces some relaxation of skeletal muscle by its central effects. It also enhances the effects of both depolarizing and nondepolarizing muscle relaxants.
  • Includes uterine smooth muscle – Isoflurane is the preferred inhalational anaesthetic for use in obstetrics (surgical) – but not natural childbirth.
36
Q

Nitrous oxide

A
  • Nitrous oxide is a weak anaesthetic with good analgesic properties and its insolubility means rapid equilibrium and so rapid onset.
  • Anaesthesia requires hyperbaric conditions (MAC=105%), however significant analgesic dose is reached much earlier (20%); consequently dental surgery doses are frequently ~50% which provides mild sedation with strong analgesia.
  • MOA is primarily non-competitive antagonism at NMDA-R; analgesia is thought to be mediated by activation of opioid neurons in periaqueductal grey and adrenergic neurons in locus ceruleus. Also activates 2 pore K+ channels
37
Q

Malignant hyperthermia- treat with Dantrolene

A
  • Malignant hyperthermia (MH) is a life-threatening clinical syndrome of hypermetabolism involving the skeletal muscle, triggered in susceptible individuals by volatile anesthetics and the muscle relaxant succinylcholine -> not allergy but an inherited disorder.
  • An abnormal ryanodine receptor (role is CICR for muscle contraction) in susceptible patients causes a build up of calcium in skeletal muscle, resulting in a massive metabolic reaction.
  • This causes increased CO2 production, metabolic and respiratory acidosis, accelerated oxygen consumption, heat production, activation of the sympathetic nervous system, hyperkalemia, disseminated intravascular coagulation (DIC), and multiple organ dysfunction and failure.
38
Q

Signs and triggers of MH

A
  • Early clinical signs of MH include an increase in end-tidal CO2 (even with increasing ventilation), tachycardia, muscle rigidity, tachypnea, and hyperkalemia
  • Anesthetics are inconsistent in triggering MH. A susceptible individual may undergo anesthesia with MH-triggering agents on multiple occasions without incident but may still react to such agents on a subsequent occasion
39
Q

Neurotoxicity

A
  • A number of mouse studies have suggested a neurotoxic effect of anesthetics.
  • In general, this is seen in neonates, raising the possibility that anesthesia may cause long-term developmental impacts when given to young children.
  • More recent work indicates that there is a particularly window of vulnerability based on the age of the individual neurons at time of exposure.
40
Q

Head injury

A

Any trauma to the head other than superficial injuries to the face

41
Q

Head injuries can be defined by

A
  • Mechanism- penetrating or blunt
  • Severity- mild, moderate or severe
  • Open or closed
  • Focal or diffuse
  • Primary or secondary
42
Q

How we define the severity of a head injury

A
  • Mild= GCS >12
  • Moderate= GCS 9-12
  • Severe= GCS 8 or less
43
Q

How do I assess a head injury patient

A
  • Primary survey (ABCDE)- cervical spine immobilisation
  • Secondary survey- ‘head to toe’
  • Neurological assessment- General (GCS), Focal (cranial nerve examination)
  • Focal neurological- peripheral nerves (tone, power, sensation, reflexes)
44
Q

How do I assess a head injury patient

A
  • Primary survey (ABCDE)- cervical spine immobilisation
  • Secondary survey- ‘head to toe’
  • Neurological assessment- General (GCS), Focal (cranial nerve examination)
  • Focal neurological- peripheral nerves (tone, power, sensation, reflexes)
45
Q

How do you inspect the Scalp and face

A

Inspect and palpate for laceration, boggy swelling and base of skull fractures

45
Q

How do you inspect the Scalp and face

A

Inspect and palpate for laceration, boggy swelling and base of skull fractures

46
Q

How does brain injury cause death

A
  • Local ischaemia plus global ischaemia from cerebral auto regulation dysfunction.
  • Brain cells are reliant on good cerebral blood flow to get their metabolic requirements.
  • A total brain ischaemic which is enough to cause a coma is associated with reduced CBF in the first few hours after death.
  • A reduced CBF is likely to be unable to meet metabolic demands of the brain
47
Q

CBF auto-regulation

A

Pre-capillary vasculature can constrict or dilate in response to changes in mean arterial pressure (can cope with 50-150mmHg). Depends on cerebral perfusion pressure

48
Q

CPP equation

A

CPP= MAP – ICP
• CPP- cerebral perfusion pressure
• MAP- mean arterial pressure (normally 50-100mmHg)
• ICP- intracranial pressure (normally around 10 mmHg)

49
Q

What causes ICP in trauma

A
  • Blood i.e. haematoma

* Brain tissue swelling i.e. high MAP

50
Q

Blood in the brain

A
  • Epidural haematoma- rapidly expanding with arterial blood. Can be caused by a skull fracture which causes a torn middle meningeal artery. The Dura is pushed away by the haematoma
  • Subdural haematoma- slowly expanding with venous blood. Due to a torn bridging vein. The Dura is attached to the skull so the blood cannot cross the falx tentorium
51
Q

Diffuse brain injury

A
  • Concussion- often mild, usually normal CT
  • Diffuse axonal injury- due to shearing forces. Associated with high velocity and deceleration. In the CT you may see widespread punctate haemorrhages
52
Q

Secondary brain injury is exacerbated by

A
  • Hypoxia
  • Hypercarbia and iatrogenic hypocapnia
  • Hypotension and hypertension
53
Q

Treatment for raised ICP

A

Reducing ICP through Mannitol injections or Hypertonic saline solution

54
Q

Brain death

A
  • GCS 3
  • Non-reactive pupils
  • Absent brainstem reflexes
  • No spontaneous ventilatory effort

Medicine year 2 semester 2 (47 decks)

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