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Integrerad sluttentament - Läkarprogrammet T11 Karolinska Institutet HT17

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Ett 6-stegs protokoll för hur man lämnar svåra besked - cancer, dödsfall, allvarlig skada eller sjukdom etc.

¤ Set-up:
Hur man ordnar inför samtalet, t.ex. avskilt utan störande moment, sitta ned, ta det lugnt, bjuda med anhöriga, ögonkontakt, informera om ev. tidsbegränsning, lämna ifrån dig ev. sökare.
Var påläst om tillståndet, patientens sjukhistoria och ha en plan för fortsatt handläggning redo för diskussion.

¤ Perception:
Hur patienten uppfattat sin situation, kan använda öppna frågor som "vad vet du om ditt tillstånd?" "vet du varför du har kommit hit idag?", "berätta hur du uppfattat situationen fram till nu" etc.

¤ Invitation:
Alla patienter är inte mottagliga för all information medan andra vill höra allt på en gång - fråga t.ex. "vill du få reda på allt nu eller ska vi bara ta det viktigaste?"

¤ Knowledge:
Varna patienten på att den kommer att få dåliga nyheter, säg t.ex. "Jag är ledsen att behöva säga att..", "Tyvärr måste jag lämna det tråkiga beskedet att..." När du ger beskedet, använd vardagliga ord (spridit sig, elakartad, återfall...) och portionera ut informationen, kolla att patienten följer med i samtalet.

¤ Emotions:
Alla känslor är tillåtna (ilska, tårar, axelryckning, shock, isolering) - svara på det du ser med empati och bekräfta känslorna, t.ex. "jag ser att du är ledsen, och jag förstår att det här inte var vad du hade hoppats på få höra", eller säg eller "berätta, vad tänker du?" om patienten är tyst. Fortsätt tills patienten återhämtat sig något och samlat sig.

¤ Strategy:
Försök ge hopp - berätta att det finns flera professionella i ett team runt om patienten som kommer finnas där för att stötta hen och göra sitt bästa, och att det finns en plan. Fråga pat om hen är redo att ta del av planen och diskutera den. Lämna aldrig en definitiv prognos. Erbjud patienten att sitta kvar i lugn och ro, och fråga om du kan kontakta någon anhörig om hen är ensam med dig.
Morfin verkar via μ-δ-opioid (Mu-Delta) receptorer. μ-receptorerna finns främst i amygdala, thalamus, hypothalamus, nucleus caudatus och putamen samt delar av cortex cerebrii och ryggmärgens substantia gelatinosa.

Morfin verkar främst i CNS och GI-trakten via μ-opioida receptorer.

Schematisk bild: http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hematology-oncology/cancer-pain/images/figure-2.jpg


Stimuli from tissue injury activate primary afferent neurons called nociceptors, found in skin, muscle, joints, and some visceral organs. Nociceptors are high-threshold receptors that are silent until significantly stimulated.18 Most nociceptors are polymodal, responding to thermal, physical, and chemical stimuli. Neuron cell bodies are located within the superficial laminae of the dorsal root ganglia and trigeminal ganglia. Once depolarized, transmission occurs proximally via thin myelinated A-δ fibers (fast) or unmyelinated C fibers (slow). Interneurons within laminae I and II of the dorsal horn amplify or dampen neurotransmission. Afferent axons terminate in lamina I or II, and second-order afferent neurons cross the midline and ascend all the way to the brainstem and thalamus in the anterolateral quadrant of the contralateral half of the spinal cord. Together with axons from second-order lamina I neurons, these fibers form the spinothalamic tract, the major ascending pathway for information about pain and temperature (Figure 2). Sensory fibers associated with affective responses also ascend in the contralateral dorsolateral spinal cord to the medial thalamus or brainstem and then to the cingulate cortex and limbic lobe. Downward modulation occurs through the periaqueductal gray (PAG) and rostral ventral medulla (RVM) with axons that transverse the dorsal lateral funiculus. These modulate pain directly by connections to secondary afferent neurons in the dorsal horn or via connections with interneurons in laminae I and II (Figure 2).19 The neurochemistry of these processes involve multiple neurotransmitters including endorphins, prostraglandins, gamma-aminobutyric acid (GABA), cannabinoids, and many others, that are targets for analgesic medications.17


Stimulation of the periaqueductal gray (PAG) matter of the midbrain activates enkephalin-releasing neurons that project to the raphe nuclei in the brainstem. 5-HT (serotonin) released from the raphe nuclei descends to the dorsal horn of the spinal cord where it forms excitatory connections with the "inhibitory interneurons" located in Laminae II (aka the substantia gelatinosa). When activated, these interneurons release either enkephalin or dynorphin (endogenous opioid neurotransmitters), which bind to mu opioid receptors on the axons of incoming C and A-delta fibers carrying pain signals from nociceptors activated in the periphery. The activation of the mu-opioid receptor inhibits the release of substance P from these incoming first-order neurons and, in turn, inhibits the activation of the second-order neuron that is responsible for transmitting the pain signal up the spinothalamic tract to the ventroposteriolateral nucleus (VPL) of the thalamus. The nociceptive signal was inhibited before it was able to reach the cortical areas that interpret the signal as "pain" (such as the anterior cingulate). This is sometimes referred to as the Gate control theory of pain and is supported by the fact that electrical stimulation of the PAG results in immediate and profound analgesia.[1] The periaqueductal gray is also activated by viewing distressing images associated with pain.[2]

Three known kinds of opioid receptors have been identified: mu (μ), kappa (κ) and delta (δ). Synthetic opioid and opioid-derivative drugs activate these receptors (possibly by acting on the PAG directly, where these receptors are densely expressed) to produce analgesia. These drugs include morphine, heroin (diacetylmorphine), pethidine, hydrocodone, oxycodone, and similar pain-reducing compounds.

receptors is associated with analgesia, sedation, euphoria, physical dependence, and respiratory depression. Morphine is also a κ-opioid and δ-opioid receptor agonist, κ-opioid's action is associated with spinal analgesia, miosis (pinpoint pupils) and psychotomimetic effects. δ-Opioid is thought to play a role in analgesia.[54] Although morphine does not bind to the σ-receptor, it has been shown that σ-agonists, such as (+)-pentazocine, inhibit morphine analgesia, and σ-antagonists enhance morphine analgesia,[56] suggesting downstream involvement of the σ-receptor in the actions of morphine.

The effects of morphine can be countered with opioid antagonists such as naloxone and naltrexone; the development of tolerance to morphine may be inhibited by NMDA antagonists such as ketamine or dextromethorphan.[57] The rotation of morphine with chemically dissimilar opioids in the long-term treatment of pain will slow down the growth of tolerance in the longer run, particularly agents known to have significantly incomplete cross-tolerance with morphine such as levorphanol, ketobemidone, piritramide, and methadone and its derivatives; all of these drugs also have NMDA antagonist properties. It is believed that the strong opioid with the most incomplete cross-tolerance with morphine is either methadone or dextromoramide.