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Samenvatting Week 2 - Zuur

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AKO abdomen 1 - week 2 zuur

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February 11, 2019
Number of pages
43
Written in
2016/2017
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ABDOMEN 1
WEEK 2 – ZUUR
ALGEMENE LEERDOELEN 2
TAAK 2.1 – OBSTRUEREND SLOKDARMCARCINOOM 6
TAAK 2.2 – HERNIA DIAFRAGMATICA MET REFLUX OESOFAGITIS 13
TAAK 2.3 – ULCUS VENTRICULI 21
TAAK 2.4 – ULCUS DUODENI 31
TAAK 2.5 – MISSELIJKHEID EN BRAKEN (AUTONOME NEUROPATHIE) 38
EXTRA INFO 42

,ALGEMENE LEERDOELEN
1) Topografische anatomie van de mondholte, farynx, slokdarm, maag en duodenum




2) Bloedvoorziening en innervatie van het bovenste gedeelte van de tractus
digestivus (slokdarm tot dunne darm)
Zie taken week 2

3) Algemene fysiologische aspecten motiliteit van bovenste gedeelte tractus
digestivus (mechanisme en regulatie)
The route of food through the digestive system:
1. Oral cavity – Mouth contains salivary glands (sublingual under tongue, submandibular
under jawbone, parotid near hinge of jaw that secretes -amylase) and the pharynx.
2. Oesophagus – consists of skeletal muscle that transitions to smooth muscle.
3. Stomach – three sections (upper fundus, central body, lower antrum). Can hold 2L of
food and fluid. Mixing of food with acid and enzymes to create chime. Pylorus is
opening between stomach and small intestine and is guarded by pyloric valve, that
regulates the amount of food entering the duodenum.
4. Small intestine – Consists of duodenum, jejunum and ileum. Digestion is carried out
by intestinal enzymes, aided by exocrine secretion from accessory glandular glands,
the pancreas and the liver. sphincter keeps pancreatic fluids and bile (gal) from entering
the small intestines except during a meal. Almost all nutrients and secreted fluids are
absorbed. 1.5L of chyme passes into the large intestine.

Week 2 – Zuur Page 2 of 43

, 5. Large intestine – watery chyme is converted to semisolid faeces in the colon as water
and electrolytes are absorbed out of the chyme into the ECF. Faeces entering the
rectum triggers a defecation reflex.

GI motility is modified by nerves, hormones and paracrine signals. The two main functions are
to move food to the anus and to mechanically mix food to maximize exposure to digestive
enzymes.

Muscle contraction occurs in three patterns:
1. Migrating motor complex - “housekeeping” function that sweeps food
remnants and bacteria out of the upper GI tract and into the large intestine.
2. Peristalsis – progressive wave of contractions. Circular muscles contract
and the bolus moves into a receiving segment, where circular muscles are
relaxed.
3. Segmental contractions – Circular muscle contract while longitudinal
muscles relax. Needed for mixing of food and absorption.

Groups of cells are electrically connected by gap junctions to create
contracting segments. Different regions show different types of
contraction.
1. Tonic contractions — occur in some smooth muscle sphincters
and in the anterior portion of the stomach and sustain for minutes
or hours
2. Phasic contractions — contraction-relaxation cycles that last
only seconds. Occur in posterior region of stomach and small
intestine. These cycles are associated with slow wave potentials.
There are 3 (stomach) - 12 (duodenum) waves/min and the
threshold isn't reached with every cycle, so no contraction
occurs. It depends on input from the enteric nervous system

When a threshold is reached, Ca2+ channels in muscle fiber open, Ca2+ enters and the cell
fires one or more action potentials. Depolarization is the result of Ca2+ entering the cell. Ca2+
also initiates muscle contraction. Contraction is graded according to the amount of Ca2+ that
enters the fiber. The longer the duration of the slow wave → the more action potentials → the
greater (and longer) the contraction force. Amplitude and duration can by modified by
neurotransmitters, hormones and paracrine molecules. Slow waves originate in a network of
cells called the interstitial cells of Cajal (ICC).

4) Algemene kenmerken ontsteking
Een complexe reactie van het aangeboren immuunsysteem waarvoor gevasculariseerd
weefsel nodig is  ophoping en activatie van leukocyten en plasmaproteïnen op de plek van
infectie, toxine afgifte en beschadiging van de cel.

Kenmerken van inflammatie zijn rubor (=rood), calor (=warmte), dolor (=pijn), tumor (=zwelling)
en functieverlies.
Oorzaken kunnen zijn micro-organismen, fysieke schade (verbranding, bevriezing), vreemd
lichaam (splinter), chemische agens en weefselnecrose.




Week 2 – Zuur Page 3 of 43

, Acute inflammatie = relatief kort en kent meerdere fases:
1) Hyperemie = verhoogde doorbloeding (rubor, calor)
a. Vaatverwijding (door histamine, bradykinine en NO) en openen nieuwe
capillairbedden   vaatverwijding en bloedflow

2) Exsudatie (tumor, dolor en functieverlies)
a. Plasma-eiwitten gaan vanuit de bloedbaan naar interstitiële ruimte.
b. Door meer bloedstroom en verhoogde permeabiliteit zijn de verhoudingen
tussen de hydrostatische druk en colloïd osmotische druk verstoord
• Door verhoogde permeabiliteit voor eiwitten wordt colloïd osmotische
druk intravasculair verlaagd en die van het interstitiële vocht verhoogd.
Hierdoor kan vochtophoping buiten het vat ontstaan.
• De verhoogde doorbloeding en hydrostatische druk aan de arteriële
kant bevorderen extra vochtophoping in het interstitiële weefsel =
exsudaat (normaal transsudaat). Dit vocht bevat hoge concentratie
eiwitten. De vochtophoping als gevolg van exsudaat = oedeem.
c. Oedeem zorgt voor de zwelling (tumor). Wanneer het oedeem rijk is aan
afgestorven neutrofielen en celresten van necrotische weefselcellen (debris)
ontstaat pus = etterig onstekingsexsudaat
d. Door de ontsteking treedt stasis op = relatieve toename van rode bloedcellen
en daardoor hogere viscositeit en vertraging van de bloedstroom (omdat vocht
en eiwitten uit de bloedbaan gaan). Stasis bevordert uittreden leukocyten uit de
bloedbaan
3) Infiltreren van immuun cellen = om de ontsteking te elimineren gaan grote aantallen
fagocyten naar de infectie. In eerste instantie neutrofielen en pas later macrofagen,
lymfocyten en plasmacellen. Leukocyten moeten de bloedbaan verlaten en dus de
endotheel laag passeren (= diapedese/extravasatie). Interactie tussen leukocyten en
endotheelcellen van cruciaal belang. Macrofagen en dendritische cellen scheiden na
stimulering cytokinen uit: TNF- en IL-1, chemokines (IL-8). Onder invloed van deze
cytokinen gaan de endotheelcellen die in de nabijheid van de infectie liggen adhesie
moleculen voor leukocyten tot expressie brengen. Dit wordt door leukocyten opgemerkt
en zullen op die plekken de bloedbaan verlaten.




a. Rollen = selectinen spelen een rol voor de primaire adhesie tussen leukocyten
en endotheelcellen. Leukocyten bewegen zich marginaals langs de vaatwand.

Week 2 – Zuur Page 4 of 43

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