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Exam 1 - Digestive organs

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1. Dyspepsia means:
- pain in the upper abdomen
- “Heartburn"
- a common term for unpleasant sensations in the upper abdomen
- regurgitation of gastric contents into the esophagus
- a common term for all symptoms that result from inadequate excretion of pepsin
Dyspepsia is a common term for the various symptoms in the upper half of the abdomen,
described by patients as a weakness,
tension, chewing, feeling fast, malaise or pain. These problems can also be accompanied by
heartburn or regurgitation. (Internal medicine, page 8)
2. A 60-year-old patient who comes to the doctor for dyspepsia
- we have to do gastroscopy
- First, in 14 days, we anticipate an antacid or H2 receptor blocker
- first, prescribe eradication treatment for H. pylori
- we perform gastroscopy in case of anemia
- First, we prescribe an ulcer diet for 14 days
3. Among the "signs of alarm" that justify immediate gastroscopy in dyspepsia are all listed
except:
- weight loss
- anemia
- palpable tumor
- pain for more than 2 weeks
- pain before meal ("on an empty stomach")
4. The color of the coffee sediment of the vomit is the most characteristic for:
- ileus
- alcohol poisoning
- overdose of black coffee
- bleeding from the upper gastrointestinal tract
- bleeding from the lower gastrointestinal tract
Coffee sediment-like color of the outbreak liquid is a sign of bleeding from the upper digestive
tube. (Internal page 14)
5. Odor of faeces of the vomit shows:
- ileus
- poisoning with organophosphates
- gastrointestinal haemorrhage
- gallbladder disease
- meteorism
By the smell of the erupted content alcohol can be identified in alcoholic drinks or fecal breath (m
iserere) in the intestinal trap (ileusu). (Internal page 14)
6. What is usually the first investigation with suspected intestinal perforation:
- ultrasound
- abdominal x-ray
- CT
- lab. blood tests
- rectal examination
For X-ray imaging of the abdomen we decide on the suspicion of ileus or penetration of the hollow
organ. (Internal page 14)
7. Colic (pain) is a typical example of:
-visceral pain
-parietal pain
-transferred pain
-phantom pain
-none of the above
8. The visceral type of pain is characterized by:
-“defense musculaire” always accompanies the pain
-accompanied by nausea and vomiting
-unlike transferred pain, it is well localized
-it gets worse when coughing, sneezing and moving
-never spreads over the diaphragm
Visceral pain causes irritation of the aferent nerve endings of the autonomic nervous system in the
wall of the hollow abdominal organs, in the mesentery or retroperitoneum. Visceral peritoneum is
not innervated, so it does not detect pain. Visceral pain causes inflammation or tenderness of the
hollow muscular abdominal organs (digestive tube, gall bladder, bile ducts, ureter, uterus). Patients
describe it as a seizure or cramping pain in the middle of the abdomen. Pain does not worsen in
sneezing or changes in body position, no defense musculaire. Its characteristic is the exhilaration
and the presence of other "visceral symptoms" (anorexia, nausea, vomiting). (internal page 17)
9.The transferred pain is:
-well-localized
-always proximal to the affected organ
-always distal from the affected organ
-worse on palpation of the dermatome, which belongs to the same spinal segment as the affected
organ
-synonymous with phantom pain
Transferred pain is a well-localized pain that is distant from the affected organ. Transmitted pain is
felt in skin dermatomes of somatic afferent nerves that enter the spinal cord at the same level as
the visceral afferent cord of the affected organ. Sometimes the pain can be transmitted by the
palpation of the affected organ. The transfer of pain from the abdominal organs to other regions is
so characteristic that after this transfer we can conclude which organ is affected.
10.If at percussion of the abdomen we find thympanism, most probable cause is the following:
-perforation of the hollow body
-free fluid in the abdomen
-free liquid retroperitoneal
-ileus
-pregnancy
11.The pain in acute appendicitis is characterized by:
-worsens with movement and cough
-radiates to the right shoulder
-is a painful palpation of the Erb point
-has a colic character, comes in attacks
-no recurrent pain
12. We suspect bowel infarction:
-with severe abdominal pain, followed by a strong bowel emptying
-when the pain stops after 3-4 hours, when the whole ischemic area dies
-with defense musculaire that arises already at the onset of pain
-with the pain that occurs in the attacks
-in young people with sudden severe abdominal pain
The characteristic of intestinal infarction is severe abdominal pain, which is usually followed by a
strong bowel discharge. The pain lasts for more than 2-3 hours. In the physical examination, I do
not discover any particularities. It is precisely the disproportion between severe pain and normal
examination of the abdomen to cause us to suspect a gut infarction, especially if the patient
belongs to a high risk group. Later on, the stomach distension and the fall in blood pressure are
associated with pain. When the necrotic necrosis develops with peritonitis, patients are vomiting,
their body temperature rises and diarrhea occurs, and blood leukocytosis and severe metabolic
acidosis with elevated lactate occur in the bloodstream. (Internal page 2
13. Jaundice becomes visible at a concentration of bilirubin, which:
-exceeds the upper limit of the normal
-exceeds the upper limit of the normal by 50%
-exceeds the upper limit of the normal by 100%
-exceeds the upper limit of the normal by 300%
-it can also be in the normal range
The normal serum bilirubin concentration is 5.1 to 17.1 μmol / l; jaundice becomes visible when
the concentration exceeds 50 μmol / l. (Itera page 23)
14. Bilirubin in urine is a sign:
-direct hyperbilirubinaemia
-indirect hyperbilirubinaemia
-prehepatic jaundice
-kidney disease
-Gilbert’s disease
Prehepatic jaundice is the result of excessive bilirubin formation due to excessive erythrocyte
decay. Elevated blood bilirubin is predominantly unconjugated (indirect). Liver enzymes are normal.
There is no bilirubin in the urine. This type of jaundice is characteristic of haemolytic anemia.
Hepatic or hepatocytic jaundice is a result of an impaired hepatocyte activity - either inadequate
conjugation or the transport of bilirubin. When conjugation of bilirubin is disturbed,
hyperbilirubinaemia is predominantly unconjugated (indirect). Such a type of jaundice is typical of
Gilbert's disease. Liver enzymes are normal. There is no bilirubin in the urine. However, when
excretion of bilirubin from hepatocytes due to impaired transport of bilirubin through the cell into
the bile, hyperbilirubinaemia is conjugated (direct). Hepatic tests are pathological and reflect the
underlying disease that caused the formation of a jaundice - hepatitis or liver cirrhosis. Bilirubin is
present in the urine. This type of jaundice is caused mostly by alcohol, hepatitis and hepatitis.
Holestatic jaundice is a failure in bile secretion due to damage to the canalicular bile secretion or
mechanical impairment of bile ducts at any level. Due to these disorders, bilirubin does not reach
the duodenum. Hyperbilirubinaemia is conjugated (direct). Hepatic tests are pathological. It leads
to an increase in alkaline phosphatase and gamma-GT. Bilirubin is present in the urine, but it does
not exist in the stool, which is why the urine is dark and the mud is bright (acholic). This type of
jaundice is caused mainly by gallstones, bile duct tumors or periampular region, and numerous
medications. In rare cases, the cholestatic form of acute viral hepatitis may also be observed.
(Internal page 23)
15. Direct hyperbilirubinaemia and an increase in alkaline phosphatase and gGT causes suspicion
of:
-obstruction of bile ducts with gallstones
-hemolytic anemia
-Gilbert syndrome
-resorption of blood from large hematomas
-none of the above
16. Indirect hyperbilirubinaemia can be found in:
-Gilbert syndrome
-alcoholic liver disease
-gallstones
-primary biliary cirrhosis
-bleeding into the gastrointestinal tract
17.An enlarged and palpatory painful liver is most likely a sign of the following causes:
-cancer
-acute cholecystitis
-alcoholic liver cirrhosis
-acute left-sided heart failure
-viral hepatitis
Enlarged liver, sensitive to touch is common in acute hepatitis, enlarged and painless
liver is a sign of chronic liver disease or tumor growth. (Internal page 25)
18. The strongly increased alkaline phosphatase concentration is most evident on:
-acute hepatitis
-obstruction of the bile duct
-alcoholic liver cirrhosis
-poisoning with carbon monoxide
-extravascular haemolysis
More than 3x is increased in choledolytia, carcinoma with water papules and cholestatic jaundice
(Interna, summarized in Table 1.23)
19. When we find higher level of direct bilirubin, the first diagnostic approach is:
-ultrasound of the liver and bile ducts
-CT abdomen
-gastroscopy (and, if necessary, endoscopic ultrasound)
-puncture of the bone marrow
-lumbar puncture
When elevated direct bilirubin, morphological diagnosis is initiated with ultrasound examination of
the liver and bile ducts. (Internal page 26)
20. The normalization of the prolonged prothrombin time in a patient with hyperbilirubinemia after
three days of vitamin K is most likely due to the following diagnoses:
-Gilbert syndrome
-alcoholic hepatitis
-viral hepatitis
-bile duct carcinoma
-poisoning with paracetamol
The K-vitamin test can help us with the differential diagnosis of parenchymal (hepatic cell) and
obstructive jaundice. The test is performed when the prothrombin time is prolonged. We perform it
for three days in a row, we inject 2 ampules of vitamin K and on the third day we measure the
prothrombin time. If it is a prison jaundice, after the addition of vitamin K, the prothrombin time will
normalize, but not in the parenchymal jaundice.
21.Diarrhea in ulcerative colitis
-osmotic
-secretory
-exudative
-motility
-none of the above
Exudative diarrhea is a consequence of a morphologically visible mucous membrane defect that
causes loss of water and electrolytes, mucus, protein, erythrocytes and leukocytes through
damaged mucous membranes. Exudative diarrhea can be a consequence of infections with
aggressive bacteria or parasites or the consequence of chronic bowel inflammation (ulcerative
colitis or Crohn's disease).
22. Osmotic diarrhea is differentiated from the secretory by:
-fasting test (not eating)
-hematesta of the feces
-rectal examination
-gastroscopy
-autopsy
Osmosis diarrhea occurs when, due to hyperosmolar intestinal content, the fluid passively passes
through the mucous membrane of the intestine into its brightness, thus restoring the osmolar
balance to body fluids. Hyperosmolar intestinal content may be caused by compounds that are
incompletely absorbed or not at all sugars (lactose, lactulose) or sugar alcohols (mannitol, sorbitol)
and certain ions (magnesium, phosphate and
sulfate). The consequences are the loss of large amounts of water and the formation of
hypernatremic dehydration. Typical cases of osmotic diarrhea are diarrhea due to malabsorption of
sugars and diarrhea following the ingestion of osmotic laxatives (eg.lactulose). Osmosis diarrhea
occurs during the day and after eating food, there is no post.
Secretarial diarrhea is the result of excessive intestinal secretion of anions (Cl-, HCO3-), which
passively follows sodium; the accumulation of NaCl in the lumen of the gut creates an osmotic
gradient that causes the diffusion of water from body fluids.
The result is the loss of a large amount of electrolytes and water in the stool and the formation of
dehydration and metabolic acidosis. A typical example of the secretory diarrhea is cholera. The
secretory diarrhea is present during day and night and is not tied to
eating food. She does not stop after the post.
Osmosis and secretory diarrhea are the result of disorders in the functioning of signaling and
transport pathways in the intestine, and the bowel mucosa is not morphologically altered. (Internal
page 27)
Hematest in the stool confirms or excludes covert bleeding. A simple test that distinguishes
between the osmotic and secretory diarrhea is also a starvation test carried out in a hospital. The
patient is fasted for 48 hours, while simultaneously with the infusion solutions, we maintain the
electrolyte and acid-base balance. If the posterior diarrhea does not disappear or even worsens, it
is a secretory diarrhea, but if the diarrhea is drowsy, it is an osmotic diarrhea. (Internal page 31)
By determining the osmolar gap in the chair, we separate the osmotic and secretory diarrhea.
(Internal page 30)
23. A sixty-year-old chronic alcoholic comes to the doctor because of the 14-day-old swelling of
the left lower limb distal to the knee. Among the causes most likely to be possible:
-heart failure (alcohol cardiomyopathy)
-hypoproteinemia due to inadequate nutrition
-nephrotic syndrome
-Local inflammation
-liver cirrhosis
Generalized edema occurs in a variety of conditions: in heart failure, liver cirrhosis, nephrotic
syndrome or nutritional disorders. Localized edema is most often the result of venous or lymph
nodes or local inflammation.
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