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GI Flashcards

1
Q

what is a mallory-weiss tear?
what membrane?

A

a tear of the tissue (mucous membrane) of lower esophagus which leads to bleeding

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2
Q

what are causes of a mallory- weiss tear?

A

violent coughing, retching, vomiting and straining (common cause)
hiatal hernia (rare)
childbirth (rare)

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3
Q

what are the signs and symptoms of mallory-weiss tear?

A

haematemesis vomiting of bright red or coffee grounds blood,
melaena (stool with blood)
dysphagia- difficulty swallowing
odynophagia- painful swallowing
anaemia
faituge, dizziness, faintness
shortness of breath
abdominal or chest pain

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4
Q

what is the diagnosis of a Mallory weiss tear?

A

signs and symptoms,
stool test,
upper gi endoscopy

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5
Q

what is the treatment of a mallory-weiss tear?

A

80-90% of cases- stop bleeding and heal on its own.
injection or a heat treatment to stop bleeding
surgical repair (rate)

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6
Q

what is the gastrin hormone?

A

produced in the stomach and plays a crucial role in digestion- the main hormone is gastrin which is secreted by g cells in the stomach lining

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7
Q

what is gastrin hormones main 2 function?

A

to simulate the secretion of gastric acid (hydrochloric acid) from the parietal cells in the stomach. this acid is essential for breaking down food and killing harmful bacteria.

gastrin also promotes gastric motility, enhancing the movement of food through the stomach

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8
Q

what are the 3 key functions of the gastric hormone?

A

gastric acid secretion, (crucial for breaking down food and creating an acidic environment that aids in digestion)
gastric motility (enhances the movement of stomach muscles)
mucosal growth (help to maintain the lining of the stomach)

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9
Q

what does hydrochloric acid do?

A

anti bacterial and converts pepsinogen to pepsin.

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10
Q

what secretes the gastrin hormone?
found where

A

G cells found in the lower half of the pyloric glands

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11
Q

what is hydrochloric acid produced by?

A

the parietal cells in the stomach

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12
Q

what is the hydrochloric acids main 3 function?

A

digestion
(break down food particles, particularly protiens, by denaturing them and activating digestive enzymes like pepsin)

acidic environment,
(essential for optimal enzyme activity and helps kill harmful bacteria and pathogens)

absorption
(certain nutrients such as vitamin B12 and minerals like iron and calcium)

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13
Q

what factors regulate hydrochloric acid?

A

-the presence of food in the stomach,
-the hormone gastrin
-neural signals

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14
Q

what is pancreatitis?

what are the 2 tupes?

A

inflammation of the pancreas. can be chronic or acute

acute pancreatitis:
sudden inflammation that lasts for a short amount of time. can be caused by gallstones, heavy alcohol consumption, certain medication and infections. symptoms are severe abdo pain, nausea, vomiting and fever

chronic pancreatitis:
long term condition that results in permanent damage to the pancreas. it is often caused by repeat episodes of acute pancreatitis- due to alcohol abuse but can also be associated with gentic factors and medical conditions.
symptoms:
persistant abdominal pain, weight loss and digestive problems

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15
Q

describe the physiology of pancreatitis?

A

in a healthy pancreas: digestive enzymes are produced and stored in an inactive form to prevent self digestion

in pancreatisis- enzymes become activated while still in the pancreas leading to inflammation and damage to pancreatic tissue. causing swelling and can disrupt its ability to produce insulin and digestive enzymes resulting in diabetes and malabsorption of nutrients.

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16
Q

explain how biliary obstruction causes pancreatitis:

A

biliary obstruction:
presence of stone in the common bile duct or sphincter of oddi.
- causes bile and pancreatic juice to mix and back flow into pancreatic tissue
- this causes inactive proteases to become activated and start of the auto-digestion of pancreatic tissue.
- autodigestion leads to oedema and ischemic injury to the pancreatic tissue
= pancreatitis

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17
Q

explain how alcohol, drugs, trauma, viruses or ischemia causes pancreatisis?

A

leads to intracellular activation of protease enzymes i.e. trypsinogen into trypsin

the activation of proteases leads to auto-digestion of pancreatic tissue and pancreatitis.

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18
Q

what are signs and symptoms of acute pancreatitis?

A

pain in epigastrium and left upper quadrant of abdomen which radiates or penetrates through to the back.
- nausea and vomiting
- tenderness on palpation
- reduction in bowel sound
-low grade fever

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19
Q

what is the diagnosis for acute pancreaitis?

A

signs and symptoms
history take
laboratory findings
blood test- increased lipase, amylase level
increased alkaline phosphate level
increased bilirubin level
increased WBC count
hypocalcemia
imaging studies

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20
Q

what is the treatment of acute pancreatitis:

A

nil by mouth
nasogastric suction
iv fluid
analgesics (remove pain by reducing inflammation)

severe:
acute necrotizing
-surgery in some cases
- mechanical ventilation
-haemodilalysis
-broad sprectrum antibiotics

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21
Q

what is appendicitis?

A

the appendix swells- no main cause
muscosal secreations increase intraluminal pressuure
pressure exceeds capillary perfusion causing venous and lymphatic obstruction
reduced perfusion=necrosis/perforation

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22
Q

how does the appendix get blocked?

A

lymphoid hyperplasia (an increase in the number of normal cells contained in the lymph nodes)
infections (parasitic)
faecaliths (stone made of feces)
tumours

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23
Q

signs and symptoms of appendixititis?

A

First symptom – usually vague epigastric pain
Can be described as cramping sensation
Over time pain becomes more localised and moves to the right lower quadrant
Sometimes flank tenderness instead of abdominal tenderness
Nausea and vomiting, diarrhoea
Low-grade fever initially – temperatures >39 C are uncommon in first 24 hours

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24
Q

what are the different points to examine for appendisitis?

A

mcburneys point- rebound tenderness on palpation- Mcburneys point

rovsings sign (LLQ palpation and feel pain in the RLQ)

psoas sign (manipulate leg to move psoas muscle over the appendix)

obturator signs (resist active hip flexion)

25
what are teh differences between chronic and acute appendicitis?
chronic: doesnt always need removal of appendix acute: immediate removal chronic: no rebound tenderness acute: rebound tenderness
26
what is ulcerative colitis?
inflammation bowel disease- causes inflammation and ulcers in the lining of the colon (large intestine) and rectum.
27
what is ulcerative colitis caused by?
unknown but people say immune response that mistakenly attacks the cells of the colon
28
what are symptoms of ulcerative colitis?
abdominal pain and cramping, diarrhea, often with blood or pus, urgency to have a bowel movement, weight loss faituge
29
how would paramedics treat ulcerative colitis?
iv fluids- for vomiting pain management monitoring vital signs hospital would do blood tests and imaging studies
30
what is the pathophyscolgy behind ulcerative colitis?
autoimmune response immune response leads to inflammation in the mucosal layer of the colon inflammation can cause the formation of ulcers in the colon lining
31
what is Crohn's disease?
a type of inflammatory bowel disease that can affect any part of the GI tract. but commonly affects the terminal ileum and colon.
32
what are the symptoms of crohns disease?
abdominal pain and cramping, diarrhea, weight loss, fatigue, fever, reduced appetite, blood in the stool.
33
what is the pathophysiology of crohns disease?
immune system mistakenly attacks the gut flora, causing inflammation. unlike ulcerative colitis (only affects the mucosal layer), crohns can cause inflammation that extends through the entire thickness of the bowel wall leading to abscesses the inflammation can lead to the formation of granulomas which are clusters oof immune cells that obstruct the intestines
34
what is the diagnosis of crohns disease?
medical history and physical exam laboratory tests- blood tests for inflammation, stool tests to rule out infection -imaging studies -endoscopy
35
what is the clinical significance of crohns complications and manageme
-chronic condition -affect quality of life -lead to complications such as: bowel obstructions, malnutrition and increased risk of colorectal cancer -magement involves: meds to control inflammatiom, dietary modifications, in some cases surgical intervention for removal of effected parts of intestine
36
what is peritonitis?
inflammation of the peritoneum- lining of the abdominal cavity- can occur due to infection
37
what are the symptoms of perionitis?
severe abdominal pain and tenderness, abdominal swelling or distension fever and chills nausea and vomiting loss of appetite changes in bowel habits such as diarrhea
38
whats the pathophysiology of periontitis?
infection- bacteria or fungi inflammatory response- leading to accumulation of fluid, immune cells and pus in the peritoneeal cavity complications- can lead to sepsis, shock and organ failure
39
what is the treatment of peritonitis?
antibiotics
40
what is pancreatic juice?
digestive fluid produced by the pancreas that plays a crucial role in the digestion of food
41
what does pancreatic juice include?
digestive enzymes: amylase- carbs to simple sugars lipase- digests fat into fatty acids and glycerol proteases- protiens into peptises and amino acid bicarccbonate iron- help to neutralise stomach acid as chyme
42
where is pancreatic acid produce into
small intestine- duodenum in response to food intake
43
what is the function of pancreatic juice?... help break down...
break down carbs, protiens, fat into absorbable units. the biacarbonate in pancreatic juice also protects the intestinal lining from the acidic content of the stomach
44
what is cirrhosis?
chronic liver disease characterised by the replacement of healthy liver tissue with scar tissue
45
what are the causes of cirrhosis??
chronic alochol abuse -viral hepatisis -non alochol fatty liver disease -autoimmune disease -gentic disorders -bile duct diseases
46
what are the symptoms of cirrohis?
fatigue, weakness, weight loss, nausea, itchy skin jaundice swelling in the legs and abdomen easy bruising or bleeding
47
what can cirrhosis lead to?
liver failure, portal hypertension (increased blood pressure in the portal veins, can lead to enlarged veins and bleeding) -hepatic encephalopathy (accumulation to toxins in the brain leading to confusion) liver cancer
48
what is the diagnosis of cirrohis?
blood tests imaging tests liver biopsy
49
what is the treatment of cirrohis?
life style changes medication for symptoms regular monitoring liver transplant
50
what are gallstones?
solid partical that form in the gallbladder, a small organ located beneath the liver that stores bile- a digestive fluid
51
what are the 2 types of gall stones
cholesterol- to much cholesterol in bile (yellow in color) pigment gallstones-excess bilirubin, such as liver cirrhosis, biliary tract infections or certain blood disorders (brown in color)
52
what are the causes of gallstones?
excess cholesterol, excess bilirubin, bile concetration (if the gallbladder does not empty effectively, bile can become overly concentarted leading to stone formation
53
what are the risk factors of gall stones?
obesity, age and gender diet rapid weight loss diabtets
54
what are symptoms of gall stones
biliary colic- sudden and intense pain in the upper right abdomen or center abdomen often after eating fatty meals. nausea or vommiting, jaundice- (if a stone blocks the bile duct) dark urine or light colored stools (indicating bile duct obstruction)
55
what are the diagnosis of gallstones?
ultrasound, ct scan or mri blood tests
56
what is the treatment for gall stones
medication to dissolve cholesterol, surgery- removal of the gallbladder
57
what is bile?
digestive fluid produced by the liver and stored in the gallbladder. plays a cruical role in digestion ad absorption of fat in the small intestine
58
what is included in bile?
water, bile salts, cholesterol, bilirubin (waste product from the breakdown of rbc), electrolytes and phospholipids
59
what is the function of bile? where is it released?
aid in the digestion of fats. its released into the small intestine. the bile salts help to break down large fat globules into smaller droplets , increasing the surface area for digestive enzymes to work on

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