GI Flashcards
(67 cards)
1
Q
causes of pneumoperitoneum and appearance on an erect CXR?
A
bowel perforation
gas-forming infection e.g. C perfringens
iatrogenic e.g. open or laparoscopic surgery
seen on CXR as air under the diaphragm
2
Q
causes of RUQ pain?
A
acute cholecystitis hepatitis right lung pneumonia appendicitis e.g. in a pregnant woman pyelonephritis duodenal ulcer
3
Q
causes of epigastric pain?
A
peptic ulcer MI acute cholecystitis pancreatitis perforated oesophagus
4
Q
causes of LUQ pain?
A
ruptured spleen gastric ulcer AA perforated colon pyelonephritis left lung pneumonia
5
Q
causes of RLQ pain?
A
appendicitis Crohn's mesenteric adenitis meckel's diverticulitis strangulated hernia renal/ureteric stone perforated caecum salpingitis TO abscess ruptured ectopic pregnancy psoas abscess
6
Q
causes of LLQ pain?
A
UC Crohn's perforated colon strangulated hernia renal/ureteric stones sigmoid diverticulitis salpingitis TO abscess ruptured ectopic pregnancy
7
Q
GI causes of clubbing?
A
cirrhosis
IBD espec. Crohn’s
GI lymphoma
malabsorption e.g. celiac disease
8
Q
causes of hepatomegaly?
A
malignancy hepatic congestion e.g. RHF infection e.g. hepatitis viruses lymphoma early cirrhosis e.g. alcoholic liver
9
Q
causes of splenomegaly?
A
portal hypertension
glandular fever
lymphoma
infections
10
Q
importance of enlarged Virchow’s node (L supraclavicular node)?
A
may indicate gastric cancer
11
Q
when might jugulo-digastric LN be enlarged?
A
tonsillitis (tonisillar node)
12
Q
which LN may be enlarged in oral cancer?
A
jugulo-omohyoid
13
Q
along which blood vessel do the deep cervical lymph nodes lie?
A
IJV
14
Q
examples of deep cervical LNs?
A
internal jugular: jugulo-digastric
jugulo-omohyoid
spinal accessory
supraclavicular (transverse cervical)
15
Q
describe Murphy’s sign
A
2 fingers laid over RUQ and ask patient to breathe in. This causes pain and arrest of inspiration as an inflamed GB impinges on your fingers. Only +ve if test repeated in LUG does not cause pain.
pain with inspiration as diaphragm flattens, so GB moves down aswell so can impinge on fingers.
+ve in acute cholecystitis- where stone or sludge impaction in neck of gallbladder which may cause continuous epigastric (foregut derived) or RUQ pain referred to right shoulder- diaphragmatic irritation as inflammtory fluid from GB can escape into subphrenic space in contact with diaphragm- central innervation phrenic nerve-C3, C4 and C5.
16
Q
contrast presentations of biliary colic, acute cholecystitis and ascending cholangitis.
A
biliary colic= just PAIN, that comes and goes- colicky with peristaltic movement of ducts when GB squeezed. symtpomatic gallstones with cystic duct obstruction or bypassing into common bile duct.
Acute cholcystitis= stone impaction in neck of GB causing inflammation- fever and pain.
Ascending cholangitis= INFECTION- stone obstructing common bile duct, so conjugated bilirubin goes into the blood, causing JAUNDICE. Charcot’s triad: RUQ pain, jaundice and rigors.
17
Q
start and end of foregut derivatives?
A
oesophagus to 2nd part of duodenum up to and including entry of common bile duct
18
Q
start and end of midgut derivatives?
A
duodenum distal to entry of common bile duct to proximal 2/3 of transverse colon.
19
Q
start and end of hindgut derivatives?
A
distal 1/3 of transverse colon to anal verge.
20
Q
causes of pancreatitis?
A
GETSMASHED: gallstones ethanol trauma steroids mumps AI scorpion venom hyperlipidaemia and calcaemia, and hypothermia ERCP drugs
21
Q
signs in acute pancreatitis?
A
tachycardia, fever, jaundice, shock, rigid abdomen, local/general tenderness
periumbilical bruising= cullen’s sign
flank bruising= grey turner’s sign, from blood vessel autodigestion adn retroperiotneal haemorrhage as elastase release within pancreas.
22
Q
marker for acute pancreatitis, raised in blood?
A
serum amylase
23
Q
Explain what Crohn’s disease is
A
- the wall of the gut, which can be thought of as a long tube travelling from your mouth down to your anus which allows that we eat to get to the areas of the body that require it in order to give us energy, become inflamed- red, hot, swollen, painful, protective mechanism in body. Any part of this tube can be affected, but most commonly affects end of small bowel/intestine= ileum, responsible for food breakdown and absorption into blood, and 1st part of large bowel where water is taken into the blood.
- symptoms and why- diarrhoea, abdominal pain, generally feeling unwell, weight loss.
- cause= unknown, may be related to immune cells normally protecting us from infection causing damage, possbile linked to a bacterial or viral infection. May be genetic link- FH? Could be that an infection triggers the immune sytem to produce an inflammatory response in someone who is genetically susceptible to the disease.
- on-going disease- chronic, not a cure, but can be managed with drugs or surgery to reduce symptoms, and symptoms might come and go- relapsing
24
Q
symptoms and signs of Crohn’s disease and why?
A
diarrhoea- can be mixed with mucus, pus or blood- if an ulcer forms and bleeds, often urgency and maybe tenesmus= feeling of wanting to go to the toilet but can’t pass anything.
weight loss- NOT INTENTIONAL! Not absorbing food into the blood in areas of gut where inflamed.
abdominal pain- often lower right side of abdomen in ileum location- RLQ/right inguinal region?
active disease= fever, malaise, anorexia
Signs:
anaemia- blood loss- pallow, pale palamar creases, fatigue, pale conjuctivae
mouth ulcers- apthous ulcers- painful
anal fissures- painful cracks in skin, and skin tags- small fleshy lumps, and perianal abscesses
right iliac fossa mass.
ALSO extra-intestinal: clubbing, conjuctivitis, large joint arthritis, renal stones, erythema nodosum= painful purple nodules, commonly on shins, regress after a few wks to leave bruised appearance, also caused by sarcoidosis, TB, drugs. Inflammation triggered in other areas?
25
common age on onset of Crohn's?
between 15 and 30
| women more often than men
26
indications from a history that a patient has Crohn's?
young- between 15 and 30
female
SH-smoker
PMH-appendicectomy in last 5 yrs
FH-Crohn's, IBD, mutations in different genes increase the risk.
DH- NSAIDs may exacerbate disease, OCP may also trigger disease onset.
27
describe the pathology of Crohn's, how would it appear macroscopically?
chronic inflammation, transmural (full thickness) granulomatous inflammation. Can affect any part of gut from mouth to anus, but most commonly terminal ileum and proximal colon.
Skip lesions- areas of unaffected bowel between areas of inflammation= active disease.
bowel thickened and narrowed
deep ulcers and fissures, cobblestone apperance- due to ulceratio, full thickness of bowel wall
radiographically= string sign of kantor= narrowed bowel regions=fibrosis, then bulge due to narrowings, them more fibrosis=barium follow through.
28
Differentials for Crohn's disease?
appendicitis- pain in right inguinal region
ulcerative colitis
diverticulitis- rare if <40yrs, and commonly left lower quadrant pain, pain relieved on defecation
irritable bowel syndrome
colonic carcinoma
29
complications of Crohn's?
strictures- narrowing due to scar tissue, creates a blockage that can cause pain and vomiting.
fistulae
perforation- can cause peritonitis- *rebound tenderness, infection
colorectal cancer
osteoporosis- poor absorption of food if severe disease- Ca2+ and Vit D
30
investigations for Crohn's?
colonoscopy and biopsies
barium enema of barium meal- special X-ray, barium shows up white
MRI/CT
blood tests- assess level of inflammation- CRP, ESR, and other signs e.g. anaemia- FBC
stool sample- check for infection
31
tment of Crohn's?
treat symptoms of flare-up- short course of steroids until symptoms ease e.g. oral prednisolone, should get better over 4 wks. Anti-inflammatory.
immunosuppressants as immune system mediating inflammation e.g. sulfasalazine= aminosalicylate- used more commonly in UC, azathioprine. In more severe cases where steroids not helped.
Biologics e.g. infliximab- target substance in body causing inflammation (e.g. cytokines- TNF alpha)
surgery if other tments don't work- remove part of bowel affected, and if complications
Regular immunomodulator, biologic or aminosalicylate prevents disease flare-ups.
32
CAGE questions to screen somebody to see if they are an alcoholic?
have you ever thought you should Cut down on your drinking?
have you ever been Annoyed by people criticising your drinking?
ever felt bad or Guilty about your drinking?
ever had a drink on a morning as an Eye-opener, steady your nerves?
yes to 2 or more is quite good at detecting alcohol abuse and dependence.
33
alcohol can cause a fatty liver, but this is reversible, whereas cirrhosis induced is irreversible. what other causes are there for a fatty liver?
obesity
diabetes mellitus
amiodarone tment= K+ channel blocker, prolongs repolarisation in tment of arrhythmias.
34
what would be seen on biopsy of alcoholic hepatitis?
mallory's hyaline= condensed cytoskeleton of hepatocytes
| may be infiltration of neutrophils
35
symptoms of alcoholism in CNS?
fits
falls
wide-based gait neuropathy
poor memory/cognition
36
effects of alcohol on GI tract?
```
obesity
diarrhoea
peptic ulcers
varices
pancreatitis
carcinoma
oral mucosal lesions
```
37
signs of liver failure?
jaundice
hepatic encephalopathy- graded 1-4, 1= mood altered/sleep disturbance, 2= increase drowsiness, confusion, slurred speech, 3= incoherent, restless, significant confusion, 4=coma.
fetor hepaticus= smell on breath result of NH3 and ketones, smells like pear drops
asterixis- indicates encephalopathy
38
3 complications of liver cirrhosis?
hepatocellular carcinoma
liver failure
portal hypertension- can produce varices e.g. oesophageal, caput medusae and rectal
39
how should someone with acute liver failure be treated?
want a liver transplant
can give laxatives to flush out NH3
can give clotting factors
can give albumin
40
what is alcoholic liver disease?
liver disease resulting from drinking excess alcohol can include 3 different conditions, which can occur by themselves or at the same time in the same person, = fatty liver, hepatitis and cirrhosis. Damge occurs to liver as alcohol we drink travels along gut tube, through stomach and into the intestines where can then be taken into the blood, but blood that it enters travels tot the liver before passing elsewhere in the body, so all of the alcohol gets taken to the liver for processing (metabolism), so that are body can use it for energy and so that the alcohol can leave our bodies.
fatty liver= fat builds up in the liver, this is a reversible change if you stop drinking, but can progress to inflammation of liver cells= hepatitis, if drinking contiues. Fatty change= initial change that takes place, occurs as liver is an important organ for processing the fats we have in our body. With too much alcohol, the liver spends too much time trying to process this and is unable to break fats down for use in providing energy to the body, so the fat accumulates**
inflammation of cells may only be mild, or if more severe can produce symptoms e.g. pain in right upper quadrant of abdomen, jaundice- skin yellowing as accumulation of bilirubin, a product formed from breaking down part of red blood cells in the liver, may just feel a bit sick, and can progress to the liver not working very well at all= failure= confusion, bleeding, jaundice.
cirrhosis= gradual change that takes place in the liver. Normal structure is altered as the tissue is replaced with fibrous scar tissue, which damages liver cells and stops them working properly. this is irreversible, but can be stopped from worsening by stopping drinking alcohol. Liver transplant may be required if liver can barely function, producing significant symptoms.
41
what is guarding?
involuntary tensing of abdominal muscles due to pain or fear of pain
42
causes of melaena?
```
peptic ulcers
gastritis
drugs e.g. NSAIDs, steroids, aspirin
duodenitis
malignancy
oesophageal varices
```
43
where should the abdomen be exposed in an abdom exam?
from above the costal margins to the level of the pubic symphysis
44
what do i also want to examine after completing GI exam?
hernial orifices
external genitalia
digital rectal examination
45
what do I want to explain to a patient when starting GI exam?
going to take a general look, look at hands and face, feel for lymph nodes, and then take a look and feel of your tummy where I'll need you to expose it, is that alright?
46
Duke's staging of colorectal cancer?
```
A= cancer has gone into but not through bowel wall, hasn't gone through muscularis mucosae.
B= cancer has gone through muscularis mucosae
C= regional LNs involved
D= distant metastases
```
47
Differentials for peptic ulcer disease?
```
GORD
gastric cancer
gallstones
crohn's
IBS
hepatitis
zollinger-ellison syndrome- gastrin secreting adenoma
```
48
explain gallstones to a patient?
gallstones= formed by bile. Bile produced by liver, and contains bile pigments, salts and cholesterol. Passes into gut, is used for fat absorption so we can get energy as helps break fats down-digestion and for neutralised acidity in the gut for digested material to be absorbed as acid produced by stomach to ensure to get rid of anything infectious in what we take in.
Gallbladder stores the bile and release it when needed. Both gallbladder and liver located in right upper part of tummy/abdomen. It contracts when we eat, emptying the stored bile back into the main bile duct. The bile passes along the remainder of the bile duct into the duodenum (the first part of the gut after the stomach).
gallstones= occur when bile, which is normally fluid, solidifies forms stones. Gallstones commonly contain lumps of fatty material that has solidified and hardened. Sometimes bile pigments or calcium deposits form gallstones. Sometimes just a few small stones are formed; sometimes a great many. Occasionally, just one large stone is formed.
49
risks for gallstones?
```
female
fat
over 40
pregnancy
rapid weight loss
diabetes
taking COCP
```
50
tment for gallstones?
non-pharm= avoid fatty foods- gallstones made up of fatty material
surgery- removal of gallbladder=cholecystectomy, and may be given painkillers and antibiotics if gallbladder gets infected due to material becoming static as stones cause obstuction, bile= toxicity, inflammation= protective mechanism in body.
ursodeoxycholic acid may dissolve small stones, may be given to prevent gallstones in those who lose weight rapidly following surgery or obesity.
51
prognosis following cholecystectomy for gallstones?
GB not needed to digest food. Bile still flows from the liver where produced to the gut once the gallbladder is removed via the common bile duct. However, there is no longer any storage area for bile between meals. The flow of bile is therefore constant, without the surges of bile that occur from a gallbladder when you eat a meal.
You can usually eat a normal diet without any problems after your gallbladder is removed. However, up to half of people who have had their gallbladder removed have some mild tummy (abdominal) pain or bloating from time to time. This may be more noticeable after eating a fatty meal. Some people notice an increase in the frequency of passing stools (motions, or faeces) after their gallbladder is removed. This is like mild diarrhoea. It can be treated by antidiarrhoeal medication e.g. loperamide, if it becomes troublesome.
52
symptoms of gallstones?
biliary colic= RUQ pain, severe, usually just below ribs. pain may last for several hrs. due to smaller stones lodging in cystic duct connecting GB with CBD, duct tries to squeeze out stone, causing pain.
cholecystitis= abdomianl pain, fever, generally feeling unwell. typically acute onset.
53
complications of gallstones?
pancreatitis
cholangitis
bowel obstruction
54
investigations for gallstones?
US scan, blood tests- may be raised ALP if obstrcutive jaundice- CBD obstructed by gallstone
55
explain stomach ulcers to a patient
most common cause= bacteria known as helicobacter pylori. causes damage to lining of stomach= essential part of food digestion. Food passes down the oesophagus (gullet) into the stomach, which makes acid to help digest food. After being mixed in the stomach, food passes into the duodenum (the first part of the small intestine). In the duodenum and the rest of the small intestine, food mixes with enzymes (chemicals). The enzymes come from the pancreas and from cells lining the intestine. The enzymes break down (digest) the food which is absorbed into the body.
Infection by Helicobacter pylori/ H. pylori is the cause in about 8 in 10 cases of stomach ulcer. Once infected, unless treated, the infection usually stays for the rest of your life. In many people it causes no problems and a number of these bacteria just live harmlessly in the lining of the stomach and duodenum. However, in some people this bacterium causes an inflammation in the lining of the stomach or duodenum which disrupts the defence mucus barrier and may cause the amount of acid to be increased) which allows the stomach acid to cause inflammation and ulcers of the lining as normal protection has been lost.
56
symptoms of gastric ulcers?
epigastric pain, worse at night, and before eating
vomiting blood (haematemesis). Pain comes and goes. Can wake you from sleep, may be worse on eating. May be eased by antacids e.g. gaviscon and rennie.
malaena= bloody stools- dark, like tar stained, smelly
may also bloat, feel sick, and partic. full after a meal.
57
what signs would you look out for examination of a patient with Crohn's disease?
```
clubbing
mouth apthous ulcers= painful
abdom tenderness, pain
weight loss
RIF mass= inflamed bowel loops matted together, or abscess
```
58
explain what UC is
1
59
most important independent RF for IBD?
family history
60
type of ulcers seen in UC?
collar button
61
gold standard investigation for IBD?
colonoscopy
62
what are you looking for in the mouth in GI examination?
dentition
mouth ulcers
dehydration
tongue- size?, enlarged- VitB12 or Fe deficiency?
63
what may cause absent bowel sounds?
paralytic ileus
| peritonitis
64
how might diarrhoea affect bowel sounds?
sounds increased
65
what produces tinkling bowel sounds?
bowel obstruction e.g. cancer, strictures, IBD, volvulus
66
investigations for peptic ulcers?
FBC- look for H pylori Abs and Fe deficiency anaemia
H pylori testing- urease breath test
endoscopy
67
lifestyle advice for peptic ulcers?
Cut down on the amount of coffee and tea you drink. This can increase the amount of acid your stomach produces. Try herbal teas instead.
Drink milk and eat milk-based foods, such as yoghurt and cheese. Milk is thought to coat the stomach and neutralise the effects of stomach acid.
Lose any extra weight you are carrying.
Eat little and often. This could help reduce the build-up of stomach acid between meals.
Limit your intake of alcohol. Too much alcohol can irritate the areas of inflammation in your stomach.
Avoid spicy or excessively rich foods if they make your symptoms worse.
Quit smoking. It may put you at greater risk of developing an ulcer and slow down your recovery.
