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Phase 2 mine > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

What type of injury can the liver recover from?

A

Acute injuries are usually recovrable

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2
Q

Wat can cause acute liver injury?

A

Viral (A,B,EBV) drugs alcohol vascular ubstruciton or congestion.

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3
Q

What can cause chronic liver failure?

A

alcohol Viral (B, C) autoimmune metabolic (iron, copper)

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4
Q

What are symptoms of acute liver injury?

A

Malaise nausea, anorexia, jaundice rarely confusion bleeding liver pain and hypoglycaemia

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5
Q

What are the presentation of chronic liver failure?

A

Ascites oedema, haematemesis (varicies, malaise, anorexia, wasting, easy bruising, itching hepatomegaly, abnormal LFTs rarely jaundice and confusion

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6
Q

What tests can gage liver function?

A

Serum bilirubin albumin prothrombin time as liver is involved in those pathways.
Serum liver enzymes like cholestatic alkaline phosphatase and gamma-GT hepatocellular transaminases give no index of liver function

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7
Q

What causes jaundice/

A

raised serum bilirubin

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8
Q

What are the types of jaundice?

A

Unconjugated prehepatic, from gilberts syndrome or haemolysis
Conjugated from cholestatic liver disease or bile obstruction so called post hepatic

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9
Q

What can be tested in liver tests?

A

Stools urine, itching and liver tests

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10
Q

What would be seen in urine stools LFT for prehepatic?

A

Normal urine normal stools and no itching and normal LFT

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11
Q

What wpuld be seen in urine stools LFT for hepatic or post hepatice?

A

Dark urine pale stools may itch and abnormal LFTs

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12
Q

What can cause liver disease?

A

Hepatitis (Viral, Drug, Immune, Alcohol) Ischaemia, Neoplasm congestion

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13
Q

What can cause obstruction of the bile duct?

A

Gallstones bile duct or Mirizzi, stricutre malignant or ischaemic inflammatory

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14
Q

What should you ask a patient with jaundice/

A

Dark urine pale stools itching? symptoms biliary pain rigors abdomen swelling weight loss, billlary disease intervention history, heart failure blod products autoimmune diseases and malignancy
drugs socual including sex IV drugs alcohol family history

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15
Q

What to test in pt with jaundice?

A

LFTs, Ultrasound for bile ducts, may need CT MR choliangiogram or endoscopic retrograde cholangiogram

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16
Q

What are gall stones made of?

A

70% choesterol 30% pigment+/- calcium,

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17
Q

What are risk factors for gall stones?

A

Femail fat fertile

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18
Q

What are symptoms of gallbladder gallstones?

A

Billary pain cholecystitis, myabe have obstructive jaundice no cholangitis or pancreatitis

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19
Q

What is the presentation of gall stones in the bile duct?

A

billary pain no cholcystitis, no obstructive jaundice no cholangitis and no pancreatitis

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20
Q

How can gall stonesbe managed/

A

Laproscopic cholecystectomy, bile acid disolution therapy, if in bile ducts ERCP with sphincterotomy and removal crushing or stent placemt or surgery

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21
Q

What the types of drug induced liver injury?

A

Hepatoceular where ALT is v high and ALT/ALK hos high

or cholestatic were it is ALK phosphatase> 2

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22
Q

When can drug induced liver injury happen/

A

Within 3 months of starting can happen after stopped, resolution within 3 months of stopping

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23
Q

What are the usual suspects for drug induced lier injury?

A

antibiotics, CNS drugs immunosupressants analgesics GI drugs suppliments

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24
Q

What is management of paracetamol induced fulminant hepatic falure?

A

N acetyl Cystine, Supportive to correct coagulationd defects fluid electrolytes and acid base balance renal failurem hypoglacaemia and encephalopathy

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25
Q

What can cause ascites?

A

Chroic liver disease portal vein thromboses hepatoma TB neoplasia of abdominal organs, pancreatitis, cardiac causes

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26
Q

Why does acites happen?

A

Systemic vasodilatation, increased fluid retention pertal hpertension low serum albumin

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27
Q

Do all alchol drinkers get alcholic liver disease?

A

No only 10 -20% of heavy drinkers

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28
Q

What can cause portal hypertenison?

A

Cirrhosis, fibrosis portl vein thrombosis from increased hepatic resistance or increased splanchnic blood flow

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29
Q

What are consequences of portal hypertension?

A

varicies splenomegaly

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30
Q

Why are chronic liver disease patients vulnerable to infection?

A

They have impared reticulo-endothelial function, reduced opsonic activity, leucocyt function, permeable gut wall

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31
Q

Is jaundice obvois?

A

No very unlikely

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32
Q

What is rigors?

A

increased temperature with shivering

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33
Q

How long for a good drug history?

A

6 months if possible

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34
Q

What does raised AST or ALT mean?

A

Might be due to liver

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35
Q

What is colic pain?

A

Coming in waves

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36
Q

What are pathologies for drug induced liver injury?

A

can be directly toxic othertimes ideosyncratic

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37
Q

What is a spider naevus?

A

brown diffuse area, it blanches

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38
Q

What is finding of acitic fluid for liver diseases?

A

Serum albumin is low and fluid is same

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39
Q

Hw can ascites be managed?

A

Fluid and salt restriction, diuretics, large-volume paracentesis+albumin, trans-jugular intrahelatic portosstemic shunt.

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40
Q

What is acute decompensation?

A

Symptoms such as formation of acites encephalopothy and bleeding when liver stops functionng correctly

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41
Q

When do most people die from alcohol related deaths?

A

50s to 70s

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42
Q

How long does it take for alcohol withdrawal symptoms to appear?

A

3 days use a withdrawl medications

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43
Q

What can precipitate liver disease decompenastion?

A

Constipation, Drugs sedatives analgesis NSAIDs diuretics ACE blockers GI bleed Infection, Hypo natraemia kalaemia glycaemia, alcohol withdrawl, other

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44
Q

What is spontaneous bacterial peritonitis?

A

Commonest serious infection in cirrhosis, vagues symptos often suspected from neutrophils in ascitic fluid, gram stain often negative use blood culutre bottules after 1 episonde should have prophylaxis and consider for transplant

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45
Q

What is renal considération liver disease?

A

Renal failure is common review drugs my need review of doses and drugs

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46
Q

What is hepatic encephalopathy?

A

Raised ammonia levels from infection GI bleed constipation hypokalaemia dru induced, hyponatramea hypohlycaemia or a stroke

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47
Q

WHat are the bedside tests for encephalopathy?

A

subtract 7, 10 animals in a minute draw 5 point star number connection test, world backwards

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48
Q

What happens with livr dysfunction?

A

Malnutrition, coagulopathy, cholestasis causes thrombocytopenia, endocrine changes gynacomastia impotence amenorrhoea hypoglycaemia

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49
Q

What to thinl about in a patient with liver disease?

A

be careful of drugs prescriptions, pain medication may need reducing, kidney injury

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50
Q

What is non-invasive liver screen?

A

autoantibdies, imunoglobulins, hepatitis B surface antigen C or virus biochemisty iron studes copper alpha1 antitrupsis lipids glucose

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51
Q

What are hepatitis differential diagnosis?

A

Alcholo autoimmune virology, drug induced

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52
Q

What is autoimmune hepatitis treated?

A

Steroids to surpress it

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53
Q

What are the types of autoimmune liver diesases?

A

Scerosisn colangitis, autoimmune hepatitis afectin hepataocytes, primary biliary cholangiatis

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54
Q

What can help with autoimmune liver dieases diagnois?

A

Family history of autoimmune disease and current other ones

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55
Q

what is the epidemiology of autoimmune disease?

A

mainly women

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56
Q

How can you treat cholestatic itch?

A

Antihistamines lotions,

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57
Q

What blood disorder can affect the liver?

A

Iron can build up in haemochromatosis can include genetic screening for the rest of the family

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58
Q

What is alpha 1 antitrypsin deficeincy?

A

inability to export alpha 1 antitrypsin from liver can cause liver disease and empysema, asthma

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59
Q

What is hepatocellular carcinoma?

A

Cancer of the liver cells Usually associated with in hepatitis BC haemochromotosis and usually already have cirrhosis, can cause decompensation,

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60
Q

What is non alcoholic fatty liver disease?

A

Build up of fat in the liver treated by weight loss improve diabetic control

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61
Q

What are non alcoholic fatty liver disease risk factors?

A

Obesity diabetes hyperlipidaemia

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62
Q

Where are most of the bacteria in the GI tract?

A

After the duodenum as gastric acid restricts the growth of organisms before this point

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63
Q

What do the intestinal microflora do?

A

Out compete pathogenic bacteria produces,mainly anaerobes, can produce antibacterial substances bile and gastric acid have antibacterial properties

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64
Q

What is diarrhoea?

A

Fluid or watery stools in 3 or more tiems in 24 hours can be watery or bloody

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65
Q

What is dysentry?

A

Bloody diarrhoeas with stomach pains

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66
Q

What non-infectious causes can casue diarrhoea?

A

Cancer cheical poising, inflammatory bowel diseae endocrine and dietary

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67
Q

What is the mechanism of diarrhoea by pathogens?

A

Adherence to epithelium in proximal small bowel and produciton of enterotoxin.

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68
Q

What usually causes bloody diarrhoea?

A

Bacteriain the colon, viruses rarely cause this

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69
Q

What are the most common cause of diarrhoea in the UK?

A

Viruses such as rotavarius in childrenand norovirus (highly infectious)

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70
Q

What are the bacterial causes of watery diarrhoea?

A

Cholera not in the uk, Enterotoxifenic E.Coli most common traveller’s diarrhoea Cperfringens Bacillus cereus reheated rice/vomiting staphylococcus all by food poisioning

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71
Q

What infections agent can cause persistent diarrhoea?

A

Giardia a parisite occures worldwide common in areas of por sanitation

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72
Q

What can cause bloody diarrhoea?

A

Slamonella from undercooked poultry eggs and upasturised dairy, shegella, person to person spread crowded living conditions and E.coli Entero invasive and shialike toxin producing, can cause haemolysis Campylobacter and yersina

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73
Q

How does shigella cause damage?

A

Shiga toxin that dammages bowel surface

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74
Q

What is colostroides difficile?

A

Spore producing toxin producing gram positive bacteria often after antibiotics that allow them to thrive

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75
Q

When does C diff infection happen?

A

up to one month after, asymptomatic carriage and can lead to toxic megacolon

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76
Q

How ar Cdiff treated?

A

Cessation of broad antibiotics, vancomycin metronidazol and barrier precations

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77
Q

What are key parts of history for diarrhoea?

A

Travel onset and duration characteristics of stools, hobbies, animal contacts, urine output drinking, medications

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78
Q

What are indications for testing of diarrhoea?

A

Signs of hypovalaemia, severe abdo pain, bloody diarrhoea+ mucus in high risk patients IBD pregnancy, more than 1 week symptoms public health concern eg if in food handler

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79
Q

What does the lab do to for testing stool?

A

microscopy, cuture, Multi-pathogen molecular panels, ova cysts parasites, toxin detection C difficile, blood for culture inflammatory markers electrolytes creatimine

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80
Q

What is main way of treating patients with diarrhoea?

A

hydration and electrolytes, may need to notify PHE, dont often give antibiotics, giardia, c diff and salmonella

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81
Q

What to do to guide intrabdominal infection investigation?

A

Pain location and other symptoms

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82
Q

What is acute cholecystitis?

A

Gallbladder inflammation cystic duct obstruction by gall stones, RUQ or epigastric pain fever and leucocytosis,

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83
Q

How is acute cholecystitis diagnosis treatment?

A

ultrasound IV fluids and analgesia and antibiotics or surgery with cholecystectomy

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84
Q

What is ascending cholangitis?

A

Obstruction of common bile duct with pain fever and jaundice charcots triad, Managed by IV antibiotics prompt admission ERCP or cholecystectomy

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85
Q

What are liver abscesses types?

A

Pyogenic following biliary sepsis usually polymicrobial enteric gram-negative bacilli and anaerobes can be amoebic occasionally

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86
Q

What are presentation of liver abscess?

A

Fever RUQ pain nausea vomiting anorexia weight loss and malaise

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87
Q

How is liver abbesses diagnosed and treated?

A

CT or ultrasound, blood cultures of the abscess material and E histolytica molecular testing.

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88
Q

What is the treatment of a liver abcess?

A

Drainage and antibiotics

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89
Q

What can cause peptic ulcers?

A

Helicobacter pylori adheres to gastric epithelium it is very common half have it it can cause dyspepsis and epigastric pain and is associated with gastritis, gastric adenocarcinoma and gALT lymphoma

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90
Q

What causes genaralised abdomainal pain/

A

Peritonitis ainflammation of peritoneaum due to infectin or inflammaton can be acute sever generalised abdominal pain with fever and diffuse abdominal tenderness and rigidity and guarding

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91
Q

What are the classes of peritonitis?

A

Primary (spontaneous) from acites TB PID and cirrhosis

Secondary from spillage from GIT in trauma or appendicitis and peritonitis secondart to ambulatory peritoneal dialysis

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92
Q

What is the presentation of enteric fever?

A

Generalised abdominal pain fever and chills, headache and myalgia and relative bradycardia rose spots constipation/green diarrhoea blood culture and bone marrow aspiration

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93
Q

What are complications of enteric fever?

A

GI bleed perforation myocarditis and abscesses

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94
Q

What is important in diarrhoea?

A

Travel history and antibiotics

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95
Q

What are general mechanisms of intestinal obstruction?

A

Intraluminal, Intramural extraluminal

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96
Q

What can cause intraluminal obstruction?

A

Tumour carcinoma lymphoma, diaphragm disease (related to NSAIDS fibrotic action), gallstone ileus (rare), meconium ileus

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97
Q

What can cause intramural obstruction?

A

diverticular disease, Crohn’s disease, Intramural tumours, Hirschprung’s disease

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98
Q

What is hirschprung’s disease?

A

When there is no ganglia so it is not innervated anganglionic bowel

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99
Q

What can cause extraluminal obstruction?

A

Adhesions often from surgery a long time ago, sigmoid volvulous ( twisted colon then obstructed itself), peritoneal tumour (ommentum potentially)

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100
Q

How common is intestinal obstrucion?

A

5-20% of emergency general surgery.

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101
Q

What is prognosis for obstructed bowel?

A

quite good when treated, around 30% mortalitiy for most types

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102
Q

What are key parts of anatomy to be aware of in the abdomen?

A

Greater sac and lesser sac, ommentum

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103
Q

What are the physiological characteristics of the bowel?

A

Distensibility, motility, segmented peristalsis, it has sphincters, secretions take place

104
Q

What is intussusception?

A

telescoping of the bowel

105
Q

What is intussusception?

A

telescoping of the bowel

106
Q

What are the ways the bowel obstruction are classified?

A

Site, extent partial/complete, anchoring to mechanism, mechanical or paralytic pseudo, according to pathology simple closed loop strangulation intussusception

107
Q

Where is intussusception most common?

A

small or large bowel

108
Q

What are the symptoms of bowel obstruction

A

poorly localised pain, colicky cramping pain, vomiting early in proximal bowel or llate in distal, constipation early in distal of bowel and late in small bowel abdominal distension

109
Q

What are clinical findings of bowel obstruction?

A

Tachycardia from dehydration low pulse pressure, abdominal (distension visible peristalsis obvious lump at the site of obstruction)

110
Q

What is paralytic ileus?

A

failure of peristalsis, no mechanical obstruction, can be caused by hypocalcaemia post operative,

111
Q

What is gastric outlet obstruction?

A

uncommon benign or malignant, chronic peptic ulcer distal gastric cancer, hypertrophic pyloric stenosis gastric paresis

112
Q

What is the most common cancer of the bowel?

A

Carcinoma

113
Q

Who does bowel cancer usually affect?

A

mainly older people and often western countries

114
Q

What structure can lead to colorectal cancer?

A

Adenomas of the bowel, polyps

115
Q

What are the genetic conditions that predispose to colorectal cancer?

A

Familial adenomatus and polyposis

hereditary nonpolyposis colorectal cancer

116
Q

What is Familial adenomatus polyposis?

A

Gorw thousands of polyps and can lead to getting adenocarinoma, caused by genetic mutation to gene that produces a protein that usually removes beta catenin so with mutation it builds up in the protein causing polyps from epithelial proliferation

117
Q

Why look for identification of HNPCC?

A

risk of further cancers in index patient and relatives, can affect therapy, tolerance of treatments

118
Q

Where does colorectal cancer occyr/

A

Mainly in the rectum rectosigmoid, meanin cn be easily felt by digital rectal examination, adenocarcinoma

119
Q

How is colorectal cancer staged?

A

resection margins Resection coding R0 completely R2 not all removed,

120
Q

How are cancers graded?

A

invasion on T and N baste on node metastases M

121
Q

What are presentation of small bowel obstruction?

A

vomiting sometiems faeculent, collicky or constant diffuse pain constipation but is a late complication distension and tenderness

122
Q

What is the presentation of large bowel obstruction?

A

abdominal discomfort, fullnes bloating nausia altered bowel habit blood in stoolsa, colicky pain tender, nausea its often from malignancy, late is vomiting if its volvulus it is sudden pain localised tenderness and distension

123
Q

What are mechanisms of obstricuion/

A

Mechanical/true intra or extraluminal and parylitic

124
Q

What is small bowel obstruction pathophysiology?

A

proximal dilatation,Increased secretions + swallowed air, with dilatation get less absorption and mucosal wal oedema, increased pressure - intramural vessels compressed leading to ischaemia and perforation

125
Q

If perforation occurs where is it most likely?

A

In the caecum

126
Q

What happens in large bowel obstruction?

A

Distension of all areas up to the blockage

127
Q

What can cause prehepatic jaundice?

A

Breakdown of blood in excess from malaria, sickle cell anaaemia and foetal Hb breakdown in newborns.

128
Q

What can cause hepatic jaundice?

A

failure of hepatocytes to take up or excrete bilirubin. dark urine and normal/ale stools increased

129
Q

What are the local complications of ulcerative collitis?

A

carcinoma rupture of the bowel, massive haemorrhage.

130
Q

What are the local complications of crohn’s disease?

A

fistula, abscess formation, stenosis/ strictures, carcinoma, lymphadenopathy

131
Q

Where can Crohn’s disease affect?

A

The whole GI tract

132
Q

Where can ulcerative colotis affect?

A

The large bowel/ colon only

133
Q

What is the pathophysiology of inflammatory bowel disease?

A

M cells usually sense the microbes in the gut to activate the immune system by using antigen presenting cells, and or impared barrier function allowing microbes into the walls. then inflammation ensues

134
Q

What environmental factors can affect Crohn’s disease and ulcerative colitis?

A

Microbes, diet infections stress NSAIDs smoking antibiotics

135
Q

What environmental factors can affect Crohn’s disease and ulcerative colitis?

A

Microbes, diet infections stress NSAIDs smoking antibiotics

136
Q

What is the inflammatory process in the bowel wall?

A

Antigen presentign presents to t cells and activates mroe APC and causes cytokine function and release including, TNF alpha, IL-1 and 6

137
Q

What are the effects of TNF alpha on the bowel mucosa?

A

Paneth cell necrosis(releases antimicrobials) angiogenesis, Intestinal endothelial cell death and increaes immune response and cayses myofibril induced destruction

138
Q

What are the systemic complication of IBD active phase?

A

Conjunctivitis, irisis, mouth ulcers, fatty liver/absecss, meseteric or portal vein thrombosis, venous thrombosis, large joint arthritis, erythema odosum and pyogenia gangreousum result of cytokine release

139
Q

What are the investigations for IBD?

A

FBC (anaemia and malabsorption) blood chemistry (decreased albumin) ESM.CRP (inflammatory markers) MCS stool microbes to rule out infection, gold standard is endoscopy- colonoscopy

140
Q

What is the features of colonoscopy for ulcerative colitis?

A

eythematus appearance, continuous lesion pseudopolyps, petuciae exudates and oedema

141
Q

What are the features of Crohn’s disease on endoscopy?

A

Cobblestone appearance strip lesions pseudopolyps granulomas

142
Q

What can you do to investigate Crohn’s disease severity?

A

Radiology looking at barium studies to stage the disease

143
Q

How is Ulcerative colitis diagnosed?

A

Chronic diarrhoea for 4 wees and evidency of activ inflamation on endoscopy and chronic changes in biopsy.

144
Q

What is needed for Croh’ns disease dianosis?

A

endoscopic findings and immagins study with clinical history

145
Q

what are the aims of treating IBD?

A

treat attacks and prevent relapse

146
Q

How can IBD be treated?

A

5- ASA terapy +- corticosteroids it is activated by colon bacteria and it reduces local inflammation. In severe issues, rehydration, and corticsteroids, no 5-asa, antibiotics or tnf-alpha inhibitors ca remove part of colons

147
Q

What are treatments for chrons?

A

Prevention, imune surpresssion diet TNF alpha antagonists, mantenance methotrexate surgery for complications of chrons and to remove sectins of damaged bowel

148
Q

What is gluten sensitivity enteropathy?

A

Coeliac disease gluten allergy

149
Q

What is gluten?

A

Found in wheat barley and rye makes doeugh elastic and binding

150
Q

What are the symptoms of coeliac disease?

A

when gluten is eaten the villi shorten and lots of intraepithelial lyphcytes prolferate. gluten initiates autoimmune reaction that shortens and atrophies villi and deapens crypts itstops water and fat absorption to cause diarrhoea and steatorrhea, weight loss fatigue anaemia ostoporosis increased risk of bleeding al from malabsorption

151
Q

What are rare complications of coeliac disease?

A

neurological disease, cancers and infertility

152
Q

What is the pathophysiology of coeliac diseae?

A

Gluten isn’t broken down properly as has lots of proline and glutamine. The large molecules can be transported by receptors between the cells or dammage the epithelium. then they are modified by an enzyme and glutamate is produced and immune system attacks this

153
Q

What is the immune response like in coeliac disease?

A

make antibodies against glutamate and cause autoantibodies for glutamate and the enzymes and causes damage to enothelium for t cell cytokines

154
Q

What makes coeliac immune problems?

A

the type of MHC II molecules they have HLA-DQ2 and 8 having this mutation and need environmental and genetic factors to contribute to it

155
Q

How is coeliac disease treated?

A

avoid gluten at all costs and will cure them

156
Q

How is coeliac disease diagnosed?

A

common in autoimmune diseases, and family history MS and type 1 diabetes the antibodies against transglutaminase but not 100% endoscopy is the most sensitive villus blunting and crypt hyperplasia

157
Q

What can cause malabsorption relating to the duodenum?

A

pancreatic failure from pancreatitis, bile salt production failure lack of digestive enzumes defetive epithelial transport, lymphatic obstruction TB or lymphoma

158
Q

What can cause damage to the absorptive surfaces of the bowel?

A

Chron’s disease, IBD and coeliac disease, small bowel infarction

159
Q

What is extensive surface parasitisation?

A

Giardia lamblia a protazoa can cause the intestine to be damaged

160
Q

What is chronic idpathic inflamatory bowel?

A

Name for Crohn’s andIBD

161
Q

What are the complications of Crohn’s disease?

A

Malabsorption disease extent surgical resection, obstruction from fibrosis, perforation, fistula formation anal skin tags fissure fistula neoplasia

162
Q

What type of inflammationos Crohn’s disease?

A

Transmural inflammation

163
Q

What type of inflammationos inflammatory bowel disease ulcerative collitis?

A

only in large intestine long strips and only affects epithelium

164
Q

What are the symptoms of upper GI cancer?

A

They are like gastritis general pains dyspepisa etc

165
Q

What is Barret’s oesophagus?

A

Metaplasia change of cell types from differentiated to another differentiated type it is also called columnar lined lower oesophagus

166
Q

What makes Barret’s oesophagus likely?

A

Obesity, males

167
Q

What are the stages of changes of oesophagus cancer formation?

A

normal tissue then GORD gives Metaplasia into glandular epithelium, then more GORD and other factors lead to dysplasia and then neoplasia

168
Q

How to treat oesophageal cancer?

A

Surgery removal if posible

169
Q

Why is oesophageal cancer got very bad outcomes?

A

It presents very late as the symptoms don’t come till later

170
Q

What are the risk factors for gastric cancers?

A

smoked pickled food? disease of later life age related, sometiems helicobacterpylori

171
Q

What are the stages of adenocarcinoma in the stomach?

A

normal mucosa is disrypted by H Pylori or other factors then has intestinal metaplasia then dysplasia happens and you get genetic changes eating to intramural carcinoma then invasive carcinoma

172
Q

Why does gastric cancer present late?

A

the tumour can get very large before symptoms become present

173
Q

What can happen to the gastric mucosa in ischaemia?

A

they stop producing enough mucous and can begin to cause an ulcer which can cause pain

174
Q

When is mucosal ischaemia likely?

A

Patients i haemodynamic shock

175
Q

What can cause gastritis?

A

ischaemia, excessive acid production (stress, Helicobacter) aspirin can cause inhibition of mucosalproduction, bile reflux, alcohol,

176
Q

Where do H.pylori live?

A

In the mucin layer they induce acid production and neutrophils to enter gastric cells

177
Q

What is important about pain sensation in the abdomen?

A

The parietal gives well localised pain the visceral only gives generalised pain

178
Q

What are the functions of the peritoneum in health and disease?

A

In health,visceral lubrication fluid and particulate absorption, in disease pain perception inflammatory and immine response and fibrinolytic activity

179
Q

How can peritonitis be classsified?

A

Acute onset chronic onset or primary or secondary

180
Q

What can cause peritonitis?

A

Bacterial from GI or other, Chemical, bile leakage or barium, Traumatic from operations/surgery, ischaemic from strangulated bowel or vascular occlusion or familial mediterranean fever

181
Q

How can the peritoneum become infected?

A

From GI ( commonly perforated ulcer, appendix, diverticulum) transmural translocation no perforation in ischaemic bowel primary bacterial peritonitis andpancreatitis, exogenous contamintation from dialysis, open surgery, trauma or drains From the femal genital tract infection or hamatogenous spread from a blood borne infection

182
Q

What microorganisms can cause peritonitis?

A

E. coli, streptoccoci Enterococci bacteroides, clostridium klebsiella

183
Q

What are the clinical features of localised peritonitis?

A

Pain, nausea and vomiting, fever, tachycardia localised guarding rebound tenderness shoulder tip (supphrenic) pain and tender rectal and or vaginal examination

184
Q

What are the early features of diffuse eritonitis?

A

abdominal pain, worse by moving, tenderness generalised guarding infrequent bowel sounds paralytic ileus, fever and tachycardia

185
Q

What are the late features of diffuse peritonitis?

A

Generalised rigidity, distentsion absent bowel sounds, ciculatory failure thready irregular pulse Hippocratic facies and loss of consciousness

186
Q

What investigations are needed for peritonitis?

A

Urine dipstix for UTI, ECG if diagnostic doubt to rule out cardiac event. Bloods U&E FBC serum amylase for pancreatitis, group and save. CT abdo or CXR

187
Q

What is the key diagnosis of coeliac disease?

A

villus atrophy intraepithelial lymphocyte increase and crypt hyperplasia

188
Q

How are patients with peritonitis treated?

A

Correction of fluid loss and circulating volume, urinary catherterisation and GI decompression antibiotics and analgesia renal support

189
Q

What is familial Mediterranean fever?

A

genetic autoinflammatory disease affecting lungs joints and abdomen mainly in 20-40, more women than men and in certain groups such as

190
Q

How much ascites is normal?

A

In men usually none women around 20mls is normal

191
Q

What are the classifications of ascities?

A

Staged 1-4, detectable only after careful examination/ultrasound, easily detectable but small volume, obvious non tense ascites and tens ascites

192
Q

What are the two types of ascites?

A

Transudatw with low protein and exudate with high protein

193
Q

What are transudate causes of ascites?q

A

Low plasma protein in malnutrition, nephrotic syndrome or protein losing eneropathy hich central venous pressure and portal hypertension.

194
Q

What are the causes of exudate ascites?

A

Peritoneal malignancy, tuberculosis peritonitis,Budd-chari syndrome, pancreatic ascites,

195
Q

Where are most cases of ascited found?

A

In liver cirrhosis then cancer

196
Q

What are clinical presentations of ascites?

A

Abdominal distension, gaining weight clothes getting tighter, nausea/loss of appetite, constipation wasting, pain and discomfort painful in malignant, and symptoms of underlying cause

197
Q

What are clinical tests for ascites?

A

Shifting dullness fluid sonds on tappingflank fullness

198
Q

What are investigations for ascites?

A

Usually part of general ones for underlying cause, utrasound most sensitive ascitic aspiration and testing of fluid

199
Q

How are ascites treated?

A

Diuretics, treatment of cause sodium restricution paracentesis indwelling drain

200
Q

What are the main types of biliary tract disease?

A

Gallstones- biliary colic, Cholecystitis, Cholangitis

201
Q

What symptoms are used to differentiate biliary tract disease?

A

Virchow’s triad- Right upper quadrant pain, Fever/incr WCC, jaundice

202
Q

Which symptoms of Virchow’s triad come with Gallstones?

A

RUW pain

203
Q

Which symptoms of Virchow’s triad come with Acute cholecystitis?

A

RUQ pain and fever

204
Q

Which symptoms of Virchow’s triad come with Cholangitis?

A

all three RUQ pain, fever WCC and Jaundice

205
Q

What is the pathophysiology for gallstones/biliary colic?

A

Blockage of the cystic or common bile duct without signs of cystic inflammation the stones are made of cholesterol pigment or both

206
Q

What are the qualities of biliary colic/ gallstones?

A

Colicky RUQ pain ofte after eating large or particularly fatty meals which trigger the gallbladder, pain can radiatd to epigastrium and back

207
Q

What investigations are needed for biliary colic/gallstones?

A

FBC, CRP, LFT Alk phos Amylase to check for pancreatitis, to confirm need ultrasound look for stones gallbladder wall thickness and duct dilatation,

208
Q

How is gallstones treated?

A

NSAIDs analgesia, optional cholecystectomy, removal

209
Q

What is cholecystitis?

A

Stone blocking the duct bile builds up distending gall bladder and vascular supply can be afected leading to inflammation of the gall bladder

210
Q

What are the signs and symptoms of cholecystitis?

A

Generalised epigastric pain to severe RUQ fever or fatigue pain associated with tenderness and guarding from inflamed gall bladder and local peritonitis

211
Q

What is a specific clinical sign for gall bladder problems?

A

Positive murphy’s sign

212
Q

What is cholangitis?

A

Blocked bile duct because bile isnt pasing through the duct so bacteria ascend fromthe gut and infect it can affect pancreas too

213
Q

What are the signs and or symptoms of Choangitis?

A

Sever RUQ pain, fever with rigors and jaundice. Patient may present as septic or have developed pancreatits

214
Q

What to do to treat cholangitis?

A

Treat sepsis, ERCP to clear blockages and might remove gall bladder

215
Q

What is acute pancreatitis?

A

self-perpetuating inflammation of the pancreas causing leakage of enzymes and autodigeston the ancreas can heal after breif acute episodes

216
Q

What is the pneumonic for acute pancreatitis?

A

I GET SMASHED
Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune(japan), Scorpion venom, Hyperlipidaemia, ERCP, Drugs NSAIDs ACEi Steroids

217
Q

What is the pathology of acute pancreatitis?

A

Alcohol contracts Ampulla of vater bstructing bile clearances and messes with Ca2+ homeostasis.
Gallstoens block bileduct and pancreatic duct causes Ca2+ relseae in oancreatic cells to actuvate tripsinogen that digests the pancreas
Also damage can lead to a leaky pancreas, causing autodigestion, can cause pancreatic dyfunction leading to hyperglycaemia

218
Q

What is the presentation of pacute pancreatitis?

A

Severe epigastric pain radiating to the back, anorexia fever jaundice Grey turners sign, N&V tachycardia

219
Q

What are the investigations for acute pancreatitis?

A

Serum amylase urinary amylase serum lipase which is more specific CRP and routine bloods erect CXray abdominal ultrasounds and CT, MRI

220
Q

How is pancreatitis treated/

A

Nil by mount to drop stimulation, prophylactve antibiotics analgesics, if gallstones are the cause treat them

221
Q

What is chronic pancreatitis?

A

Generally caused by chronic alcohol abuse but can be hereditary autoimmune or from CKD, obstructs bicarbonate secretion causes early activation of trypsinogen and autodigestion of pancreas and fibrosis,

222
Q

What is the presentation of chronic pancreatitis?

A

Epigastric pain boring through the back, worse after alcohol better leaning forward, usually 50+ maleHistory usualy fits, nausea vomiting decreased appedite malabsorption

223
Q

What are treatments for chronic pancreatitis?

A

stop drinking pancreatic enzyme supplements and PPI to aid digestion insulin for Diabetes and duct drainage

224
Q

What can cause infective diarrhoea?

A

Viral, bacterial, paneatic, antibiotics C diff,

225
Q

What are the risk factors for infective diarrhoea?

A

Foreign travel poor hygiene and crowded area

226
Q

What is haemochromatosis?

A

Too much iron in body cant store properly so end AR inheritance

227
Q

When does haemochromatosis present?

A

40s and later in women due to menstruation

228
Q

What is the presentation of haemochromotosis?

A

Chronic tiredness, Joint pain, pigmentation of skin, hair loss, sexual problems, cognitive problems, mood disturbance pancreas problems

229
Q

How is hameochromotisis?

A

Genetic testing to confirm, transferrin, and ferratin levels

230
Q

What is wilson’s disease?

A

Too much copper in liver and CNS

231
Q

Wat is the pathophysiology of Wilson’s disease?

A

Error of copper matabolism copper is deposited in liver basal ganglia and cornea

232
Q

What is the presentation of wilson’s disease?

A

Depression, neurotic behavioural patterns, CNS problems tremor dysarthria involuntary motions reduced memory, hapatitis cirrosis, Kayser-Fleischer ring copper in cornea

233
Q

What investigations are needed for Wilkinson’s diagnosis?

A

Serum copper and ceruloplasmin reduced, 24hour urinary copper excretion high, liver biopsy

234
Q

What is the treatment for Wilkinson disease?

A

Avoid high copper foods, use Chelating agent, Penicillamin or liver transplant

235
Q

What is alpha 1 antitrypsin deficiency?

A

autosomal recessive may result in lung and liver disease protease inhibitor that inhibits elastase. It causes COPD like symptoms with emphyseuma, bronchiectasis, chronic bronchitis

236
Q

What are complications of alpha 1 antitrypsin deficiency?

A

COPD lung dammage mucous chronic cough, liver disfynction, toxin buildup prota hypertension

237
Q

How to investigate alpha 1 antitrypsin deficiency?

A

Bloods serum A1AT CXR pulmonary functon tests liver function tests and liver biopsy

238
Q

How is A1ATD treated?

A

treat liver problems, and lung problems as symptomatic

239
Q

What is the pathophysiolgy of acities?

A

Excessive buildup of fluid in the peritoneal cavity from poor liver function and low albumin, low oncotic pressure, leads to fluid losss to the peritoneal cavity.

240
Q

What is the presentation of acites?

A

Large distended abdomen, shifting dullness

241
Q

How to treat ascites?

A

Low sodium diet spironolactome and furosimede and identyfy and treat cause

242
Q

How can peritonitis occur?

A

Spontaneous bacterial infection, secondary o perforated bowel or appendice or GU tract

243
Q

Where are the sites a hernia can take place?

A

epigastric, umbilical spigelian inginal femoral or obturator

244
Q

What are the complications of hernias?

A

Obstruction and strangulation of the bowel

245
Q

How do inguinal hernias occur/

A

Direct uncommon passes through posterior wall direct is medial to the inferior epigastric artery and indirect is lateral to it

246
Q

What are the symptoms of a hernia?

A

Swollen lump, discomfort in the gut, pain in abdomen, constipation and expands on coughing

247
Q

What is acute appendicitis?

A

infection of it it is surgical emergency

248
Q

What can cause appendicitis?

A

faecoliths, bezoars foreighn bodies trauma intestinal worms or lymphoid hyperplasia. leads to swelling and infection

249
Q

What is clinical presentation of Acute appendicitis/

A

early pain discomfort around umbilicus then passes towards tight illiac fossa to mcBuneys poing can be les severe, get guarding tender mass in RIF pyrexia anorexia nasusa and vomiting rosvings sign pain on movment and coughing

250
Q

What investigations are needed for Appendicits?

A

FBC raised WCC Raised CRP ESR less likely ultrasound can ddetect but gold standart is CT

251
Q

How is acute appendicitis managed?

A

Appendiectomy is gold standard IV antibiotics

252
Q

What is complicatin of acute appendicitis?

A

Perforation appendix mass, adhesions PID

253
Q

What is clinical presentation of ischaemic bowel disease?

A

Acute sever abdo pain, no abdo pain hypovalaemic shock often out of proportion symptoms with signs

254
Q

What is likely to case memsenteric schaemia

A

Superior mesenteric artery embolismu of ten from Atrial fibrilation

255
Q

What is gold standard for diagnosisng coeliac?

A

Duodenal biopsy

Phase 2 mine (13 decks)

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