CPC 8 acute abdo Flashcards

1
Q

What stimulates the acute phase response?

A

Cytokines IL-1, IL-6 and TNF

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2
Q

What does the acute phase response increase (blood results)

A

CRP and fibrinogen, increased ESR, fever, increased leukocytes and negative nitrogen balance.

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3
Q

What does a CRP of 100-200 suggest

A

Marked inflammation, bacterial infection

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4
Q

What does a CRP of more than 200 suggest?

A

Severe bacterial infection or extensive trauma.

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5
Q

What is pyelonephritis?

A

Suppurative inflammation of the kidney, with neutrophils within the tuules and interstitioum, although glomeruli are only involved in severe disease. Generally there are yellow-white cortical abscesses and surrounding hyperaemia.

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6
Q

What are some complications of pyelonephritis

A

Pyonephritis
Peri-nephric abscess
Papillary necrosis,

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7
Q

Causes of papillary necrosis - acronym

A

POST CARDS

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8
Q

Causes of papillary necrosis, POST CARDS

A
Pyelonephritis
Obstruction of the urogenital tract
Sickle cell disease
Tuberculosis
Chronic liver disease
Analgesia/alcohol abuse
Rejection of renal transplant
Diabetes mellitus
Systemic vasculitis.
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9
Q

First line investigations for suspected pyelonephritis

A

MSU and blood cultures.

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10
Q

Treatment for uncomplicated pyelonephritis

A

Ciprofloxacin for 7 days.

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11
Q

How do you treat an infection which is resistant to several antibiotics i.e. has extended spectrum beta lactamase?

A

With meropenem.

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12
Q

What are the components of human bile?

A

bile salts (primary and secondary), phospholipids, cholesterol, protein, bilirubin and electrolytes.

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13
Q

Discuss the pathogenesis of gall stones

A

Cholesterol supersaturation in bile (with mucin hypersecretion
gall bladder hypomotility
and increased intetinal conversion to deoxycholate also involved.)
Crystal nucleation
Stone growth

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14
Q

What are the types of gall stones?

A

Cholesterol and pigment. Cholesterol is most common in western populations, while pigment stones are predominantly in others.

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15
Q

What populations are susceptible to cholesterol stones?

A

Western populations. Forty, fat, female, fertile, also those who have just had rapid weight loss and or have inborn errors of bile acid metabolism.

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16
Q

What populations are risk factors for pigment stones?

A

Chronic hemolytic syndromes, biliary infection, ileal disease (crohn’s, resection or bypass), cystic fibrosis with pancreatic insufficiency.

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17
Q

Where does gallstone pain radiate?

A

Epigastric pain radiating to the back (in waves if in CBD), vomiting. If gall stone ileus, also pain and distension. If in bile duct, jaundice.

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18
Q

What investigation do you do for a suspected bile duct stone?

A

EUS is best, but MRCP if this is not available. US not really good for duct stones.

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19
Q

Complications of gallstones?

A

Biliary sepsis
Gall bladder empyema
Gall stone ileus
Acute cholecystitis.

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20
Q

What organisms cause biliary sepsis (mostly)

A

E. coli and bacteroides fragilis.

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21
Q

What immune cells are mostly involved in gall bladder empyema?

A

Neutrophils.

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22
Q

What is the treatment for biliary sepsis which is mild and community acquired?

A

Co-amoxiclav

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23
Q

What is the treatment for biliary sepsis which is mild and community acquired with penicillin allergy?

A

ciprofloxacin and metronidazole

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24
Q

What is the treatment for biliary sepsis which is hospital acquired MRSA positive?

A

Vancomycin (for MRSA) and Piperacillin-Tazobactam (for anaerobes)

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25
Q

What is the treatment for biliary sepsis which is hospital acquired MRSA positive in penicillin allergic patient?

A

vancomycin, ciprofloxacin and metronidazole.

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26
Q

What causes acute cholecystitis?

A

Diabetes mellitus, gallstones, sepsis, immunosuppression and trauma.

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27
Q

What is the appearance of a gallbladder with cholecystitis?

A

Fibrinous exudate on external surface
Subserosal haemorrhage
Gallbladder wall is thickened, oedematous and hyperaemic
Neutrophilic inflammation

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28
Q

What is the most common cause of chronic cholecystitis?

A

Gallstones (90%)

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29
Q

General chronic cholecystitis info

A

Supersaturation of bile leads to chronic inflammation and stone formation.
⅓ have E. coli or enterococcus in bile.

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30
Q

Appearance of gallbladder in chronic cholecystitis

A

Thickened wall, variable chronic inflammation, sub-epithelial and sub-serosal fibrosis, outpouchings of epithelium through the wall.

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31
Q

Imaging of choice for right iliac fossa pain, fever and diarrhoea

A

CT the best, but US has less radiation.

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32
Q

Differential diagnoses for right iliac fossa pain, fever and diarrhoea

A
Appendicitis
Carcinoid tumour
Endometriosis
Enterobius vermicularis
Idiopathic inflammatory bowel disease. 
Ectopic pregnancy
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33
Q

Pathophysiology of appendicitis

A

Obstruction of lumen → stasis and loss of venous outflow → bacterial proliferation, inflam.response and ischaemia → neutrophilic inflammation and necrosis.

34
Q

Appearance of appendix in appendicitis

A

Hyperaemic dilated vessels and/or fibrinious exudate on surface and/or perforation.
Neutrophilic infiltrate at least as far as muscularis propria. Serosal involvement suggests peritonitis.

35
Q

Complications of appendicitis

A
Perforation and peritonitis 
Appendix mass
Pyelophlebitis
Portal vein thrombosis
Liver abscess
Bacteraemia
36
Q

Basic info on carcinoid tumours

A

Well differentiated neuro-endocrine tumour.

40% jejunum/ileum,

37
Q

Carcinoid syndrome symptoms

A

Flushing
Diarrhoea
Secondary restrictive cardiomyopathy.

38
Q

What would be your imaging method of choice in the 74 year old with central abdominal pain radiating to the back and down into the legs?

A

CT

39
Q

What would be your imaging of choice for suspected acute diverticulitis?

A

CT, unless young patient in which case expert US can be ok.

40
Q

Causes of acute pancreatitis acronym

A

I GET SMASHED

41
Q

Causes of acute pancreatitis I GET SMASHED

A
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia. 
ERCP and emboli
Drugs (azathioprine)
42
Q

Biochemistry of acute pancreatitis.

A

Increased serum amylase levels within first 24 hr
Rising serum lipases
10% have glycosuria
Hypocalcaemia secondary to deposition of calcium salts.

43
Q

Histology of pancreatitis

A
Microvascular leak and oedema
Fat necrosis
Acute inflammation
Destruction of parenchyma
Destruction of blood vessels and interstitial haemorrhage.
44
Q

Complications of acute pancreatitis

A

ARDS
Renal failure
Pseudocyst formation
Sterile abscess.

45
Q

Hereditary pancreatitis - what genes cause it?

A

Gain of function in trypsinogen gene (PRSS1)
CFTR mutation
Loss of function of SPINK1, a trypsin inhibitor

46
Q

What are the complications of hereditary pancreatitis

A

Pancreatitic carcinoma - 40% lifetime risk.

47
Q

Chronic pancreatitis - general

A

Prolonged inflammation with irreversible injury and fibrosis

Exocrine injury occurs first, endocrine later.

48
Q

Causes of chronic pancreatitis

A

alcohol, long-standing obstruction, autoimmune pancreatitis, hereditary pancreatitis.

49
Q

What is diverticular disease?

A

Multiple outpouchings through the muscularis mucosae at taeniae coli where the vasa recta penetrate.

50
Q

What is the pathology of diverticular disease

A

Inflammation, perforation, abscess formation, fistula.

51
Q

What are the risk factors for colorectal carcinoma?

A

Diet high in refined carbs
NSAIDS are protective
FAP or HNPCC

52
Q

How does the position affect the shape of a colorectal carcinoma?

A

Exophytic in proximal, annular if distal

53
Q

Colorectal carcinoma prognosis depends on…

A

Prognosis depends on depth of invasion (vascular?) lymph node mets, differentiation and whether or not it is mucinous.

54
Q

Histology of colorectal carcinoma

A

Dysplastic glands

Stromal changes

55
Q

Pathophysiology of ischaemic colitis.

A

Acute compromise vs chronic hypoperfusion
Mucosal infarction may follow either
Transmural infaction typically follows acute vascular obstruction.

56
Q

Causes of acute obstructive ischaemic colitis.

A
Severe atherosclerosis at the origin of the mesenteric vessels
Abdominal aortic aneurysm
Oral contraceptive pill  use
Embolisation of cardiac vegetations.
Hypercoagulable states
57
Q

Causes of intestinal hypoperfusion.

A

Cardiac failure
Shock
Dehydration
Vasocconstrictive drugs.

58
Q

Macro appearance of ischaemic colitis

A

Congested and dusky
Bloodstained contents
Perforation
Serositis with fibrin.

59
Q

Histopathology of ischaemic colitis.

A
Mucosa haemorrhagic and ulcerated
Atrophy and sloughing of surface epithelium
Crypts regenerative
Neutrophils after reperfusion
Fibrosis if chronic.
60
Q

Ectopic pregnancy general

A

2% of confirmed pregnancies

Risk factors: appendicitis, endometriosis, previous surgery, IUCD.

61
Q

Likely causes of peritonism with epigastric pain with nausea.

A

Peptic ulceration
Acute pancreatitis
Acute cholecystitis
(be aware appendicitis, lower lobe pneumonia, MI)

62
Q

If someone has peritonism and pain, with cool peripheries, what does this mean?

A

He may have a degree of hypovolaemia - give him fluids.

63
Q

Treatment for acute pancreatitis.

A

80%-90% resolve with conservative treatment - IV fluids, nil by mouth, possible Abx.

64
Q

What is Wilson’s disease?

A

Autosomal recessive condition characterized by toxic accumulation of copper in the liver and brain. Neurological problems may manifest as dementia, tremor or dyskinesias.
Onset between 10-25 years

65
Q

Features of Wilson’s disease

A

liver: hepatitis, cirrhosis
neurological: basal ganglia degeneration, speech and behavioural problems are often the first manifestations. Also: asterixis, chorea, dementia
Kayser-Fleischer rings
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails

66
Q

Diagnosis of Wilson’s disease

A

reduced serum caeruloplasmin

increased 24hr urinary copper excretion

67
Q

Treatment of Wilson’s disease

A

penicillamine (chelates copper) has been the traditional first-line treatment
trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
tetrathiomolybdate is a newer agent that is currently under investigation
Next question

68
Q

Probable cause of painless enlarged gallbladder with mild jaundice on background of alcoholism

A

Pancreatic cancer

69
Q

Likely cause of diarrhoea 1-6 hr after exposure

A

Staphylococcus aureus, Bacillus cereus

70
Q

Likely cause of diarrhoea 12-48 h after exposure

A

Salmonella, Escherichia coli

71
Q

Likely cause of diarrhoea 48-72 h after exposure

A

Shigella, Campylobacter

72
Q

Likely cause of diarrhoea more than 7 days after exposure.

A

Giardiasis, Amoebiasis

73
Q

What is Budd-Chiari syndrome?

A

Budd–Chiari syndrome is a condition caused by occlusion of the hepatic veins that drain the liver.

74
Q

What is primary sclerosing cholangitis?

A

a biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts

75
Q

What is primary sclerosing cholangitis associated with?

A

ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC
Crohn’s (much less common association than UC)
HIV

76
Q

How to manage post-operative ileus

A

Nil by mouth and NG tube for stomach decompression

77
Q

Charcot’s triad for ascending cholangitis

A

Right upper quadrant pain, fever and jaundice

78
Q

Medication for renal colic

A

Diclofenac for pain relief

Alpha-adrenergic blockers to help stone pass.

79
Q

What medication can help prevent calcium renal stones?

A

Thiazide diuretics, which increase Ca++ reabsorption.

80
Q

Common features of viral hepatitis

A

nausea and vomiting, anorexia
myalgia
lethargy
right upper quadrant (RUQ) pain