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Medicine Year 1 > Case 10 SAP > Flashcards

Case 10 SAP Flashcards

1
Q

Biliary dyskinesia

A

problem with emptying gallbladder

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2
Q

Cholelithiasis

A

gallstones

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3
Q

Biliary colic

A

sudden pain in RUQ due to gallstones, also known as symptomatic cholelithiasis. Colicky and in waves, typically after eating. Usually from obstruction of cystic duct

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4
Q

Cholecystitis

A

inflammation of gallbladder likely from obstruction in cystic duct. RUQ pain, positive Murphy’s sign, pain more constant than biliary colic. get fever, nausea etc.

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5
Q

Positive Murphy’s sign

A

pain on inspiration while palpating gallbladder

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6
Q

Cholangitis

A

inflammation of any bile duct. can be infective, obstructive, autoimmune, or malignant. Charcot’s triad or Reynold’s pentad (in severe cases)

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7
Q

Charcot’s triad

A

Cholangitis. RUQ pain, jaundice, fever.

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8
Q

Reynold’s pentad

A

RUQ pain, jaundice, fever, altered mental status, shock (low BP, tachycardia)

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9
Q

Gallbladder mucocele

A

dilation of gallbladder due to chronic obstruction of cystic duct

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10
Q

Risk factors for gallstones

A

Crohn’s, diabetes, diet high in triglycerides and refined carbohydrate, diet low in fibre, female gender, genetic and ethnic factors, increasing age, medications (somatostatin analogue octreotide, glucagon-like peptide-1 analogues, ceftriaxone), non-alcohol related fatty liver disease, obesity, prolonged fasting/weight loss, use of HRT.

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11
Q

Morphology of obstructive gallbladder disease

A

gallbladder becomes enlarged, distended, and red. Gallbladder walls thicken. Can exude pericholecystic fluid when inflamed. Necrosis from ischaemia can occur. Bile ducts dilated.

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12
Q

Cardinal symptoms of gallbladder disease

A

RUQ pain, shoulder blade pain, pain after fatty meal, fever, nausea, vomiting, heartburn, indigestion, excessive gas, tenderness in RUQ, Murphy’s sign. If stones in duct: jaundice, dark urine, pale faeces, itching

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13
Q

Cardinal symptoms of pancreatic disease

A

pain which radiates to the back, jaundice, dark urine and pale stool (cancer), nausea, vomiting, loss of appetite, fever, shock in acute pancreatitis, chronic fatigue, weight loss, diabetes.

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14
Q

Define pancreatitis

A

Inflammation of the pancreas. can be acute or chronic

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15
Q

describe acute pancreatitis

A

sudden onset in response to short-term injury leading to autodigestion by its own enzymes. limited impact on secretory function and no gross structural damage

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16
Q

types of acute pancreatitis

A

mild, moderate, and severe

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17
Q

mortality from severe pancreatitis

A

50%

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18
Q

describe chronic pancreatitis

A

chronic fibro-inflammatory disease resulting in progressive and irreversible damage to the pancreatic parenchyma. loss of exocrine and endocrine capacity, although this may take years to develop

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19
Q

Risk factors for acute pancreatitis

A

I GET SMASHED
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Malignancy/mumps (infection)
Autoimmune
Scorpion sting
Hypertriglyceridemia/hypercalcaemia
Endoscopic retrograde cholangiopancreatography
Drugs (thiazide diuretics, ACEis, statins etc.)

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20
Q

Top three causes of acute pancreatitis

A

idiopathic, gallstones, alcohol

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21
Q

Risk factors for chronic pancreatitis

A

Alcohol in 70-80% cases
Others include smoking, recurrent acute, chronic obstructive cases, genetic abnormalities, metabolic conditions (hypertriglyceridemia and hypercalcaemia)

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22
Q

Pathology of acute pancreatitis

A

inappropriate release and activation of pancreatic enzymes → damage to pancreatic tissue → acute inflammatory response triggered

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23
Q

What three events cause enzyme release in acute pancreatitis?

A

Duct obstruction, acinar cell injury, defective intracellular transport

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24
Q

Duct obstruction in acute pancreatitis

A

accumulation of enzyme rich fluid and increased pressure in interstitium, lipase accumulation leads to local fat necrosis → inflammatory response compromises local blood flow leading to ischaemia of acinar cells resulting in release of digestive enzymes

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25
Q

Acinar cell injury in acute pancreatitis

A

can cause autodigestion from release and activation of zymogens

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26
Q

Defective enzyme transport within acinar cells in acute pancreatitis

A

normally the enzymes and hydrolases are transported via different pathways, but in pancreatitis distension of the ducts disrupts membrane trafficking leading to fusion of granules and lysosomes causing digestive enzyme activation

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27
Q

How does repeated acute pancreatitis cause chronic pancreatitis? (LADS)

A

may lead to ductal dilatation due to high back pressure, stellate cells laying down fibrotic tissue causing ductal stenosis, atrophy of pancreatic tissue, and low flow through the duct facilitating calcium stone formation

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28
Q

How does alcohol cause chronic pancreatitis?

A

stimulation of acinar cells to release cytokines leading to an immune response, neutrophils release superoxide and proteases acting on pancreatic tissue. reactive oxygen species from oxidative metabolism of alcohol may overwhelm cell defences. Impact on cellular secretion leading to plug formation in the ducts causing an obstruction. Transient contraction of sphincter of Oddi causing duct obstruction

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29
Q

Morphology in mild acute pancreatitis

A

oedema from vascular permeability, focal areas of fat necrosis

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30
Q

Morphology in severe acute pancreatitis

A

necrosis of islets, ducts, and acinar cells, vascular injury leading to haemorrhage

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31
Q

Morphology in chronic pancreatitis

A

atrophy, fibrosis, deformation of large ducts, calcium carbonate deposits

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32
Q

Clinical presentation in acute pancreatitis

A

severe epigastric pain which can radiate through to the back, associated with nausea and vomiting. Pain relieved by leaning forwards, exacerbated by lying down. Other features include high temperature, tenderness and swelling of the abdomen, and tachycardia.

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33
Q

Clinical features in chronic pancreatitis

A

repeated episodes of epigastric pain - burning or shooting pain that lasts hours or days. eventually constant mild to moderate pain between bouts of severe pain. advanced - steatorrhea (foul-smelling, oily stools), diabetes, weight loss.

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34
Q

Risks for alcohol-related liver disease

A

alcohol consumption, drug misuse, overweight/obese, female sex, pre-existing liver condition, and genetics (alcohol dependence and problems processing alcohol often run in families)

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35
Q

Risk factors for non-alcoholic fatty liver disease

A

type 2 diabetes, insulin resistance, conditions that affect the use of insulin, underactive thyroid, hypertension, high cholesterol, metabolic syndromes, aged over 50, and smoker.

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36
Q

Describe fatty liver disease

A

build-up of fat inside the hepatocytes that leads to hepatomegaly.

37
Q

Causes of fatty liver disease

A

alcoholic liver disease, NAFLD (obesity, type 2 diabetes, hypertension, hypercholesterolaemia), drugs, hep C, nutritional disorders, systemic disorder (IBD etc.), non-insulin related metabolic disorders (Wilson’s disease etc.), and small bowel diverticulosis with bacterial overgrowth

38
Q

Describe alcoholic hepatitis

A

acute inflammation of the liver which causes death of hepatocytes and is often followed by permanent scarring

39
Q

Four steps of NAFLD:

A

fatty liver (steatosis) –> non-alcoholic steatohepatitis (inflammation) –> fibrosis/cirrhosis –> cirrhosis –> potentially to cancer

40
Q

Which steps of cirrhosis are reversible?

A

Fatty liver, inflammation, and fibrosis (with treatment like diet, exercise, weight loss, bariatric surgery)

41
Q

Non-alcoholic steatohepatitis (NASH) morphology

A

evidence of cell injury/cytoskeletal disruption, cell death, and accompanying inflammation

42
Q

NASH histopathology

A

ballooned hepatocytes – essential finding indicative of microtubular disruption, may contain Mallory-Denk bodies.
Necroinflammation and lobular inflammation from immune response.
Hepatic fibrosis – perivenular/pericellular which may be accompanied by portal and periportal fibrosis

43
Q

Difference between NASH and NAFLD

A

NAFLD is just fat with no damage to the liver, NASH has damage to the liver itself

44
Q

Acute liver failure/fulminant hepatitis

A

characterised by acute liver injury with hepatic encephalopathy and coagulopathy that occurs <26 weeks of initial liver injury in the absence of pre-existing liver disease

45
Q

Hyperacute liver failure timescale

A

<7 days since injury

46
Q

Acute liver failure timescale

A

7-21 days after injury

47
Q

Subacute liver failure timescale

A

> 21 days and <26 weeks since injury

48
Q

Causes of acute liver failure

A

ABCs
A = acetaminophen, hep A, autoimmune hepatitis, adenovirus, amanita phalloides (mushroom poisoning)
B = hep B, Budd-Chari syndrome
C = cryptogenic, hep C, cytomegalovirus
D = hep D, drugs (and toxins)
E = hep E, Epstein-Barr virus
F = fatty infiltration (acute fatty liver of pregnancy, Reye’s syndrome)
G = genetic e.g. Wilson disease
H = ), hypoperfusion (ischaemic hepatitis, sinusoidal obstruction syndrome, sepsis), haemolysis elevated liver enzymes low platelets (HELLP), herpes simplex, heat stroke, hepatectomy, hemophagocytic lymphohistiocytosis

49
Q

Chronic liver failure

A

progressive deterioration of liver functions which follows years of insidious progressive liver disease, is most associated with cirrhosis

50
Q

Acute-on-chronic liver failure

A

decompensation of the diseased liver by other diseases/conditions that place demands on the liver. In most cases, liver transplantation is the only hope for survival.

51
Q

Morphology of liver failure

A

liver is initially enlarged by swelling and oedema related to inflammation, but as parenchyma is destroyed the liver shrinks dramatically. Hepatocellular necrosis

52
Q

Initial clinical features of liver failure

A

fatigue, anorexia, nausea, vomiting, and jaundice.

53
Q

More advanced clinical features of liver failure

A

coagulopathy, hepatorenal syndrome, portal hypertension

54
Q

Hepatorenal syndrome

A

renal failure with liver failure with no cause for kidney failure, decreased urine output, increased BUN and creatinine

55
Q

Portal hypertension

A

increase in pressure leading to resistance to portal blood flow, splenomegaly, anaemia, leukopenia, thrombocytopenia, portosystemic shunting, shunting from intestine into general circulation, hepatic encephalopathy, development of collateral channels, caput medusae, oesophageal varices, haemorrhoids, ascites, and spontaneous bacterial peritonitis

56
Q

Cardinal symptoms of liver disease

A

abdominal pain, dark urine, pale faeces, pruritus (itch), nausea, vomiting, loss of appetite, chronic fatigue, encephalopathy (confusion)

57
Q

Cardinal signs of liver disease

A

jaundice (colour comes from bilirubin), fever, hair loss, as well as compensated or decompensated signs

58
Q

Signs of compensated liver failure

A

Xanthelasmas, parotid enlargement, spider naevi, gynaecomastia, small or large liver, splenomegaly, clubbing, duputren’s contracture, xanthomas, scratch marks, testicular atrophy, purpura, pigmented ulcers

59
Q

Signs of decompensated liver failure

A

Neurological i.e. disorientation, drowsy –> coma, hepatic flap, fetor hepaticus, ascites, dilated veins on abdomen, oedma

60
Q

Dupuytren’s contracture

A

thickening and shortening of palmar fascia that leads to flexion deformities of the fingers. (benediction sign)

61
Q

Palmar erythema

A

exaggerations of normal speckled mottling of the palm due to altered sex hormone metabolism leading to hyperoestrogenaemia

62
Q

Spider naevi

A

vascular lesions consisting of a central arteriole surrounded by many smaller vessels due to an increase in oestrogen

63
Q

Hepatic encephalopathy

A

occurs when toxins that are normally cleared from the body by the liver accumulate in the blood, eventually travelling to the brain. Ranges from subtle behavioural abnormalities, marked confusion and stupor to deep coma and death. Develops over days, weeks to a few months. Neurological signs include rigidity, hyperreflexia, and asterixis.

64
Q

Precipitations of hepatic encephalopathy

A

alcohol, excess dietary protein, constipation, GI bleeding, and infection

65
Q

Define cirrhosis

A

build-up of scar tissue in the liver that stops it from functioning properly. Insult to the liver can lead to inflammation or death of the hepatocytes. Inflammation then causes death of the hepatocytes and scarring, and the scarring leads to a fibrotic, nodular liver. Death of hepatocytes leads to regeneration of hepatocytes which in turn leads to a fibrotic, nodular liver.

66
Q

Compensated cirrhosis

A

fibrosis present but liver functions also present, asymptomatic over many years, or symptoms are non-specific

67
Q

Decompensated cirrhosis

A

liver cannot function properly, more severe symptoms like jaundice, ascites, GI bleeding, and hepatic encephalopathy

68
Q

What can cirrhosis lead to? (Symptoms and diseases)

A

Portal hypertension, ascites, hypersplenism, oesophageal varices, synthetic dysfunction (coagulopathy, hypoalbuminemia), hepatorenal syndrome, hepatopulmonary syndrome, encephalopathy, hepatocellular carcinoma

69
Q

Three main morphological features of cirrhosis

A

bridging fibrous septa, parenchymal nodule formation, disruption of architecture of entire liver

70
Q

Stages of liver fibrosis histology

A

1 and 2 around central veins, 3 is bridging fibrosis, 4 is cirrhosis

71
Q

Most common causes of cirrhosis in developed countries (top 3)

A

Alcoholic liver disease, fatty liver disease, chronic viral hepatitis (hep C)

72
Q

Other causes of cirrhosis

A

autoimmune hepatitis, biliary diseases, genetic and metabolic liver disease, vascular disease, drugs and toxins, systemic diseases, idiopathic causes, developmental abnormalities, and infections

73
Q

Unusual causes of cirrhosis

A

hereditary haemochromatosis, alpha-1 antitrypsin deficiency, Wilson’s disease, primary sclerosing cholangitis, and primary biliary cholangitis.

74
Q

Hereditary haemochromatosis

A

Iron overload with deposition in liver, pancreas, heart, joints etc. Can cause hepatomegaly

75
Q

Alpha-1 antitrypsin deficiency (liver)

A

Pulmonary emphysema and liver disease

76
Q

Wilson’s disease

A

copper overload in liver, eye, and brain

77
Q

Primary sclerosing cholangitis

A

bile ducts decrease in size due to inflammation and fibrosis, associated with chronic ulcerative colitis

78
Q

Primary biliary cholangitis

A

bile ducts become injured, inflamed, and eventually destroyed

79
Q

Hepatitis

A

inflammation of the liver

80
Q

What does hepatitis look like histologically?

A

Pattern of liver injury characterised by portal and lobular inflammation with or without necrosis, depending on severity

81
Q

Acute hepatitis

A

Duration of less than six months. Three possible pathways: resolution, chronic hepatitis, or hepatic failure

82
Q

Causes of hepatitis

A

Infection, autoimmune, drug induced liver injury

83
Q

Hepatotropic hepatitis

A

Inflammation to the liver only

84
Q

Causes acute hepatotropic hepatitis

A

hep A and hep E via oral route

85
Q

Causes chronic hepatotropic hepatitis

A

hep B, C, and D via the blood rout

86
Q

Non-hepatotropic hepatitis

A

systemic with liver involvement

87
Q

Causes acute non-hepatotropic hepatitis

A

Epstein-Barr virus, cytomegalovirus, herpes simplex virus

88
Q

What test is diagnostic for acute pancreatitis?

A

Serum amylase or lipase 3x normal upper limit

Medicine Year 1 (23 decks)

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