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Year 3 > Block 32 Week 8 > Flashcards

Block 32 Week 8 Flashcards

1
Q

acute pancreatitis?

A
  • acute inflammation of the pancreas
  • uncontr release of activated pancreatic enzymes -> autodigestion
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2
Q

most common cause of acute panc?

A

1) Gallstones
2) alcohol

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3
Q

I GET SMASHED

A
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4
Q

gallstones -> panc?

A
  • most common cause
  • almost half of cases
  • can obstruct the ampulla -> biliary reflux
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5
Q

alcohol -> acute panceatitis?

A
  • increased production of digestive enzymes
  • alcohol commonly causes chronic panc but also causes acute
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6
Q

ERCP?

A

-> acute panc

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7
Q

endocrine function of pancreas?

A
  • islets of langerhans
  • insulin and glucagon
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8
Q

exocrine function of panc?

A
  • pancreatic ductal cells
  • produce pancreatic juice
  • trypsin imp in pancreatitus
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9
Q

pain in acute panc?

A
  • sudden onset epigastric pain
  • vomiting
  • worse on movement
  • radiation to back
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10
Q

why may patients have reduced urinary output in panc?

A
  • vomiting and third spacing of fluid - fluid exits the vascular space into tissues due to inflammation
  • can result in a significant fluid deficit and as such patients may have dry mucous membranes and reduced urinary output
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11
Q

Sx of acute panc?

A
  • Abdominal pain (may radiate to the back)
  • Nausea
  • Vomiting
  • Anorexia
  • Diarrhoea
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12
Q

Signs of acute panc?

A
  • Abdominal tenderness
  • Abdominal distention
  • Tachycardia
  • Tachypnea
  • Pyrexia
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13
Q

Acute panc - 2 signs?

A

Cullens sign and grey turners

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14
Q

Cullens sign =

A

peri-umbilical bruising

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15
Q

grey turner sign?

A

flank bruising

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16
Q

diagnostic test of acute panc?

A

amylase 3x the reference range

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17
Q

how long does amylase stay elevated?

A
  • 3 days
  • patients who present late may have a missed peak
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18
Q

amylase in acute on chronic panc?

A

even in severe pancreatitis the amylase may be normal, particularly in those with acute-on-chronic disease. In these cases, a CT abdomen and pelvis is generally needed to confirm the diagnosis and exclude alternative causes.

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19
Q

mild elevation of amylase?

A
  • parotitis
  • bowel obstruction
  • intestinal inflammation
  • trauma
  • malignancy
  • ruptured ectopic pregnancy
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20
Q

Lipase vs amylase?

A
  • lipase is more specific for panc
  • has a longer half life so levels remain elevated for longer
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21
Q

lipase levels suggesting acute panc?

A

3x above reference range

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22
Q

bedside Ix for acute panc?

A
  • Observations
  • ECG
  • Blood sugar
  • Pregnancy test
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23
Q

Bloods for panc?

A
  • amylase/ lipase
  • U&Es
  • LFTs - assessing for cholangitis
  • LDH
  • glucose
  • lipids
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24
Q

US in acute panc?

A

used to demonstrate gallstones or a dilated common bile duct. The pancreas may be visualised.

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25
Q

CT in acute panc?

A

used to confirm diagnosis when uncertainty remains and to exclude complications of disease.

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26
Q

MRCP in acute panc?

A

most commonly indicated in suspected gallstone pancreatitis to help evaluate for CBD stones.

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27
Q

scoring for acute panc?

A

glasgow

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28
Q

glasgow score indicating severe panc?

A

> 3

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29
Q

Tx of acute panc?

A
  • supportive
  • IV fluids
  • Analgesia
  • Nutritional support
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30
Q

nutrition in acute panc?

A

in mild cases low fat diet reintro

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31
Q

Severe panc - feeding?

A
  • enteral feeding is preferred to total parenteral nutrition (TPN).
  • It is thought enteral feeding helps maintain the mucosa and prevents translocation of bacteria. Nasojejunal feeding is commonly used.
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32
Q

when should ab be used?

A
  • NOT for acute panc
  • should be used for suspected cholangitis
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33
Q

ERCP?

A
  • Gallstone panc
  • stone extraction
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34
Q

pancreatic necrosis?

A
  • continued inflammation -> local thrombosis, haemorrhage and necorsis in the panc
  • high infection risk
  • major cause of mortality
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35
Q

Ix for pancreatic necrosis?

A
  • CT guided fine needle aspiration and culture
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36
Q

panc pseudocyst?

A
  • present 4+ weeks after an episode
  • psudo means epithelial lining around the cyst rather than granulation tissue
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37
Q

vascular complications of acute panc?

A
  • pseudoaneurysm
  • venous thrombosis
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38
Q

pseudoaneurysm?

A
  • rare but life threatning haemorrhages
  • often seen in splenic and hepatic arteries
  • normally occur in association w pancreatic pseudocysts
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39
Q

venous thrombosis?

A
  • venous thrombosis may affect the portal, splenic and superior mesenteric veins
  • requires AC
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40
Q

Severe acute pancreatitis can lead to ->

A
  • Acute respiratory distress syndrome
  • Renal failure
  • Shock - disrtibutive
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41
Q

mortality in acute panc?

A
  • 1% in mild panc
  • sterile pancreatic necrosis: 10%
  • infected panc necrosis: 25% mortality
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42
Q

Chronic pancreatitis refers to

A

chronic, irreversible, inflammation and/or fibrosis of the pancreas.

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43
Q

leading cause of chronic panc?

A

alcohol

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44
Q

endocrine dysfunction in chronic panc?

A

Endocrine dysfunction: damage to the islet cells result in lack of insulin and development of diabetes mellitus

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45
Q

exocrine dysfunction in chronic panc?

A

Exocrine dysfunction: damage to the acinar cells results in lack of pancreatic enzymes and malabsorption

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46
Q

Classification of the causes of panc?

A

TIGAR-O

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47
Q

Tigar-O?

A

T (toxic/metabolic): alcohol, smoking, high triglycerides, hypercalcaemia, chronic kidney disease

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48
Q

tIgar-O?

A
  • idiopathic
  • may be late onset, early onset or tropical
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49
Q

tiGar-O?

A
  • genetics
  • mutation in PRSS1
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50
Q

autoimmune panc?

A
  • type 1
  • type 2
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51
Q

Type 1 autoimmune panc?

A
  • IgG4 disease
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52
Q

Type 2 autoimmune panc?

A

limited to the pancreas and associated with inflammatory bowel disease

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53
Q

tigaR-O?

A
  • recurrent and severe acute panc
  • patients with a severe episode of necrotising pancreatitis or those with acute recurrent pancreatitis can progress to chronic pancreatitis due to tissue destruction
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54
Q

tigar-O?

A
  • chronic obstruction of the main pancreatic duct can lead to tissue damage and chronic pancreatitis upstream.
  • Typical causes of obstruction include strictures, stones, cysts, and tumours
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55
Q

autosomal dominant hereditary panc?

A
  • PRSS1 mutation
  • encodes cationic trypsinogen
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56
Q

autosomal recessive hereditary panc?

A
  • mutation in CTFR gene
  • spink 1 gene
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57
Q

most common feature of chronic panc?

A

abd pain

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58
Q

pain in chronic pain?

A
  • epigastric discomfort
  • worse post-prandially and on lying down
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59
Q

pain in chronic panc may be assoc w ?

A
  • nausea
  • vomiting
  • anorexia
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60
Q

CP - exocrine insufficiency?

A
  • destruction of acinar cells -> loss of digestive enzymes -> malabs
  • inability to digest fatty foods due to lack of lipase
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61
Q

features of panc exocrine insufficiency?

A
  • Weight loss
  • Bloating
  • Flatulence
  • Abdominal pain/discomfort
  • Loose stools
  • Steatorrhea
  • > 90% of the pancreatic exocrine function needs to be lost before patients develop steatorrhea - consq of long standing panc damage
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62
Q

loss of endocrine cells in CP?

A
  • Type 3c DM
  • Polyuria, polydispsia, weight loss
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63
Q

assessment of chronic panc?

A
  • CT or MRI with MRCP
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64
Q

features of chronic panc on CT?

A
  • CT is excellent at looking for calcification changes within the pancreas.
  • Features of chronic pancreatitis include atrophy, calcification, and ductal changes (e.g. dilatation, strictures).
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65
Q

Fecal elastase?

A
  • indirect marker of panc function
  • used to assess for panc exocrine insufficiency
  • low levels suggest PEI
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66
Q

Bloods in CP?

A
  • FBC, U&Es, LFTs
  • lipid profile
  • bone profile
  • mag
  • hbalc
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67
Q

general management of chronic panc?

A
  • nutritional assessment
  • alcohol cessation
  • smoking cessation
  • vitamin replacement e.g. vitamin D
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68
Q

Pain relief in chronic panc?

A
  • basic first: paracetamol and NSAIDs
  • then weak opiods: tramadol, codeine
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69
Q

PEI management?

A
  • pancreatic enzyme replacement therapy
  • abs can be improved using a PPI
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70
Q

Endoscopic management for chronic panc when:

A
  • Pancreatic pseudocysts
  • Pancreatic stones
  • Main pancreatic duct strictures
  • Other complications (e.g. biliary strictures,
    duodenal obstruction)
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71
Q

complications of chronic panc?

A
  • PEI
  • DM
  • osteoporosis
  • panc cancer
  • duodenal and biliary obst
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72
Q

Hb ab interpretation?

A

HBsAg = ongoing infection, either acute or chronic if present > 6 months

anti-HBc = caught, i.e. negative if immunized

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73
Q

Transmission of hep A?

A
  • faecal-oral
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74
Q

hep A disease coruse?

A
  • self limiting
  • doesn’t cause chronic disease
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75
Q

features of hep A?

A
  • flu-like prodrome
  • abdominal pain: typically right upper quadrant
  • tender hepatomegaly
  • jaundice
  • deranged liver function tests
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76
Q

immunisation for hep?

A
  • A
  • B
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77
Q

hep B is a

A

double standed DNA hepadanvirus

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78
Q

how is hep B spread?

A
  • exposure to infected blood or body fluids
  • mother to child
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79
Q

incubation period for hep B?

A

6-20 weeks

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80
Q

features of hep B?

A
  • fever
  • jaundice
  • elevated LFTs
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81
Q

features of chronic hep B on LM?

A

ground glass hepatocytes

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82
Q

complications of hep B

A
  • HCC
  • glomerulonephritis
  • fulm liver failure
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83
Q

hep E spread?

A
  • faecal oral
  • Can be transmitted by seafood
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84
Q

incubation period of hep E?

A

3-8 WEEKS

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85
Q

Where is hep E common?

A
  • central and south asia
  • mexico
  • north and west africa
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86
Q

hep E is especially problematic in?

A
  • pregnancy - causes sig mortality
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87
Q

hep E does not cause ?

A

does not cause chronic disease or an increased risk of hepatocellular cancer

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88
Q

hep C affects?

A
  • IV drug users
  • patients who receive a blood transfusion
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89
Q

incubation period of hep C?

A

6-9 weeks

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90
Q

transmission of HepC?

A
  • Needle stick injury
  • mother to child
  • sexual intercourse
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91
Q

what is not contra-indicated in hep C?

A

breastfeeding

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92
Q

there is no vaccine for ?

A

hep C

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93
Q

Comps of chronic hep C?

A
  • Sjogren’s syndrome
  • cirrhosis
  • HCC
  • glomerulonephritis
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94
Q

hep D?

A
  • single stranded RNA virus
  • transmitted parenterally (blood and body fluids)
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95
Q

how does hep D cause infection?

A
  • requires hep B surface antigen to repllicate
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96
Q

how is hep D transmitted?

A

transmitted in a similar fashion to hepatitis B (exchange of bodily fluids) and patients may be infected with hepatitis B and hepatitis D at the same time.

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97
Q

Co-infection vs superinfection?

A

Co-infection: Hepatitis B and Hepatitis D infection at the same time.
Superinfection: A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection.

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98
Q

superinfection of hep B and D is assoc w a higher risk of?

A

Superinfection is associated with high risk of fulminant hepatitis, chronic hepatitis status and cirrhosis.

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99
Q

Ascending cholangitis is?

A
  • infection of the biliary ducts
  • caused by obstruction
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100
Q

how does ascending cholangitis present?

A

Charcots triad: fever, jaundice, RUQ pain

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101
Q

Reynol’d pentad?

A
  • Ascending cholangitis
  • fever, jaundice, RUQ pain, septic shock and mental confusion
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102
Q

common causes of asc cholamgitis?

A

choledocholithiasis (gallstones) and strictures of the biliary tree.

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103
Q

Reynold’s pentad indicated?

A

inc risk of septic shock -> medical emergency

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104
Q

LFTs with Ascending cholangitis?

A

hyperbilirubinaemia and elevated serum alkaline phosphatase

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105
Q

imaging for Ascending cholangitis?

A
  • ERCP: when history of biliary disease
  • transabd US: CBD dilatation
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106
Q

Mx of ascending cholangitis?

A
  • pieracillin/ tazobactam
  • IV fluids
  • analgesia
  • sepsis 5
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107
Q

definitive management of ascendinh cholngitis?

A
  • biliary decompression
  • ERCP or surgery
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108
Q

biliary colic pain?

A
  • RUQ pain
  • intermittent
  • usually begins abruptly and subsides gradually
  • attacks often occur after eating
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109
Q

Biliary colic - mneumonic?

A
  • female
  • forties
  • fat
  • fair
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110
Q

Acute cholesystitis pain?

A
  • similar to biliary colic but more severe and persistent
  • pain may radiate to back or right shoulder
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111
Q

acute cholesytitis sign?

A
  • pyrexial
  • murphy’s sign positive: arrest of inspiration on palpation of the RUQ
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112
Q

Gallstone ileus?

A
  • SBO
  • secondary to impacted gallstone
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113
Q

features of gallstone ileus?

A

Abdominal pain, distension and vomiting

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114
Q

Features of cholangiocarcinoma?

A
  • persistent biliary colic symptoms
  • anorexia
  • jaundice
  • weight loss
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115
Q

Signs of cholangiocarcinoma?

A
  • Courvoiser’s sign
  • sister mary joseph nodes
  • virchow node
116
Q

Courvoisier sign?

A

palpable mass in the right upper quadrant

117
Q

Sister mary joseph nodes?

A

periumbilical lymphadenopathy

118
Q

virchow node?

A

left supraclavicular adenopathy

119
Q

acute panc pain is usually due to?

A

alcohol or gallstones

120
Q

features of acute panc pain?

A
  • Severe epigastric pain
  • Vomiting is common
  • Examination may reveal tenderness, ileus and low-grade fever
121
Q

pancreatic cancer features?

A
  • painless jaundice
  • anorexia
  • weight loss
122
Q

differentiating pain

A
  • Biliary colic –> pain
  • Acute cholecystitis –> pain + fever
  • Ascending cholangitis –> pain + fever + jaundice
123
Q

Mirrizi syndrome?

A

In Mirizzi syndrome the stone may compress the bile duct directly- one of the rare times that cholecystitis may present with jaundice

124
Q

infection in cholangitis is due to?

125
Q

Panc cancer?

A

Typically painless jaundice with palpable gallbladder (Courvoisier’s Law)

126
Q

cholangiocarcinoma is linked to

127
Q

RF for gallstones?

A
  • Fat
  • Female
  • Fertile - pregnancy
  • Forty
128
Q

Other RF for gallstones?

A
  • diabetes
  • chrons
  • rapid weight loss
  • drugs - fibrates, oral contraceptive
129
Q

Features of gallstones?

A
  • colicky right upper quadrant abdominal pain worse postprandially, worse after fatty foods
  • the pain may radiate to the right shoulder/interscapular region
  • N and V
130
Q

distinguishing biliary colic from other gallstone related conditions?

A

in biliary colic there is no fever and liver function tests/inflammatory markers are normal

131
Q

choledocholithiasis=

A

gallstones in common bile duct

132
Q

cholelithiasis =

A

Cholelithiasis (gallstones) refers to the development of a solid deposit or ‘stone’ within the gallbladder.

133
Q

who do gallstones tend to affect?

A

They are more common in women and tend to affect those of caucasian, Native American and hispanic backgrounds more.

134
Q

RF for gallstones?

A
  • age
  • female
  • obesity
  • rapid weight loss/ prolonged fasting
  • diabetes
  • crohns
135
Q

medications linked to gallstones?

A

oestrogen replacement therapy, ceftriaxone, octreotide

136
Q

CF of gallstones?

A
  • intermittent RUQ/ epigastric pain
  • nausea and vomiting
137
Q

Ix for gallstones?

A
  • USS - can also assess for CBD dilation
  • LFTs
138
Q

symptomatic management of gallstones?

A
  • analgesia - paracetamol and NSAIDs
  • diet - low fat
139
Q

surgical management of gallstones?

A
  • elective cholecystectomy
140
Q

cholethiasis refers to?

A

Cholelithiasis (gallstones) refers to the development of a solid deposit or ‘stone’ within the gallbladder.

141
Q

Choledocholithiasis =

A

gallstones within the biliary tree.

142
Q

biliary colic =

A

refers to a self-limiting pain in the RUQ/epigastrum associated with gallstones.

143
Q

acute cholecystitis =

A

refers to the acute inflammation of the gallbladder, most commonly caused by gallstones.

144
Q

acute cholangitis =

A

refers to the acute inflammation of the gallbladder, most commonly caused by gallstones.

145
Q

cholesterol stones?

A
  • most common type
  • occur due to crystalisation of cholesterol in bile due to supersaturation of cholesterol
146
Q

black pigment stones?

A
  • dark stones composed primarily of calcium bilirubinate
  • They occur in people with increased amounts of bilirubin in their bile - hyperbilirubinbilia
  • occurs w inc haemolysis
147
Q

brown pigment stones?

A
  • mix of calcium bilirubinate and a calcium salts of fatty acids
  • mostly occur in association with infection
148
Q

comparison of abd pain?

149
Q

biliary colid observations?

A
  • normal
  • BTs normal
150
Q

acute cholesystitis symptoms?

A

RUQ pain, fevers, malaise

151
Q

observations of acute cholesytitis?

A
  • fever
  • haemodynamic instability
152
Q

examination in acute cholesystitis?

A
  • tenderness
  • localised guarding may be present
153
Q

USS of acute cholesystitis?

A
  • gallstones
  • inflamed, thickened GB
  • pericholesytitic fluid
154
Q

acute cholangitis obs?

A

fever and haemodynamic instability

155
Q

acute cholangitis features?

A
  • jaundice
  • tenderness
156
Q

acute cholangitis findings on US?

A

CBD stone, duct dilatation

157
Q

acute panc summary?

A
  • epi pain radiating to back
  • fever and tachy
  • epigastric tenderness
  • raised amylase
158
Q

Prostate cancer should be suspected in people who have any of the following symptoms that are unexplained:

A
  • Lower back or bone pain.
  • Lethargy.
  • Erectile dysfunction.
  • Haematuria.
  • Anorexia/weight loss.
  • Lower urinary tract symptoms (LUTS), such as frequency, urgency, hesitancy, terminal dribbling, and/or overactive bladder.
159
Q

Which anti-glycaemic drugs can be used to reduce CVD events, kidney failure and heart failure hospitalisation?

A
  • SGLT2 inhibitors: cardiovascular and renal benefits - e.g. CREDENCE trial
  • GLP-1 analogues -> CV benefit
160
Q

ppl w diabetes experience high rates of?

A

people with diabetes experience disproportionately high rates of mental health problems such as depression, anxiety and eating disorders.

161
Q

diabulimia?

A
  • diabulimia involves the deliberate manipulation of insulin doses to control weight -> poor glycaemic control and ketosis
162
Q

MH problems in diabetes?

A
  • Diabetes disress - constant vigilance -> stress
  • depression and anxiety - stress of a chronic condition, stress about a hypo
  • increased risk of EDs - condition called diabulimia
  • Chronic hyperglycemia and fluctuations in blood sugar levels can affect cognitive function in individuals with type 1 diabetes
163
Q

disordered eating in diabetes may be due to?

A
  • Insulin omission/ manipulation
  • Fear of hypos -> restrictive eating
  • Food rules and rituals - only eating at certain times and developing strict meal plans
  • Body image concerns - focus on weight
164
Q

main interventions to reduce CV morbidity and mortality in T1D - CV risk assessment?

A
  • eGFR and ACR
  • Smoking
  • BP control
  • full lipid profile
  • age
  • FHx of CVD
  • abd adiposity
165
Q

Interventions to reduce risk and manage CVD - T1D?

A
  • Stop smoking
  • BB for those who have had a stroke or MI
166
Q

Offer statin treatment for the primary prevention of CVD to adults with type 1 diabetes who:

A
  • are older than 40 years or
  • have had diabetes for more than 10 years or
  • have established nephropathy or
  • have other CVD risk factors.
167
Q

Consider ? Treatment in T1D for CVD prevention

A

Consider statin treatment for the primary prevention of CVD for people aged 18 to 40 with type 1 diabetes, including those who have had diabetes for 10 years or less.

168
Q

the role of transplant in t1d?

A
  • for adults w T1D who have recurrent severe hypoglycaemia that has not responsed to other treatments
  • consider referral to for islet and/or pancreas transplantation
  • Consider islet or pancreas transplantation for adults with type 1 diabetes with suboptimal diabetes control, if they have had a renal transplant and are currently on immunosuppressive therapy.
169
Q

appetite control centre is in the?

A
  • in the hypothalamus
  • arcuate nucleus -> appetite controle
170
Q

excitatory vs inhibitory NTs?

A
  • Excitatory neurons release NPY -> hunger
  • Inhibitory neurons release -> POMC
171
Q

ghrelin?

A
  • Ghrelin is a peptide hormone produced in the pancreas and released from the stomach wall when the stomach is empty.
  • This stimulates the excitatory primary neurones, and therefore stimulates appetite. When the stomach is full, ghrelin release is inhibited, thus the appetite stimulus is also inhibited
172
Q

PPY?

A

from the ileum in response to feeding. Causes appetite suppression

173
Q

Leptin?

A
  • leptin is produced by fat cells
  • stimulates inhibitory neurones and inhibits excitatory neurons in the arcuate nucleus -> appetite suppression
174
Q

Insulin?

A
  • Insulin is a hormone released from beta cells in the islets of Langerhans of the pancreas. This suppresses appetite in a similar way to leptin.
175
Q

How does the stomach signal to the brainstem?

A

vagus nerve

176
Q

How do we detect that we’re hungry?

A
  • Empty stomach senses by stretch receptors in the stomach -> signal to BS
  • Ghrelin -> arcute nucleus of hypothalamus
  • Ghrelin -> paraventicular nucleus to increase food intake and decrease energy expenditure
177
Q

Stomach distension?

A
  • distension of stomach stops ghrelin production
  • Gut peptides like GLP-1 and CCK are released which then act on the BS and hypothalamus
  • suppressing appetite and increasing energy expenditure
178
Q

LT metabolism regulation?

A
  • High fat -> stop feeding and spend energy
  • Low fat -> feed more, preserve more energy
179
Q

Leptin release is dependent on?

A
  • Leptin release is dependent on insulin and is released from adipose tissue
  • Increased leptin -> stop eating and spend energy
  • Inhibit food intake at hypothalamus
180
Q

Obesity results from?

A
  • results from disregulation of this system
  • assoc w chronic low leptin - makes the body think its starved which leads to obesity
181
Q

Lifestyle in obesity development?

A
  • high fat diet -> saturated fats -> inflammation -> leptin resistance -> starvation response
  • Leptin deficiency or mutations leading to leptin resistance
182
Q

Roles of insulin?

A
  • Insulin -> GLUT4 insertion -> glucose enters cell
  • Causes glycogen production, inhibits glucogonegenesis
183
Q

Roles of glucagon?

A
  • Glucagon - released when all the glucose
  • inactivates glycogen synthesis
  • inc glucogenolysis
  • Adrenaline acts the same as glucagon but faster
184
Q

Roles of BMI?

A
  • screening tool - quick and easy way to assess weight
  • health risk assessment - Individuals with higher BMI values are generally at increased risk of developing these conditions compared to those with lower BMI values.
  • population health monitoring
  • clinical decision making
185
Q

-Limitations of BMI

A
  • Doesn’t distinguish between fat and lean body mass
  • not applicable to different age and ethniticities
  • BMI does not account for distrubution of body fat
  • not suitable for pregnancy
186
Q

classification of obesity?

A
  • healthy weight: BMI 18.5 kg/m2 to 24.9 kg/m2
  • overweight: BMI 25 kg/m2 to 29.9 kg/m2
  • obesity class 1: BMI 30 kg/m2 to 34.9 kg/m2
  • obesity class 2: BMI 35 kg/m2 to 39.9 kg/m2
  • obesity class 3: BMI 40 kg/m2 or more
187
Q

Waist circumference indicating obesity?

A

Men: ≥ 102 cm (40 inches)
Women: ≥ 88 cm (35 inches)

188
Q

lifestyle Ix of obesity?

A
  • dietary changes - lifestyle interventions
  • reducing calories
  • increasing fruit and veggies
  • physical activity
  • behavioural strategies - goal setting, self monitoring
  • education - nutrition, exercise. weight management
189
Q

Limitations of lifestyle Ix in obesity?

A
  • complexity of disease - multifactorial so won’t address underlying genetic factors
  • indiv variability
  • sustainability - challenging to do long term
190
Q

Psych factors in using lifestyle Ix in obesity?

A

Emotional eating, stress, depression, and other psychological factors can undermine efforts to adopt healthier lifestyles. Lifestyle interventions may need to incorporate strategies to address these psychological barriers effectively.

191
Q

when is bariatric surgery indicated in obesity?

192
Q

Least restrictive bariatric surgery?

193
Q

LABG

A
  • least restrictive
  • first line
  • less weight loss but less comps
194
Q

What does a sleeve gastrectomy do?

A

reduces size of stomach

195
Q

What does the duodenum abs?

A

= Metal ions + Folate (first)

196
Q

Jejenum vs ileum abs?

A
  • Jejunum = all vitamins except
  • Ileum = B12
197
Q

What does the LI abs?

A

Na, K, water

198
Q

Initial Ix of Pituitary disease?

A
  • ACTH
  • FSH/ LH
  • TSH
  • GH
  • prolactin
199
Q

pathophys of thyroid eye disease?

A
  • autoimmune response against an autoantigen, possibly the TSH receptor → retro-orbital inflammation
  • the inflammation results in glycosaminoglycan and collagen deposition in the muscles
200
Q

RF for Thyroid eye disease?

A
  • most imp: smoking
  • radiodine treatment - predinoslone can reduce risk
201
Q

CF of thyroid eye disease?

A
  • the patient may be eu-, hypo- or hyperthyroid at the time of presentation
  • exophthalmos
  • conjunctival oedema
  • optic disc swelling
  • ophthalmoplegia
  • inability to close the eyelids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
202
Q

Mx of thyroid eye disease?

A
  • smoking cessation
    topical lubricants may be needed to help prevent corneal inflammation caused by exposure
  • steroids
  • radiotherapy
  • surgery
203
Q

thyroid issues in the pregnancy/ post-partum period?

A
  • the typical symptoms of pregnancy often emulate symptoms of thyroid dysfunction, creating a significant diagnostic challenge during this time
  • during pregnancy, thyroid gland enlarges and TFTs change - T3 and T4 increases but TSH decreases
204
Q

TFTs in pregnancy?

A
  • due to human chorionic gonadotropin (hCG) cross-reacting with TSH receptors; total T4 (TT4) levels increase while free T4 (FT4) levels remain unchanged.
205
Q

Roles of meds in causing thyrotoxicosis?

A

amiodarone and immune checkpoint inhibitors in causing thyroid hormone excess

206
Q

Subclinical hyperthyroidism TFTs?

A
  • normal T3 and T4 levels
  • TSH is low (suppressed)
207
Q

Causes of subclin hyperthyroidism?

A

MNG paticularly in elderly females

208
Q

Problems in subclinical hyperthyroidism?

A
  • AF
  • osteoporosis
209
Q

Mx of subclinical hyperthyroidism?

A
  • TSH levels often revert to normal - therefore levels must be persistently low to warrant intervention
  • a reasonable treatment option is a therapeutic trial of low-dose antithyroid agents for approximately 6 months in an effort to induce a remission
210
Q

Subclinical hypothyroidism TFTs?

A

TSH raised T3 and T4 normal

211
Q

Significance of subclin hypothyrodisim?

A
  • risk of progressing to overt hypothyroidism - higher in men
  • risk increased by presence of thyroid autoantibodies
212
Q

Mx of subclin hypo?

A
  • TSH >10 -> levothyroxine
213
Q

What is an adrenal incentaloma?

A
  • Incidentaloma - mass found upon imaging
  • was not carried out for sus of adrenal disease
214
Q

Signs and symptoms of adrenal incidentaloma?

A
  • usually no typical findings
  • mild autonomous cortisol excess
215
Q

sig of an adrenal incidenataloma?

A
  • Have an increased incidence of metabolic disease like T2DM, HTN, osteoporosis, dyslipidemia
216
Q

Ix for an adrenal incidentaloma?

A
  • CT for diagnostic uncertainty on whether it’s a cancer
  • Urine metanephrines
  • > 4cm mass requires urgent assessment for malignancy
217
Q

Other Ix of adrenal incidentaloma?

A
  • Glucocorticoids - Dexamethasone suppression test
  • Urine and plasma metanephrines
218
Q

Mx of an adrenal incidentaloma?

A
  • Benign and no hormone excess -> no follow up
  • Clinically overt cortisol excess or aldosterone or catecholamines -> surgery?
219
Q

site of origin for a phaechromocytoma?

A
  • chromaffin cells of the adrenal medulla -> catecholamine hypersecretion
  • may also develop at extra-adrenal sites -> paraganlionomas
220
Q

Triad for phaechromocytoma?

A

episodic headache, diaphoresis, and tachycardia

221
Q

Diagnosis of phaechrocytoma?

A
  • Plasma or urinary fractioned metanephrines
  • Followed by CT/ MRI for localisation
222
Q

associations

Pathophys of Phaechromoytoma?

A
  • MEN11 association
  • Von Hippel Lindau syndrome
223
Q

CF of a phaechromocytoma?

A
  • can be bilateral or unilateral
  • episodic
  • HTN - v high
  • headaches
  • palpitations
  • anxiety
  • sweating
224
Q

Ix of a phaechromytoma - 1)

A
  • 24 hr urine metanephrines NOT catecholamines
225
Q

Other Ix for a phaechromocytoma?

A
  • CT/ MRI
  • Functional imaging modalities like MIBG scintigraphy or PET scans may be employed in cases of metastatic or extra-adrenal disease.
  • genetic testing e.g. VHL
226
Q

Mx of phaechromocytoma?

A
  • Surgery definitive
  • but medically stabilise with BB or alpha blocker like phenyoxybenzamine first - pre-op
227
Q

most common cause of primary hyperaldosteronism?

A
  • bilateral idiopathic adrenal hyperplasia causes most cases followed by adrenal adenomas
228
Q

Top 2 causes of primary hyperaldosteronism?

A

1) bilateral adrenal hyperplasia
2) Conns = adrenal adenoma

229
Q

CF of primary hyperalds?

A
  • HTN
  • hypokalaemia - e.g. muscle weakness
  • metabolic alkalosis
230
Q

When should Conns be suspected?

A
  • hypertension w hypokal
  • Tx resistant HTN
231
Q

First line Ix in primary hyperalds?

A
  • first line: plasma A/R ratio
  • should show high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone
232
Q

Other Ix for PHA?

A
  • High res CT abdo and adrenal vein sampling can be done to distinguish between unilateral and bilateral hyperplasia
233
Q

Secondary hyperaldosteronism is caused by?

A

caused by excessive renin stimulating the release of excessive aldosterone.

234
Q

SHA: Excessive renin is released due to disproportionately lower blood pressure in the kidneys, usually due to:

A
  • Renal artery stenosis
  • Heart failure
  • Liver cirrhosis and ascites
235
Q

Ix of Renal artery stenosis?

A
  • Renal artery stenosis (atherosclerosis of renal artery) is confirmed w Doppler US and CT angiogram oe MRA
236
Q

ARR result interpretation?

A
  • High aldosterone and low renin indicate primary hyperaldosteronism
  • High aldosterone and high renin indicate secondary hyperaldosteronism
237
Q

Mx of primary HA?

A
  • eplerenone and spironolactone - aldosterone antagonists
238
Q

who should we consider testing for hyperalds in?

A
  • Consider testing for hyperaldosteronism in patients with hypertension, who are younger, fail to respond to treatment or have a low potassium.
  • Be aware that potassium levels may be normal in hyperaldosteronism.
239
Q

Complication of immune checkpoint inhibitors?

A
  • Addisons is a complication of ICI
  • ACTH excess (lack of negative feedback)
  • T cells activated by ICIs may mistakenly recognize adrenal antigens as foreign and mount an immune response against them, leading to adrenal gland inflammation.
240
Q

CFs of addisons?

A
  • fatigue weakness and lethargy
  • hypotension - dizziness, fainintg, lightheadedness
  • Nausea, vomiting, abdo pain
  • Hyponatreamia
  • Hypoglycaemia - cortisol deficiency
241
Q

confirmation of addisons through…

A

synthacten

242
Q

hypophysitis is…

A
  • inflammation of PG -> inadequate production of one or more of the hormones secreted by the pituitary gland.
243
Q

most common cause of hypophysitis?

A
  • compression of the pituitary gland by non-secretory pituitary macroadenoma (most common)
244
Q

Pituitary causes of hypophysitis?

A
  • pituitary apoplexy
  • Sheehan’s syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage
  • hypothalamic tumours e.g. craniopharyngioma
245
Q

other causes of hypophysitis?

A
  • trauma
  • iatrogenic irradiation
  • infiltrative e.g. hemochromatosis, sarcoidosis
246
Q

Hypophysitis - low ACTH?

A
  • tiredness
  • postural hypotension
247
Q

Hypophysitis - low FSH/LH?

A
  • amenorrhoea
  • infertility
  • loss of libido
248
Q

Hypophysitis - low TSH?

A
  • feeling cold
  • constipation
249
Q

Hypophysitis - low GH?

A
  • if occurs during childhood then short stature
250
Q

Hypophysitis - low prolactin ->

A
  • problems with lactation
251
Q

Pituitary macroadenoma vs apoplexy?

A
  • pituriary macroadenoma → bitemporal hemianopia
  • pituitary apoplexy → sudden, severe headache
252
Q

Mx of hypophysitis?

A
  • replacement of deficient hormones
  • Tx of underlying cause - e.g. surgery for removal of tumour
253
Q

drugs causing hypopituitarism?

A
  • high dose steroids
  • Checkpoint Inhibitors
254
Q

med induced adrenal insufficiency?

A
  • Prolonged use of glucocorticoids or drugs that inhibit steroidogenesis (e.g., ketoconazole) can suppress the hypothalamic-pituitary-adrenal (HPA) axis, leading to adrenal atrophy and insufficiency.
255
Q

what can lead to adrenal haemorrhage -> adrenal insufficiency?

A
  • Trauma, anticoagulation, and sepsis can lead to adrenal haemorrhage, resulting in acute adrenal insufficiency.
256
Q

Physiological causes of hyperprolactinaemia?

A
  • stress
  • pregnancy
  • lactation
  • exercise
  • sexual intercourse
257
Q

Drugs causing hyperprolactinaemia?

A
  • AP
  • AD - SSRIs, MAO inhib, antienetics like domperidone and metoclopramide
258
Q

most common cause of pathological hyperprolactinomas?

A

prolactinomas

259
Q

hyperprolactinomas - compression of pituitary stalk?

A

Compression of pituitary stalk due to meningiomas, craniphrayngiomas, GH secreting adenomas -> acromegaly

260
Q

other causes of hyperprolactinomas?

A
  • CKD, cirrhosis, PCOS, hypothyroidism
261
Q

lab investigations of prolactinomas?

A
  • Serum prolactin: to confirm the diagnosis of hyperprolactinaemia
  • Pregnancy test: to exclude pregnancy, a common physiological cause of hyperprolactinaemia
  • Thyroid function tests: to identify hypothyroidism
  • Urea & electrolytes: to identify reduced renal function (chronic kidney disease)
  • Pituitary function testing: to assess pituitary function and possible hypopituitarism
262
Q

Ix of a prolactinomas?

A
  • type of pituitary adenoma
  • macroadeoma >1cm
  • hormonal status: a secretory/functioning adenoma produces and excess of a particular hormone and a non-secretory/functioning adenoma does not produce a hormone to excess
263
Q

Features of a prolactinoma - excess prolactin in women?

A

amenorrhoea
- infertility
- galactorrhoea
- osteoporosis

264
Q

Features of a prolactinoma - excess prolactin in men?

A
  • impotence
  • loss of libido
  • galactorrhoea
265
Q

Symptoms seen in a macroadenoma?

A
  • headache.
  • visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia)
  • symptoms and signs of hypopituitarism
266
Q

diagnosis of a pituitary adenoma?

267
Q

Medical management of a prolactinoma?

A
  • in the majority of cases, symptomatic patients are treated medically with dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland
268
Q

Surgical Mx of prolactinomas?

A
  • surgery is performed for patients who cannot tolerate or fail to respond to medical therapy.
  • A trans-sphenoidal approach is generally preferred unless there is a significant extra-pituitary extension
269
Q

Follow up for prolactinomas

A
  • Follow up every 6 -12 months
  • measurement of prolactin levels
  • visual fields
270
Q

Signs of non-functioning tumours of PG - mass effects?

A
  • headache
  • bilateral heminaopia
  • symptoms of hypopituitarism
271
Q

2 initial tests in DI?

A
  • 1) Water deprivation
  • 2) desmopressin
272
Q

Cranial DI vs nephrogenic DI?

A
  • cranial DI: increase conc of urine after desmopressin
  • Nephrogenic: no change following desmopressin
273
Q

sIADH ?

A
  • Increased release of ADH from PP
  • increases water reabs from the urine, causing dilution of the blood -> hyponatreamia
274
Q

DI vs siADH?

A
  • DI: hypernatreamia
  • siADH: hyponatraemia
275
Q

Pathophys of sIADH?

A
  • ADH produced in the hypothalamus and secreted the PP
  • ADH stimulates water reabs in CDs diluting blood
  • causes hyponatreamia
  • extra water doesn’t cause fluid overload so this is a euvolaemic hyponatreamia
276
Q

Urine osmolarity vs sodium?

A
  • high urine osmolarity
  • high urine sodium
277
Q

The symptoms of SIADH relate to low sodium (hyponatraemia). Depending on the sodium level and how rapidly it occurs, they may be asymptomatic or present with non-specific symptoms:

A
  • Headache
  • Fatigue
  • Muscle aches and cramps
  • Confusion
278
Q

Severe hyponatraemia- >

A

seziures and reduced consciousness

279
Q

causes of siADH?

A
  • pre-op after surgery - transphenoidal surgery
  • lung infection
  • subarachnoid haemorrhage
  • Meds - SSRI and carbamazepine
  • small cell lung cancer
  • HIV
280
Q

pre-op after surgery?

A

transsphenoidal surgery

281
Q

CFs of siADH?

A
  • Euvolaemia
  • Hyponatraemia
  • Low serum osmolality
  • High urine sodium
  • High urine osmolality
282
Q

Excluding other causes w siADH?

A
  • synacthen test
  • CKD
  • HF or liver disease
283
Q

Primary polydipsia?

A
  • primary polydipsia involves excessive water consumption.
  • Causes euvolaemic hyponatreamia but there is low urine sodium and low urine osmolality
284
Q

Mx of siADH?

A
  • Stop med and treat underlying infection
  • Fluid restrict
  • Vasopressin antagonists - tolvaptan
285
Q

why must sodium be corrected slowly?

A
  • It is essential to correct the sodium slowly to prevent osmotic demyelination. The sodium concentration should not change more than 10 mmol/L in 24 hours.
287
Q

hyponatreamia - fluid must be?

A

Patients should be fluid restricted, to increase serum sodium and correct the hyponatremia

Year 3 (45 decks)

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