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Year 5 notes > GI and endocrine > Flashcards

GI and endocrine Flashcards

1
Q

management of hypoglycaemia if conscious

A
  • initially 10-20g glucose PO either liquid/sugar lumps - can repeat after 10-15 minutes
  • then snack providing sustained carbohydrate given
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2
Q

management of hypoglycaemia if unconscious

A
  • community/can’t get access = IM glucagon

- 20% IV glucose - 10g

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3
Q

treatment of hypoglycaemic coma (follows profound hypo lasting >5 hours causing cerebral oedema)

A

IV mannitol and dexamethasone

with IV glucose and constant glucose monitoring to keep glucose level at 5-10mmol

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4
Q

criteria for diagnosing DKA

A
  • urine ketones ++ or in blood >3mmol/l
  • capillary blood glucose >11mmol/L or known T1DM
  • ABG - pH <7.3 or HCO3 <16mmol
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5
Q

drugs which can cause diabetes

A

steroids
antipsychotics
thiazides

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6
Q

steps 1, 2, 3 and 4 for T2DM drug management

A

1) if >48, metformin 500mg BD after food - if metformin not tolerated or CI: give gliptin or gliclazide or pioglitazone

2) if >58 16 weeks later: metformin + sulphonylurea (gliclazide 40mg OD) or pioglitazone or SGLT2 inhibitor
- if >58 6 months after use INSULIN

3) if >58 triple therapy:
- metformin + sitagliptin + gliclazide
- metformin + pioglitazone + gliclazide
- metformin + gliclazide + SGLT2 inhibitor

4) if not tolerated, side effects or contraindicated AND BMI >35
- metformin + gliclazide + GLP-1 mimetic

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7
Q

chief cause of death in diabetes

A

CVD - 75% have heart attack/stroke

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8
Q

how to check for diabetic nephropathy

A

check for microalbuminuria (ACR >3 but dipstick not positive for protein)

keep BP under control

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9
Q

when to avoid metformin

A

if eGFR <36

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10
Q

what procedures to stop metformin for

A

before GA or contrast containing iodine

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11
Q

diabetes drugs causing hypoglycaemia and weight gain

A

sulphonylureas - e.g. gliclazide

pioglitazone

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12
Q

which diabetes drug can cause fractures, fluid retention and increased LFTs

A

pioglitazone

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13
Q

which diabetes drug is contraindicated in CCF or osteoporosis

A

pioglitazone

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14
Q

diabetes drug increasing the risk of UTI/thrush

A

SGLT-2 inhibitors e.g. empaglifozin

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15
Q

what is Charcot’s arthropathy

A

diabetic foot injury:

osteoporosis, fracture, acute inflammation and disorganisation of architecture

usually presents as hot swollen foot after minor trauma

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16
Q

what is necrobiosis lipoidica

A

inflammatory condition where shiny, red-brown or yellow patches develop in the skin usually on the shins

associated with diabetes

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17
Q

what is the SINBAD system used for

A

to document severity of diabetic foot ulcer:

site, ischaemia, neuropathy, bacterial infection area and depth

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18
Q

antibiotic treatment for osteomyelitis (often in diabetic foot disease)

A

flucloxacillin +/- gentamicin/metronidazole for at least 7 days put o 6 weeks

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19
Q

annual screening for diabetic foot disease

A
  • palpating pulses

- 10g monofilament on sole of foot (neuropathy)

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20
Q

what do the antibodies do in graves

A

stimulate TSH receptor

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21
Q

what is acropachy

A

soft tissue swelling of hands and clubbing of fingers (periostitis)

in graves disease

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22
Q

complication of carbimazole

A

agranulocytosis - warn to come for FBC if sore throat

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23
Q

management of graves

A
  • BBs for rapid symptom control (or CCB)
  • carbimazole - usually euthyroid within 4-8 weeks
  • repeat TFTs monthly and alter dose according to T4 level
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24
Q

when is radioiodine for graves disease contraindicated

A

pregnancy
age <16
thyroid eye disease

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25
Q

causes of Addison’s disease

A
  • autoimmune (most common)
  • TB
  • metastases
  • HIV
  • APS
  • meningococcal septicaemia
  • secondary - pituitary disorders (tumours, irradiation, infiltration)
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26
Q

which endocrine disorder causes hypotension

A

ONLY Addison’s

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27
Q

electrolyte imbalances in Addison’s

A

hyponatraemia (in 90%)

hyperkalaemia

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28
Q

how does the short Synacthen test work

A

plasma cortisol measured before and 30 minutes after given 250mcg of Synacthen IM

should cause a rise in cortisol - in adrenal insufficiency this doesn’t occur

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29
Q

cortisol levels to investigate for Addison’s

A
  • <100 = urgent investigation

- 100-500 = refer to endocrinology

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30
Q

ACTH levels in primary insufficiency (Addison’s) vs secondary

A

primary/Addison’s = ACTH high

secondary = ACTH normal/low

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31
Q

management of adrenal crisis

A

high dose hydrocortisone and IV fluids (with dextrose if hypoglycaemic)

6 hourly hydrocortisone until patient stable

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32
Q

drugs which can cause hypothyroidism

A

lithium
amiodarone
carbimazole

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33
Q

secondary causes of hypothyroidism

A
  • pituitary failure

- associated with Down’s syndrome, Turner’s and coeliac disease

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34
Q

TFTs in primary vs secondary hypothyroidism

A
  • primary = increased TSH, low T4, low/normal T3

- secondary = low/normal TSH, low T4, low/normal T3

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35
Q

antibodies present in hypothyroidism (usually)

A

anti-TPO

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36
Q

when to lower dose of levothyroxine for hypothyroidism

A

elderly
ischaemic heart disease

NB: increase dose in pregnancy

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37
Q

when should TFTs be checked after changing dose of levothyroxine

A

after 8-12 weeks

goal is TSH 0.5-2.5

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38
Q

complications of levothyroxine

A
  • hyperthyroidism
  • AF
  • worsening of angina
  • reduced bone mineral density
  • interacts with iron and calcium carbonate - five at least 4 hours apart
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39
Q

most common cause of primary hyperparathyroidism

A

solidary adenoma

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40
Q

cause of secondary hyperparathyroidism

A

decreased vit D / chronic renal failure

= hypocalcaemia, leading to more PTH secreted = hyperplasia

serum calcium level will be low/normal but PTH will be high

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41
Q

treatment of secondary hyperparathyroidism

A

correcting underlying cause - vit D deficiency, renal failure

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42
Q

cause of tertiary hyperparathyroidism

A

when secondary continues for a long time - parathyroid hyperplasia = baseline PTH increases dramatically

when treating secondary and reduced need for increased PTH - PTH still high as it used to be producing large amounts = hypercalcaemia

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43
Q

characteristic XR finding of hyperparathyroidism

A

pepper pot skull

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44
Q

investigation results for hyperparathyroidism

A
  • raised calcium
  • LOW phosphate
  • PTH raised or normal (inappropriately given the raised calcium)
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45
Q

definitive management of primary and tertiary hyperparathyroidism

A

total parathyroidectomy

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46
Q

when can you do conservative management for hyperparathyroidism

A

if calcium <0.25 mmol/l above upper limit of normal

AND patient >50

AND no evidence of end organ damage

calcimimetic agents e.g. cinacalcet

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47
Q

complications post parathyroidectomy

A
  • hypocalcaemia

- recurrent laryngeal nerve injury

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48
Q

ECG findings in hypercalcaemia

A
  • bradycardia
  • short QT
  • wide T waves
  • prolonged PR
  • BBB
  • arrhythmia
  • HTN
  • arrest?
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49
Q

what is premature arcus senilis

A

white/grey opaque ring in corneal margin - sign of hyperlipidaemia

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50
Q

cholesterol level to refer for familial hyperlipidaemia

A

consider if >7.5

refer if >9 or LDL >7.5

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51
Q

primary prevention for hyperlipidaemia

A

if QRISK2 >10% or T1DM >40 or DM >10 years or CKD if eGFR <60

atorvastatin 20mg OD

if non-HDL hasn’t fallen by 40%+ then consider titrating up to 80mg

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52
Q

secondary prevention for hyperlipidaemia (known IHD/CVD/PAD)

A

atorvastatin 80mg OD

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53
Q

what is primary hypoparathyroidism

A

decreased PTH secretion e.g. secondary to thyroid surgery

LOW calcium, high phosphate, low/inappropriately normal PTH

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54
Q

treatment of hypoparathyroidism

A

alfacalcidol

diet rich in calcium and vit D

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55
Q

what is Trousseau’s sign

A

carpal spasm if brachial artery occluded by inflating BP cuff - sign of hypoparathyroidism

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56
Q

what is Chvostek’s sign

A

tapping over parotid causes facial muscles to twitch - sign of hypoparathyroidism

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57
Q

how is pseudohypoparathyroidism characterised

A

similar findings to hypoparathyroidism - but PTH is elevated due to PTH resistance

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58
Q

when to FNAC a thyroid nodule

A

any nodule ?1cm

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59
Q

any patient with thyroid lump + stridor =

A

same day referral - may be recurrent laryngeal nerve involvement

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60
Q

TFTs in a non toxic/simple goitre

A

normal - non-functioning nodules

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61
Q

what is Riedel’s

A

rare cause of hypothyroidism - dense fibrous tissue replacing normal thyroid parenchyma = hard, fixed painless goitre

associated with retroperitoneal fibrosis

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62
Q

when to give FFP in active bleeding

A

if fibrinogen level <1/litre

if PT/APTT >1.5 normal

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63
Q

when should endoscopy be offered in acute GI bleed

A

should be offered immediately after resuscitation in patients with severe bleed - all patients within 24 hours

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64
Q

what to do before endoscopy in ?varices

A

give terlipressin 2mg QDS before endoscopy - stop once haemostasis achieved

also give ciprofloxacin 200mg IV for 72 hours before

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65
Q

definitive management of oesophageal varices

A
  • band ligation

- transjugular intrahepatic portosystemic shunts (TIPS) if band ligation unsuccessful

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66
Q

type of laxative to use in opioid induced constipation and impaction

A

osmotic - Macrogol/movicol 1st line, lactulose 2nd line

add stimulant (Senna) if response inadequate

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67
Q

what is Beriberi

A

HF with general oedema or neuropathy - due to lack of B1 (thiamine)

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68
Q

what is pellagra

A

diarrhoea, dementia, dermatitis

due to lack of nicotinic acid (B6)

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69
Q

what is Kwashiokor

A

malnutrition due to severe deficiency of proteins/essential amino acids

can cause abdominal distension with fatty liver

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70
Q

investigation results in Kwashiokor

A
  • hypoalbuminaemia

- normo and microcytic anaemia

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71
Q

what is Marasmus

A

malnutrition due to severe energy (calories) deficiency

hypoalbuminaemia found

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72
Q

how should refeeding be started if at risk of refeeding syndrome

A

started at <50% energy requirements if eaten little/nothing for 5+ days - increase slowly over 4-7 days

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73
Q

drugs which can cause GORD

A
  • TCA
  • anticholinergics
  • nitrates
  • CCB
  • NSAIDs
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74
Q

when to do an upper GI endoscopy for GORD

A
  • > 55
  • symptoms >4 weeks/despite treatment t
  • dysphagia
  • relapsing symptoms
  • weight loss

If endoscopy is negative - do 24 hour oesophageal pH monitoring

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75
Q

how is oesophagitis graded on endoscopy

A

Savary-Miller grading (1-5 - 5 is Barrett’s)

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76
Q

management of endoscopically proven oesophagitis

A
  • full dose PPI for 1-2 months

- if no response - double dose PPI for 1 month

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77
Q

management of endoscopically negative oesophagitis

A
  • full dose PPI for 1 month

- if no response - H2 receptor antagonist or pro kinetic for 1 month

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78
Q

most common type of oesophageal carcinoma in UK

A

adenocarcinoma (most likely in GORD/Barrett’s)

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79
Q

what is bird beak sign

A

back up of food in oesophagus (in achalasia - where the LOS doesn’t open fully during swallowing)

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80
Q

most common type of hiatus hernia

A

sliding (GOJ moves above the diaphragm)

other type = rolling (GOJ remains below diaphragm and separate part of stomach herniates through oesophageal hiatus)

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81
Q

what is diagnostic of hiatus hernia on CXR

A

retrocardiac air-fluid level

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82
Q

pharmacological management of hiatus hernia

A

PPI (also H2 antagonists but less effective)

only do surgery if high doses of meds not helping (respiratory complications, risk of strangulation)

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83
Q

drugs which can cause a peptic ulcer

A
  • NSAIDs
  • SSRIs
  • corticosteroids
  • bisphosphonates
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84
Q

most common type of peptic ulcer

A

duodenal

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85
Q

when is endoscopy required for a peptic ulcer

A

IDA
weight loss
progressive dysphagia
epigastric mass

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86
Q

management of H. pylori negative peptic ulcer

A

PPIs until ulcer healed

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87
Q

management of H. pylori positive peptic ulcer

A
  • PPI + amoxicillin + clarithromycin OR

- PPI + metronidazole + clarithromycin

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88
Q

most common type of gastric carcinoma

A

> 90% adenocarcinoma

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89
Q

infection associated with gastric cancer

A

H. pylori

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90
Q

when to do 2 week referral for suspected gastric cancer

A

dyspepsia AND:

  • progressive dysphagia, persistent vomiting, IDA, epigastric mass etc
  • > 55 and unexplained persistent dyspepsia
  • dysphagia
  • unexplained upper abdo pain and weight loss
91
Q

management of proximal gastric carcinoma (5-10cm from OG junction)

A

subtotal gastrectomy

92
Q

management of gastric carcinoma if tumour <5cm from OG junction

A

total gastrectomy

93
Q

what is Trousseau sign

A

migratory thrombophlebitis - sign of pancreatic cancer

94
Q

endocrine tumours of the pancreas - by cell type and hormone secreted

A
  • Gastrinoma (G cells)
  • Glucagonoma (alpha cells)
  • Insulinoma (beta cells)
  • Somatostatinoma (gamma cells)
95
Q

genes associated with coeliac disease

A

HLA-DQ2 and HLA-DQ8

96
Q

duodenal biopsy findings in coeliac disease

A
  • villous atrophy
  • crypt hyperplasia
  • increase in intraepithelial lymphocytes
  • lamina propria infiltration with lymphocytes
97
Q

why are people with coeliac offered pneumococcal vaccine

A

may have functional hyposplenism

98
Q

drugs which can cause acute pancreatitis

A
  • mesalazine
  • azathioprine
  • NSAIDs
  • bendroflumethiazide
  • furosemide
  • sodium valproate
  • steroids
  • pentamidine
99
Q

indications of severe pancreatitis

A
  • hypocalcaemia, hyperglycaemia
  • hypoxia
  • neutrophilic
  • elevated LDH and AST
100
Q

what does a Glasgow Prognostic score of >3 suggest

A

severe acute pancreatitis

101
Q

what does an APACHE II score of >8 suggest

A

severe acute pancreatitis

102
Q

amylase level diagnostic of acute pancreatitis

A

3x normal

> 1000

103
Q

VACCINE mnemonic for acute pancreatitis management

A
  • Vital signs monitoring
  • Analgesia/abx (NOT morphine, don’t usually give abx)
  • Catheterise (due to potential for 3rd space losses)
  • IV access and fluids
  • NG tube
  • ERCP
  • Surgery if infection and necrosis
104
Q

when does spontaneous bacterial peritonitis occur

A

in patients with ascites secondary to chronic liver disease

105
Q

antibiotics to treat SBP

A

IV cefotaxime

106
Q

when to give antibiotic prophylaxis to patients with ascites (risk of SBP)

A
  • previous episode of SBP

- fluid protein <15g/L and Child-Pugh score 9+ (until ascites has resolved)

107
Q

location of femoral hernia (more common in women)

A

lateral and inferior to pubic tubercle (medial to femoral pulse)

108
Q

how quickly should femoral hernias be treated

A

within 2 weeks - due to high strangulation risk

109
Q

when would an umbilical hernia require repair

A

if >1.5cm or >4 years

110
Q

what may cause acalculous cholecystitis

A

seen in hospitalised and v ill patients - gallbladder stasis, hypo perfusion, infection

111
Q

pain management given in acute cholecystitis

A

usually parenteral morphine/pethidine

112
Q

definition of significant portal hypertension

A

hepatic venous pressure gradient of >=10mmHg

113
Q

pre-hepatic causes of portal HTN

A

blockage of portal vein before the liver:

  • congenital atresia/stenosis
  • portal vein thrombosis
  • splenic vein thrombosis
  • extrinsic compression - e.g. tumours
114
Q

hepatic causes of portal HTN

A
  • cirrhosis
  • chronic hepatitis
  • fibropolycystic disease
  • schistosomiasis
  • toxins
  • nodular
  • idiopathic
  • granulomata e.g. sarcoid
115
Q

post-hepatic causes of portal HTN

A
  • Budd-Chiari (hepatic vein obstruction)
  • constrictive pericarditis
  • right heart failure
  • veno-occlusive disease
116
Q

viruses (other than hep A-4) which can cause viral hepatitis

A

CMV, EBV, adenovirus, HSV

117
Q

common type of hepatitis in travellers

A

hep A (faeco-oral route)

118
Q

most common type of hepatitis worldwide

A

hep B (transmitted through body fluids/blood)

119
Q

how is hep C transmitted

A

via IVDU, haemodialysis, sexual contact, needle stick injuries, vertically

120
Q

what does hep D require to replicate

A

presence of hep B

121
Q

what does a fibroscan do

A

measures ‘stiffness’ of liver using 50-MHz wave from US probe - for liver cirrhosis

122
Q

who to do screening for liver cirrhosis

A
  • people with hep C
  • men drinking >50 units of alcohol a week
  • women drinking >35 units of alcohol a week
  • diagnosed with alcohol-related liver disease
123
Q

what can be given for pruritis in liver cirrhosis

A

colestyramine

124
Q

prevention of liver cirrhosis

A
  • immunisation against hep B

- sensible drinking

125
Q

investigation results in NAFLD

A

ALT>AST

126
Q

what is the ELF blood test

A

enhanced liver fibrosis test

127
Q

how much ascitic fluid needed to be detectable on clinical examination

A

> 1.5L

USS can detect >500ml

128
Q

types of hepatitis increasing risk of ascites

A

hep B/C

129
Q

management of ascites

A
  • treat cause
  • salt restriction to <90 mmol/day
  • diuretics (usually spironolactone)
  • paracentesis
  • prophylactic abx to reduce risk of SBP
  • transjugular intrahepatic portosystemic shunt (TIPS) if needing frequent paracentesis
130
Q

what does UC never spread beyond

A

ileocaecal valve (and continuous disease)

so basically never beyond large bowel

131
Q

endoscopy results in Crohn’s

A

deep ulcers, skip lesions, ‘cobblestone’ appearance

132
Q

endoscopy results in UC

A

widespread ulceration with preservation of adjacent mucosa

133
Q

type of IBD increasing the risk of colorectal cancer

A

UC (higher risk than Crohn’s)

134
Q

pANCA in Crohn’s vs UC

A

Crohn’s = negative

UC = positive

135
Q

what indicates bowel stricture in Crohn’s

A

small bowel enema - ‘Kantors string sign’ in terminal ileum

136
Q

drugs increasing the risk of diverticulae perforation

A

NSAIDs
opioids
steroids

therefore avoid these - give paracetamol for analgesia

137
Q

what is notorious for concealing colon cancer

A

diverticular disease

138
Q

presentation of acute diverticulitis

A
  • severe abdo pain in LLQ (may be RLQ in some asian patients)
  • N+V
  • change in bowel habit (constipaiton more common)
  • urinary sx (irritation of bladder)
  • PR bleeding?
  • tachycardia, low pyrexia
139
Q

treatment of acute diverticulitis

A
  • abx (metronidazole)

- fluids, liquid diet, analgesia

140
Q

Rosving’s sign

A

pain felt in the RIF on pressing over the LIF (appendicitis)

141
Q

Psoas sign

A

pain on extending hip if retrocaecal appendicitis

142
Q

Cope sign

A

pain on flexion and internal rotation of right hip if appendix is in close relation to obturator internus

143
Q

prophylactic abx to give in appendicitis to reduce post op infection

A

Metronidazole 500mg/8hr + cefuroxime 1.5g/8hr

144
Q

what might an ABG show in bowel obstruction

A

high lactate - ischaemia?

145
Q

what are haustra

A

transverse bands in large bowel - DON’T cross the full diameter of the bowel

146
Q

what are valvulae conniventes

A

transverse bands of small bowel - DO cross the full diameter of bowel

147
Q

3, 6, 9 rule

A
  • dilated small bowel = >3cm is abnormal
  • dilated large bowel = >6cm is abnormal
  • dilated caecum = >9cm is abnormal
148
Q

management of bowel obstruction is absence of signs of ischaemia/strangulation

A

drip and suck - NBM, insert NGT to decompress bowel

IV fluids and correct electrolyte disturbance

149
Q

when does bowel obstruction require urgent surgery

A
  • closed loop bowel obstruction/evidence of ischaemia
  • SBO with no surgical history
  • failure to improve within 48 hours of conservative measures
150
Q

what can paralytic ileus occur in association with

A
  • chest infection
  • MI
  • stroke
  • AKI
  • trauma
  • severe hypothyroidism
  • electrolyte disturbance
  • DKA
151
Q

congenital causes of colorectal carcinoma

A
  • HNPCC
  • FAP
  • Gardner’s syndrome
152
Q

screening for colorectal cancer

A
  • faecal occult blood tests (offered every 2 years to those aged 60-74)
  • sigmoidoscopy screening at 55, if normal, bowel screening at 60
  • FIT testing
153
Q

Duke’s staging for CRC

A
  • A = confined to bowel wall
  • B = invasion through bowel wall
  • C = LN involvement
  • D = distant mets
154
Q

type of CRC more likely to benefit from radiotherapy

A

rectal carcinoma

don’t usually give for colon cancer - due to toxicity of adjacent organs

155
Q

chemotherapy given in Dukes C CRC (LN involvement but no distant mets)

A

5-FU

156
Q

what is IBS-C

A

loose stools <25% of the time

constipation >25% of the time

157
Q

what is IBS-D

A

loose stools >25% of the time

hard stools <25% of the time

158
Q

what is IBS-M

A

both hard and soft stools >25% or the time

159
Q

diagnostic criteria for IBS

A 
6+ months 
diagnosed clinically if: 
- abdo pain relieved by defectation/or associated with bowel frequency/stool form AND at least 2 of: 
- altered passage of stool 
- abdo bloating 
- aggravated by eating 
- passage of mucus rectally
160
Q

grading I-IV of haemorrhoids

A

I = don’t prolapse
II = prolapse on straining, reduce spontaneously
III = prolapse on straining, can be reduced manually
- IV = permanently prolapsed, can’t be reduced

161
Q

when would haemorrhoids show pain

A

if thrombosed/ strangulated

162
Q

treatment of acutely thrombosed external haemorrhoids

A
  • if presents within 72 hours - consider referral for excision
  • otherwise give stool softeners, ice packs, analgesia - usually settles within 10 days

can develop skin tags

163
Q

most common form of anorectal abscess

A

peri-anal abscess - risk factors include IBD, DM (poor wound healing), underlying malignancy

164
Q

usual pathogens causing peri-anal abscess

A

colonised by gut flora e.g. E. coli

those caused by staph. aureus are more likely to be infection of skin rather than digestive tract

165
Q

gold standard investigation for peri-anal abscess

A

MRI - but rarely used except for complications/associated with IBD

usually is a clinical diagnosis - but can do transperineal USS

166
Q

when are abx used in peri-anal abscesses

A

if systemic upset secondary to abscess - don’t seem to help with healing of wound after drainage

may be used if diabetes/immunosuppression

167
Q

common complication of peri-anal abscess

A

fissure in ano (up to 30%) - reduced by early surgical drainage

168
Q

location of anal fissure

A

longitudinal or elliptical tears of the squamous lining of the distal anal canal (>6 weeks = chronic)

MOST COMMON on posterior midline

169
Q

what if an anal fissure is not on the posterior midline

A

consider underlying cause e.g. IBD

170
Q

acute vs chronic appearance of anal fissure

A
  • acute = clear edge, linear

- chronic = deeper, may be associated with external skin tag

171
Q

management of acute anal fissure (<6 weeks)

A
  • dietary
  • bulk forming laxatives - if not tolerated, try lactulose
  • lubricants e.g. petroleum jelly
  • topical anaesthetics, analgesia
172
Q

management of chronic anal fissure (>6 weeks)

A
  • continue management of acute
  • topical GTN first line (2x a day for up to 8 weeks)
  • if not effective after 8 weeks - consider secondary care referral
173
Q

when does sigmoid volvulus occur

A

in cases of long-standing chronic constipation - large sigmoid loop full of faeces and distended with gas twists on its mesenteric pedicle to create a closed-loop obstruction

174
Q

complications of sigmoid volvulus

A
  • bowel obstruction

- venous infarction = perforation and faecal peritonitis

175
Q

investigations to do in sigmoid volvulus

A
  • plain abdo XR (coffee bean sign)
  • may need barium enema
  • CT scan allows assessment of bowel wall ischaemia
176
Q

management of sigmoid volvulus

A
  • LL position
  • decompression - sigmoidoscope passed into rectum
  • need for surgical intervention if indication of ischaemia (sigmoidectomy with primary anastomosis)
177
Q

barium swallow - achalasia

A

bird’s beak sign

178
Q

management of achalasia

A
  • CCB/nitrates may reduce pressure in LOS (only effective in 10%)
  • heller myotome
  • pneumatic dilatation for older unfit patients
179
Q

most common cause of chronic pancreatitis

A

alcohol excess

can also be due to CF, haemochromatosis, ductal obstruction

180
Q

what is a subphrenic abscess

A

collection of infected fluid between diaphragm, liver and spleen - develops after surgery e.g. splenectomy

181
Q

antibiotics used in liver abscess (as well as drainage)

A

amoxicillin, ciprofloxacin and metronidazole

open surgery if ruptured/peritonitis/>5cm

182
Q

imaging used for hepatocellular carcinoma

A

CT/MRI

alpha fetoprotein usually elevated

avoid biopsy

183
Q

main risk factor for cholangiocarcinoma

A

primary sclerosing cholangitis

184
Q

tumour markers in cholangiocarcinoma

A

Ca19-9
CEA
Ca125

all often elevated

185
Q

what can be used to reduce ammonia in hepatic failure (which can cause encephalopathy)

A

lactulose

186
Q

what is an epigastric hernia

A

lump in midline between umbilicus and xiphisternum (in linea alba)

surgical repair is essential - high risk of strangulation/incarceration

187
Q

most common type of anal cancer

A

80% SCC

188
Q

risk factors for anal cancer

A
  • HIV
  • immunosuppression
  • cervical cancer
  • smoking
189
Q

usual cause of fistula-in-ano

A

when an abscess heals

can also be caused by Crohn’s, diverticulitis, surgery and cancer

190
Q

management of fistula-in-ano

A

Seton procedure (allows drainage to help fistula to heal)

fistulotomy etc.

191
Q

causes of hypopituitarism

A
  • most commonly = anterior pituitary tumours
  • infections - abscess, meningitis, encephalitis, TB
  • head injury
  • congenital
192
Q

presentation of hypopituitarism

A
  • asymptomatic
  • ACTH deficiency - Addison’s
  • TSH deficiency - hypothyroidism
  • gonadotrophin deficiency - oligomenorrhoea, loss of libido, dyspareunia, infertility, osteoporosis
  • GH deficiency - short stated, dyslipidaemia
  • ADH deficiency - polyuria, polydipsia, hypernatraemia
  • stroke-like symptoms
193
Q

acute pituitary failure symptoms

A

sudden onset headache, vomiting, visual impairment, decreased consciousness

194
Q

cause of acute pituitary failure

A

haemorrhage/infarction of pituitary

195
Q

management of acute pituitary failure

A

hydrocortisone replacement, surgery, resuscitation, IV fluids

196
Q

what is Sheehan’s syndrome

A

post partum pituitary necrosis - due to severe hypotension/shock during delivery

197
Q

what condition can a pituitary adenoma be associated with

A

MEN I

198
Q

conditions associated with phaeochromocytoma

A
  • MENII
  • neurofibromatosis
  • von Hippel-Lindau
199
Q

management of phaeochromocytoma

A

surgery - stabilise with alpha and beta blockers first

200
Q

what can cause pseudo-Cushing’s

A

alcohol excess/severe depression

causes false positive dexamethasone suppression test

201
Q

what is adrenal-genital syndrome

A

congenital adrenal hyperplasia - 95% 46XX with ambiguous genitalia

autosomal dominant

leading cause of pseudo-hermaphrodism

202
Q

how might someone with adreno-genital syndrome present when born

A

salt losing crisis at 7-14 days = vomiting, weight loss, extreme tiredness, severe dehydration

203
Q

most common cause of hyperaldosteronism

A

bilateral idiopathic adrenal hyperplasia

used to be thought to be due to adrenal adenoma (Conn’s syndrome)

204
Q

how does adreno-genital syndrome happen

A

low cortisol = anterior pituitary secretes lots of ACTH = production of adrenal androgens

205
Q

first line investigation in hyperaldosteronism

A

plasma aldosterone/renin ration

high aldosterone and low renin

206
Q

management of hyperaldosteronism

A
  • adrenal adenoma = surgery

- bilateral hyperplasia = aldosterone antagonism e.g. spironolactone

207
Q

what causes secondary hyperaldosteronism

A

excessive renin - e.g. from diuretics, HF, hepatic failure, nephrotic syndrome, malignant HTN

208
Q

causes of hypoaldosteronism

A
  • primary adrenal insufficiency
  • congenital adrenal hyperplasia
  • NSAIDs, heparin
  • ciclosporin
  • diabetic nephropathy
209
Q

electrolyte abnormalities in hypoaldosteronism

A
  • hyponatraemia (salt craving)
  • hyperkalaemia
  • metabolic acidosis
210
Q

investigations for hypoaldosteronism

A

measure plasma renin activity (PRA), serum aldosterone and serum cortisol

211
Q

drugs which can cause hirsutism

A
  • phenytoin

- corticosteorids

212
Q

topical treatment for hirsutism on the dace

A

topical eflornithine

213
Q

what is hypertrichosis

A

androgen-independent hair growth:

familial, phenytoin, ciclosporin, anorexia

214
Q

plasma osmolality and glucose in HHS

A

osmolality >320

glucose >30

215
Q

2 types of diabetes insipidus

A

cranial (not secreting enough ADH)

nephrogenic (insensitive to ADH

216
Q

causes of cranial DI

A
  • idiopathic
  • head injury
  • pituitary surgery
  • craniopharyngiomas
  • haemochromatosis
217
Q

causes of nephrogenic DI

A
  • genetic
  • hypercalcaemia/hypokalaemia
  • lithium
  • tubulointerstitial disease
218
Q

what urine osmolality excludes DI

A

> 700

because urine osmolality is LOW in DI (and plasma osmolality is high)

219
Q

how is nephrogenic DI managed

A

thiazides

low salt/protein diet

220
Q

why does SIADH feature hyponatraemia

A

secondary to dilutional effects of excessive water retention

221
Q

cancers causing SIADH

A

SCLC

pancreatic

222
Q

neurological causes of SIADH

A

stroke
SAH
subdural haemorrhage
meningitis/ encephalitis / abscess

223
Q

infectious causes of SIADH

A

TB

pneumonia

224
Q

drugs which can cause SIADH

A 
sulfonylreas
SSRIs
TCAs
carbamazepine
vincristine
cyclophosphamide

Year 5 notes (10 decks)

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