Gastro + Endo + Nephro Flashcards
H pylori post eradication therapy
Consider retest if:
- poor compliance to eradication therapy
- Aspirin or NSAID is indicated
- FHx of gastric malignancy
- The person requests re-testing
They advise that re-testing should ideally be done 8 weeks after initial eradication therapy and the carbon-13 urea breath test should be used first-line.
GI bleed scoring system
blatchford bleeding risk
rockall rebleeding risk
1st-3rd line therapy c diff
first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy: oral vancomycin +/- IV metronidazole
C peptide and type 1 vs type 2 diabetes?
C peptides raised in type 2
Prolactinoma treatment
Dopamine agonist (e.g cabergoline, bromocriptine)
surgery if fail to respond
acromegaly and elevated IGF-1 (insulin growth factor) investigations
OGTT and serial GH levels
acromegaly how to diagnose
1st = serum IGF-1
2nd= OGTT+ serial GH
in normal patients if hyperglycaemic then GH reduced, but in acromegaly GH still high
what marker monitors disease In acromegaly
IGF-1
crushing syndrome metabolic disturbance
hypokalaemia metabolic alkalosis
Bicarbonate resorption is increased in the tubules with potassium depletion causing metabolic alkalosis.
Gynaecomastia causes: drugs
spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids
Treatment for galactorrhoea
bromocriptine (dopamine agonist)
how do thiazides impact Ca level
HYPERcalacemia
what is subclinical hypothyroid
TSH above range but normal thyroxine
Subclinical hypothyroidism with TSH level of level is 5.5 - 10mU/L: offer patients < 65 years a 6-month trial of thyroxine if TSH remains at that level on 2 separate occasions 3 months apart and they have hypothyroidism symptoms
what medication interacts with thyroxine absorption
iron
Kallman’s syndrome hormone level
low LH & FSH and testosterone (failure of GnRH secreting neurones in hypothalamus)
Kallman = Fallman
Poor Kall the man cannot smell
chromosome = X linked drecessive
Klinefelter Sx
High FSH and high LH. But low testosterone. Tall, no secondary sexual characteristics. Small firm testes + gynecomastia.
Addisons and hyperpigmentation
primary Addison’s is associated with hyperpigmentation whereas secondary adrenal insufficiency is not
secondary causes= tumours, irradiation, infiltration, exogenous steroids
Diabetes-specific autoantiboits T2DM vs T1DM
in type 1 C peptide LOW but others present
OGTT test: IMPAIRED glucose tolerance
Fasting plasma glucose < 7.0 mmol/l
OGTT 2-hour value: 7.8 to 11.1 mmol/l
drug causes raised prolactin (and –> galacctoreoa)
metoclopramide, domperidone
phenothiazines
haloperidol
very rare: SSRIs, opioids
non drug causes raised prolactin
prolactinoma
pregnancy
oestrogens
physiological: stress, exercise, sleep
acromegaly: 1/3 of patients
polycystic ovarian syndrome
primary hypothyroidism (due to thyrotrophin releasing hormone (TRH) stimulating prolactin release)
T1DM with bloating, vomiting and erratic CGMs? what med to try
metoclopramide
tender goitre, hyperthyroidism and raised ESR. The globally reduced uptake on technetium thyroid scan is also typical
Sub acute (De Quervains) thyroiditis
diabetes medicaition and BMI>35 - what to consider?
GLP-1 (e.g. exenatide)
FOR SPECIALSITS ONLY
GLP-1 receptor agonists should only be continued if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months.
Who avoids SGLT-2?
FOOT ULCER
should be avoided in active foot disease (such as skin ulceration, osteomyelitis, or gangrene) due to the possible increased risk of lower limb amputation (mainly toes).
T2DM triple therapy not worked.. what to do?
if a triple combination of drugs has failed to reduce HbA1c then switching one of the drugs for a GLP-1 mimetic is recommended, particularly if the BMI > 35
most common cause of cushings SYDNROME
pituitary adeoma (aka cushings DISEASE) - ACTH
Thiazolinediones - what is the the side effects?
e.g. Pioglitazone
T2DM medication
weight gain
liver impairment
fluid retention –. CONTRAINDICATED in hearty failure
increased fractures
bladder cancer
which diabetic meds cause weight gain
gliclazide and prioglitazone
thyrotoxicosis with tender goitre
de Quervains thyroiditis
Addisons and vomiting
take IM hydrocortisone until vomiting stops
hypoglycaemia - what two things to measure to investigate cause? (2)
What does this show? (2)
Serum insulin and C-peptite
Insulin HIGH C peptide HIGH = endogenous insulin production (insulinoma/ sulfonylrea)
Insulin HIGH C peptide LOW = exogenous (added too much)
Insulin Low C peptide LOW = non inulin cause e.g. alcohol, critical illness, adrenal insufficient, GH deficiency, fasting/ starvation
a HbAlc value of less than 48 mmol/mol (6.5%)
does not exclude diabetes (i.e. it is not as sensitive as fasting samples for detecting diabetes) –> consider fasting glucose sample
T4 vs T3
T4 is the synthetic form
raised ESR
AUTOIMMUNE CONDITIONS e.g. hashimotos thyroiditis
Addisons - high or low aldosteronism
PRIMARY HYPOaldosteronism
hypercalacemia- two most common causes
malignancy and PTH
-> PTH best test for confimin diagnosis
e.g. if PTH raised or normal = Primary hyperparathyroidism
PTHrP tumour
squamous cell lung cancer
how do sulfonyluyrea work
bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells
–> insulin release
(hence why you get weight gain)
Crohns:
how to induce remission (3)
fistulating disease (1)
peri-anal disease (1)
what diet? (1)
1st line - glucocorticoids (budesonide as alternative)
THEN
2nd line - 5-ASA drugs (e.g. mesalazine)
3rd line= azathioprine or mercaptopurine as add on
fistulating/ reflractory= inflixamab
peri-anal disease= metronidazole
diet= enteral feeding with an elemental diet may be used in addition to or instead of other measures to induce remission, particularly if there is concern regarding the side-effects of steroids (for example in young children)
Crohns:
maintaining remission? (1)
smoking: what to do? (1)
perianal disease (3)
azathioprine or mercatopurine
stop smoking
peri-anal disease: MRI
metronidazole
anti-TNF (infliximab)
draining seton for complex
Crohns:
common complications (3)
small bowel cancer
colorectal cancer
osteoporosis
Diarrhoea:
acid-base balance seen on arterial blood gas?
Normal anion gap metabolic acidosis
diarrhoea= loose bicarbonate = loose alkaloid ions = blood is acidotic
It is a normal anion gap as acidosis is not a result of acidotic ion production, such as lactate, ketosis, or salicylate acid.
Causes of anion gap metabolic acidosis
lactate (shock, sepsis, hypoxia)
ketones: diabetic ketoacidosis
alcohol
urate: renal failure
acid poisoning: salicylates, methanol
Iron studies:
how to tell difference between deficiency anaemia vs. anaemia of chronic disease (1)
TIBC is high in IDA, and low/normal in anaemia of chronic disease
ACD:
normochromic/hypochromic, normocytic anaemia
reduced serum and TIBC
normal or raised ferritin
- TIBC measures the number of binding sites on transferrin available for iron. It therefore also increases in ID and decreases in ACD.
Transferrin: how does it change in iron deficiency
- Transferrin is the body’s carrier of iron around the blood. In states of iron deficiency, transferrin increases as the body tries to ‘make the most’ of what iron it has left, meaning that transferrin levels go up.
- Anaemia of chronic disease is the body’s physiological response to a danger, such as a potentially harmful pathogen. Like humans, pathogens require iron for metabolism and survival. Therefore, in ACD, the body reduces iron available for pathogens by circulating less around the blood. This means that transferrin decreases.
- TIBC measures the number of binding sites on transferrin available for iron. It therefore also increases in ID and decreases in ACD.
Iron studies:
when is ferritin high/low? (2)
high= inflammatory disorders
low= IDA
Which Abx causes C diff? (1)
what other drug linked to it? (1)
Clindamycin
PPI !
C diff:
distinguishing features for severe/ life threatening? (2)
severe:
increased WCC, temperature
life threatening:
hypotension, partial/complete ileus, toxic megacolon
C diff:
diagnosis (1)
is made by detecting C. difficile toxin (CDT) in the stool
C. difficile antigen positivity only shows exposure to the bacteria, rather than current infection
C diff: 1st/2nd/3rd management (3)
if recurrent (2)
life-threatening (1)
first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy: oral vancomycin +/- IV metronidazole
Recurrent episode
recurrent infection occurs in around 20% of patients, increasing to 50% after their second episode
within 12 weeks of symptom resolution: oral fidaxomicin
after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin
Life-threatening C. difficile infection
oral vancomycin AND IV metronidazole
specialist advice - surgery may be considered
flushing, diarrhoea, bronchospasm, hypotension, and weight loss.
carcinoid tumor
5-HIAA (the tumor will serete serotonin)
usually occurs when metastases are present in the liver and release serotonin into the systemic circulation
may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver
Coagulopathy:
all clotting factors are low except for factor VIII. Both PT and APTT prolonged.
liver failure
Coagulopathy:
VIII low only (1)
IX low only (1)
Haemophilia A
Haemophilia B
Diabsts insipidus: causes
either ADH decreased secretion from pituitary OR insensitivity to ADH
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis
Pernicious anaemia:
which Vitamin? (1)
other causes of deficiency (3)
diagnosis (1)
B12
Other causes include atrophic gastritis (e.g. secondary to H. pylori infection), gastrectomy, malnutrition (e.g. alcoholism)
Anti intrinsic factor antibodies
Pernicious anemaia: feature
anaemia features
lethargy
pallor
dyspnoea
neurological features
peripheral neuropathy: ‘pins and needles’, numbness. Typically symmetrical and affects the legs more than the arms
subacute combined degeneration of the spinal cord: progressive weakness, ataxia and paresthesias that may progress to spasticity and paraplegia
neuropsychiatric features: memory loss, poor concentration, confusion, depression, irritabiltiy
other features
mild jaundice: combined with pallor results in a ‘lemon tinge’
atrophic glossitis → sore tongue
Pernicious anaemia management
Management
vitamin B12 replacement
usually given intramuscularly
no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections
more frequent doses are given for patients with neurological features
there is some evidence that oral vitamin B12 may be effective for providing maintenance levels of vitamin B12 but it is not yet common practice
folic acid supplementation may also be required
A BMI >30 kg/m², increased hepatic echogenicity on liver ultrasound, and an ALT:AST ratio >2
NAFLD
Barretts:
management
high-dose proton pump inhibitor
whilst this is commonly used in patients with Barrett’s the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited
endoscopic surveillance with biopsies
for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
if dysplasia of any grade is identified endoscopic intervention is offered. Options include:
radiofrequency ablation: preferred first-line treatment, particularly for low-grade dysplasia
endoscopic mucosal resection
Haemochromatosis:
how inherited?
how to monitor (1)
why is serum iron useless (1)
Autosomal recessive
Ferritin and transferrin saturation
ferritin is a measure of total iron stores, and transferrin saturation also measures how much serum iron is bound to proteins in the blood.
Similarly, serum iron fluctuates throughout the day and is based on diet. Furthermore, it is likely to fluctuate significantly with regular phlebotomies.
CKD on haemodialysis:
most likely cause of death (1)
causes (5)
IHD
diabetes
chronic glomerulonephritis
chronic pyelonephritis
HTN
adult PCKD
Granulomas: Crohns vs UC
Crohns
Pseudopolyps: Crohns vs UC
UC
Skip lesions: Crohns vs UC
Crohns
Goblet cells + granulomas: Crohns vs US
Crohns
Primary sclerosing cholangitis more common: C vs UC
UC
Gallstones are more common secondary to reduced bile acid reabsorption
Oxalate renal stones*: Crohns Vs UC
CrohnsWidespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
Widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
UC
Radiology results UC vs Crohns
Crohns: Small bowel enema
high sensitivity and specificity for examination of the terminal ileum
strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae
UC: loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’
Mild/ moderate/ severe UC: diarrhoea
mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
UC: mild-moderate disease
how to induce remission
1st LINE: RECTAL +/- LEFT SIDED
topical (rectal) aminosalicylate
if remission not achieved in 4 weeks add oral
if still not achieved add steroids oral
1st LINE: EXTENSIVE (RIGHT SIDED)
topical (rectal) and high dose oral aminosalicylate
UC: severe disease remission
HOSPITAL for IV steroids 1st line
UC: maintenance
aminosalicylate
Following a severe relapse or >=2 exacerbations in the past year
oral azathioprine or oral mercaptopurine
Other points
methotrexate is not recommended for the management of UC (in contrast to Crohn’s disease)
there is some evidence that probiotics may prevent relapse in patients with mild to moderate disease
Diagnosis of non-alcoholic fatty liver diseases
Enhanced liver fibrosis blood test
H pylori test:
when to stop meds before urea breath test
4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)
peritonitis post dialysis organism
Staphylococcus epidermidis.
UC most common site
rectum
triad of normocytic anaemia, thrombocytopenia and acute kidney injury.
Haemolytic uraemia syndrome
HUS most common cause (what bacteria) (1)
treatment (1)
E coli
supporitive (no Abx)
cancer Sx in coeliac disease
enteropathy-associated T cell lymphoma (EATL),
acute interstitial nephritis:
features? (1)
causes (4)
ffeawtures (4)
Acute interstitial nephritis causes an ‘allergic’ type picture consisting usually of raised urinary WCC and eosinophils, alongside impaired renal function
Classically urine shows elevated white cell counts and eosinophils. IgE is also often elevated.
drugs: the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci
Features
fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension
Acute interstitial nephritis
histology (1)
investigations (2)
histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules
Investigations
sterile pyuria
white cell casts
CKD stage 1 and 2 diagnosis needs..
Some Sx/ features other than low eGFR
Oesophageal bleeding:
prophylaxis? (1)
acute management drug (1)
NS BB e.g. propranolol
Terlipressin is a vasopressin analogue that is indicated in the acute management of variceal bleeding.
(+ prophylactic Abx)
primary biliary cholangitis: Management (1)
associations (4)
urideoxycholic acid
(cholestyramine for the itch)
liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
Associations
Sjogren’s syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease
primary biliary cholagitis:
features (5)
early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
around 10% of patients have right upper quadrant pain
xanthelasmas, xanthomata
also: clubbing, hepatosplenomegaly
late: may progress to liver failure
primary biliary cholangitis: complications (3)
Complications
cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)
Coeliac disese: WHAT biopsy?
JEJUNAL biopsy
Liver Hepatitis bloods
HBsAg = ongoing infection, either acute or chronic if present > 6 months
anti-HBc = caught, i.e. negative if immunized
Hepatic encepalopathy:
grading (4)
precipitating factors (5)
management (2)
Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma
infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)
1st= lactulose
2nd= Abx e.g. rifaximin
other options = protosystemic shunts/ liver transplant
Size of kidneys: CKD in diabetes?
AKI vs CKD?
other features differentiating CKD and AKI? (1)
Chronic diabetic nephropathy will have large/normal sized kidneys on ultrasound whereas most patients with chronic kidney disease have bilateral small kidneys
One of the best ways to differentiate between acute kidney injury (AKI) and chronic kidney disease (CKD) is renal ultrasound - most patients with CKD have bilateral small kidneys. Exceptions to this rule include:
autosomal dominant polycystic kidney disease
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy
HYPOcalceamia = due to vit D = CKD
visible haematuria following a recent URTI
IgA nephropathy (Bergers disease)
Associated conditions
alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura
IgA nephropathy and post-streptococcal glomerulonephritis
time difference?
protein and haematuria?
IgA= 1-2 days after URTI, PSGN= 1-2 weeks after
IgA= haematuria, PSGN= proteiuira AND haematuria
IgA= macroscopic haematuia, PSGN= low complement
Cholestatis +/ hepatitis: which drugs cause it?
combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine
which drugs cause liver cirrhosis
methotrexate
methyldopa
amiodarone
SBP:
most common organism? (1)
how to diagnose (1)
treatment (1)
prohplayxis? 91)
E coli
paracentesis (neutrophils >250)
IV cefotaxime
ABX : patients who have had an episode of SBP
patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’
Primary biliary cholangitis - what rule
the M rule
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females
dyspepsia, abdominal pain, nausea and anorexia
Early symptoms of stomach cancer include:
All patients who’ve got an upper abdominal mass consistent with stomach cancer
Patients aged >= 55 years who’ve got weight loss, AND any of the following:
upper abdominal pain
reflux
dyspepsia
Non-urgent
Patients with haematemesis
Patients aged >= 55 years who’ve got:
treatment-resistant dyspepsia or
upper abdominal pain with low haemoglobin levels or
raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
Managing patients who do not meet referral criteria (‘undiagnosed dyspepsia’)
This can be summarised at a step-wise approach
1. Review medications for possible causes of dyspepsia
2. Lifestyle advice
3. Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori
if symptoms persist after either of the above approaches then the alternative approach should be tried
Testing for H. pylori infection
initial diagnosis: NICE recommend using a carbon-13 urea breath test or a stool antigen test, or laboratory-based serology ‘where its performance has been locally validated’
test of cure:
there is no need to check for H. pylori eradication if symptoms have resolved following test and treat
however, if repeat testing is required then a carbon-13 urea breath test should be used
live screening for hepatocellular carcinoma is for who
Screening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:
patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
men with liver cirrhosis secondary to alcohol
Risk factors for HCC
alpha-1 antitrypsin deficiency
hereditary tyrosinosis
glycogen storage disease
aflatoxin
drugs: oral contraceptive pill, anabolic steroids
porphyria cutanea tarda
male sex
diabetes mellitus, metabolic syndrome
diagnosis post-streptococcal glomerulonephritis
raised anti-streptolysin O titre
most common nephrotic syndrome in kids
minimal change disease
(IgA nephropathy and post streptococcal glomerulonephritis are nephrITICs syndrome)
abdominal pain, arthritis, haematuria and a purpuric rash over the buttocks and extensor surfaces of arms and legs
HSP
The risk of which one of the following cancers is he most at risk of following renal transplantation?
squamous cell carcinoma
Rhabdomyolysis:
features - electrolytes? (3)
acute kidney injury with disproportionately raised creatinine
elevated creatine kinase (CK)
the CK is significantly elevated, at least 5 times the upper limit of normal
elevations of CK that are ‘only’ 2-4 times that of normal are not supportive of a diagnosis and suggest another underlying pathophysiology
myoglobinuria: dark or reddish-brown colour
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia (may develop before renal failure)
metabolic acidosis
Rhabdomyolysis
management (1)
IV fluids to maintain good urine output
urinary alkalinization is sometimes used
Triad: haematuria, loin pain, abdominal mass
renal cell carcinoma
Renal cell carincoma:
features
classical triad: haematuria, loin pain, abdominal mass
pyrexia of unknown origin
left varicocele (due to occlusion of left testicular vein)
endocrine effects: may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH
25% have metastases at presentation
young person, dysuria. Treated for UTI already. Urine dipstick is positive for blood + and leucocytes +. A MSSU shows no organism.
chlamydia
Hypokalaemia:
management if <2.5? (1)
management if 2.5-3.4? (1)
The infusion rate should not exceed 20mmol/hr. In this case, 3 bags of 0.9% Saline with 40mmol KCL
IV +/- oral replacement
U waves
T wave flattening
ST segment changes
hypokalaemia
Glucose requirement when prescribing fluids
50-100g /day irrespective of weight
0.9% salie- if large volumes used then concerns RE….
hyperCHLORAEMIC metabolic acidosis
how to calculate anion gap
(sodium + potassium) - (bicarbonate + chloride)
loss of P waves
broad QRS complexes
sinusoidal wave pattern
(and tented T waves)
HYPERkalaemia
Diagnosis of AKI:
Creatine % (1) and amount (1)
urine output (1)
↑ creatinine > 26µmol/L in 48 hours
↑ creatinine > 50% in 7 days
↓ urine output < 0.5ml/kg/hr for more than 6 hours
AKI: when to refer? (10)
Renal tranplant
ITU patient with unknown cause of AKI
Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
AKI with no known cause
Inadequate response to treatment
Complications of AKI
Stage 3 AKI (see guideline for details)
CKD stage 4 or 5
Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
AKI:
when stage 2 and 3?
doubles (2x), its stage 2. If it triples (3x), its stage 3
Additionally, a patient is deemed in stage 3 AKI if they are commenced on renal replacement therapy irrespective of creatinine or urine production.
tachycardia, fatigue, pallor and an aortic flow murmur.
anaemia
(murmur due to increased blood flow through the valves/ chambers –> turbulence –> soft murmur)
SBP:
Abx management? (1)
who gets it? (1)
ciprofloxacin IF protein concentration <=15 g/L
with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’
Alcoholic liver disease is a marker of poor prognosis in SBP.
Metabolic ketoacidosis with normal or low glucose
Alcohol ketoacidosis
Haemochromatosis:
how to monitor treatment? (2)
transferrin saturation + serum ferritin
Transferrin saturation measures the amount of iron bound to a protein (transferrin) in the blood. This is the first marker to rise in haemochromatosis and levels above 45% are considered too high.
‘double duct’ sign on MRCP
pancreatic cancer
Achalasia:
management (1)
pneumatic (balloon) dilation
surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
Hepatitis:
IgG vs IgM
IgM: Mmmm, yeah you’re infected
IgG: Golly, it’s chronic (G looks like C so chronic)
HBsAg = ongoing infection, either acute or chronic if present > 6 months
anti-HBc = caught, i.e. negative if immunized
Crohns - most common site affected
ileum
watery travellers diarrhoea
E coli
Bile acid malabsopriton management (1)
cholestyamine
Creon
replace pancreatic enzymes, for example in cystic fibrosis where there is a reduction in pancreatic enzymes reaching the intestine.
most common extra-intestinal feature in both Crohn’s and UC
arthritis
Melanosis coli
laxative abuse
numerous hamartomatous polyps in the GI tract and pigmented freckles on lips/ face/ palms/ soles
Peutz-Jeghers syndrome
Oesophageal cancer: SCC vs adenocarcinoma
location? (1)
risk factors adenocarinoma (4)
risk factors SCC? (5)
lower 1/3 = adenocinoma
GORD
barretts
smoking
obesity
smoking
alcoohl
achalasia
Plummer vinson syndrome
nitrosamine rich diet
Crohns:
with extra-intestinal Sx related to disease activity
erythema nodosum
Which TB therapy causes B6 deficiency
Isoniazid
IBS: laxative
isphagula husk (bulk forming)
High ferritin:
what to look at first in iron studies (1)
TRANSFERRIN= if normal then you know it’s without iron overload
IF NORMAL –>
inflammation,
alcohol excess
liver disease
CKD
malignancy
IF HIGH–
primary iron overload (hereditary haemochromatosis)
secondary iron overload (transfusions)
ferritin is reduced in iron deficiency anaemia
diarrhoea, floating stool greasy, swimming pools
Giardia lamblia
A 76-year-old woman presents with abdominal pain, distension and vomiting. She recently had an episode of acute cholecystitis and is awaiting a cholecystectomy. She feels her symptoms have returned over the past few days. On examination her abdomen is distended.
gallstone ileus
Persistent biliary colic symptoms, associated with anorexia, jaundice and weight loss. A palpable mass in the right upper quadrant (Courvoisier sign), periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
cholangiocarcinoma
Typical symptoms are malaise, anorexia and weight loss. The associated RUQ pain tends to be mild and jaundice is uncommon.
amoebic liver abscess
A 72-year-old man is admitted with an episode of brisk haematemesis. Following resuscitation an upper GI endoscopy is performed and a prominent blood vessel is identified in the mucosa approximately 6 cm from the O-G junction on the lesser curve of the stomach.
dieulafoy lesion
These small arterial lesions are a rare cause of bleeding and are characterised by a single large tortuous arteriole in the sub mucosa. Extra gastric lesions may occur.
Usually haematemesis and epigastric discomfort. Usually, there is an underlying cause such as recent NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise
diffuse erosive gastritis
Glasgow-Blatchford
outpatient vs not for UGI bleed
Rockhall
AFTER endoscopy - risk of Rebleed and mortality
includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage
AST/ALT ration 2:1
Alcohol hepatitis
When to give IV fresh frozen plasma
either a fibrinogen level of less than 1 g/litre or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal.
Typical symptoms are malaise, anorexia and weight loss. The associated RUQ pain tends to be mild and jaundice is uncommon.
amoebic liver disease
Common symptoms include:
nausea and vomiting, anorexia
myalgia
lethargy
right upper quadrant (RUQ) pain
forge in travel/ IVDU
viral hepatitis
The liver only usually causes pain if stretched. One common way this can occur is as a consequence of congestive heart failure. In severe cases cirrhosis may occur.
congestive hepatomegaly
RUQ pain, intermittent, usually begins abruptly and subsides gradually. Attacks often occur after eating. Nausea is common.
It is sometimes taught that patients are female, forties, fat and fair although this is obviously a generalisation.
biliar colic
acute cholecystitis
Pain similar to biliary colic but more severe and persistent. The pain may radiate to the back or right shoulder.
The patient may be pyrexial and Murphy’s sign positive (arrest of inspiration on palpation of the RUQ)
Persistent biliary colic symptoms, associated with anorexia, jaundice and weight loss. A palpable mass in the right upper quadrant (Courvoisier sign), periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
cholangiocarcinoma
Usually due to alcohol or gallstones
Severe epigastric pain
Vomiting is common
Examination may reveal tenderness, ileus and low-grade fever
Periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare
pancreatitis acute
The main symptoms are severe nausea and vomiting which can last from a few hours to a few days, occurring in discrete episodes. There is also an association with migraine as can be seen in this case. Reduced appetite and weight loss can occur.
cyclical vomiting syndrome
Painless jaundice is the classical presentation of pancreatic cancer. However pain is actually a relatively common presenting symptom of pancreatic cancer. Anorexia and weight loss are common
pancreatic cancer
Cyclical vomiting syndrome:
management (3)
Avoidance of triggers
Prophylactic treatments include amitriptyline, propranolol and topiramate.
Ondansetron, prochlorperazine and triptans in acute episodes.
ALP vs ALT in:
hepatocellular disease
cholestatic disease
mixed disease
hepatocellular: ALT/ALP 5+ (high ALT)
cholestatic: ALT/ALP <2
mixed disease; ALT/ALP 2-5
There may be a history of heartburn
Odynophagia but no weight loss and systemically well
oesophagi’s
A 46-year-old man presents to the emergency department complaining of 3 days of watery diarrhoea which is occasionally bloody. On further questioning, he reveals cramping abdominal pain over the same period. He has dry mucous membranes and a prolonged capillary refill. Five days ago, he was started on a new medication by his GP.
Clindamycin ( C diff)
Dysphagia_ There may be a history of HIV or other risk factors such as steroid inhaler use
oesophageal candidacies
Dysphagia of both liquids and solids from the start
Heartburn
Regurgitation of food - may lead to cough, aspiration pneumonia etc
achalasia
Other features of CREST syndrome may be present, namely Calcinosis, Raynaud’s phenomenon, oEsophageal dysmotility, Sclerodactyly, Telangiectasia
As well as oesophageal dysmotility the lower oesophageal sphincter (LES) pressure is decreased. This contrasts to achalasia where the LES pressure is increased
systematic sclerosis
Other symptoms may include extraocular muscle weakness or ptosis
Dysphagia with liquids as well as solids
myasthenia travis
Acute liver failure in paracetamol overdose- what measure
PT
ALT 1465 iu/L is incorrect. Whilst ALT is a good measure of hepatotoxicity in paracetamol poisoning, it is not a measure of synthetic function so is an inferior test for assessing acute liver failure.
Scleroderma + low ferritin, Vita B and folate + diarrhoea
malabsorption syndrome
the underlying diagnosis of scleroderma which can cause small intestinal bacterial overgrowth (SIBO) leading to malabsorption.
A combination of liver and neurological disease points towards …..
Wilsons disease
Wilsons disease:
features
liver: hepatitis, cirrhosis
neurological:
basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism
Kayser-Fleischer rings
green-brown rings in the periphery of the iris
due to copper accumulation in Descemet membrane
present in around 50% of patients with isolated hepatic Wilson’s disease and 90% who have neurological involvement
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
How is Wilsons disease:
investigated (4)
diagnosed (1)
slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
free (non-ceruloplasmin-bound) serum copper is increased
increased 24hr urinary copper excretion
the diagnosis is confirmed by genetic analysis of the ATP7B gene
Management Wilsons disease
penicillamine (chelates copper) has been the traditional first-line treatment
trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
tetrathiomolybdate is a newer agent that is currently under investigation
crohns 1st line remission
azathioprine or mercaptopurine is used first-line to maintain remission
azathioprine. This medication is used as first-line management to maintain remission in patients with Crohn’s. Remember that the function of the enzyme thiopurine methyltransferase (TPMT) needs to be assessed before starting a patient on azathioprine because a deficiency in this enzyme (present in 1% of the population) could lead to bone marrow suppression with potentially deadly consequences.
2nd=
flushing, diarrhoea, bronchospasm, hypotension, and weight loss.
carcinoid tumor
urinary 5-HIAA, as the tumour will secrete serotonin
Carcinoid syndrome
usually occurs when metastases are present in the liver and release serotonin into the systemic circulation
may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver
urea breath test; when to stop drugs
no antibiotics in past 4 weeks, no antisecretory drugs (e.g. PPI) in past 2 weeks
all clotting factors are low except for factor VIII which is supra-normal. Both PT and APTT can be prolonged.\(factor VIII is made in endothelial cells round the body but al others made in liver)
liver failure
UC most common site
rectum
prophylaxis of oesophageal bleeding
propanolol
coeliac disease - how to diagnose? (gold standard)
jejunal biopsy
haemochromatosis treatment: how to monitor
Ferritin and transferrin saturation are used to monitor treatment in haemochromatosis
IgG
Golly its chronic
Chrons most common site
ilieium
Bile-acid malabsorption may be treated with
cholestyramine
most common extra-intestinal feature in both Crohn’s and UC
Arthritis
Clindamycin important GI side effect
C diff
used to monitor treatment in haemochromatosis
What is Ferritin and transferrin saturation
ferritin= stored iron
transferrin= transferring iron
Liver problems + amenorrohoea
AUTOIMMUNE
severe UC
IV steroids and ADMIT (less severe you can give aminosalicylate)i
in liver cirrhosis liver enzymes are..
relatively normal
drug induced liver dissease
The following drugs tend to cause a hepatocellular picture:
paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
nitrofurantoin
The following drugs tend to cause cholestasis (+/- hepatitis):
combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine
Liver cirrhosis
methotrexate
methyldopa
amiodarone
Peutz-Jehgers =
Polyps (GI) + Pigments (skin/mucosa)
Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Although the polyps themselves don’t have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.
conservative unless complications develop
Ispaghula husk
bulk forming laxative used in IBS
lansoprazole vs omeprazole
lansoprazole apparently has less impact on CYP2c19 enzyme –> better for preventing drug interactions
The demographic (middle-aged female), history (lethargy, pruritus) and liver function tests (rise in ALP and γGT) all point to a diagnosis of
primary biliary cirrhosis (PBC). Anti-mitochondrial antibodies are found in 98% of patients with PBC.
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females
adequate response to immunisation heptitis
Anti-HBc = cirrhosis (previous or current infection)
Anti-HBs = safe (you are safe because of your immunisations)
LFTS:
hepatocelluar
cholestatic
mixed disease
HEPATOCELLULAR: (e.g,paracetamol) raised ALT, normal APT, ALT/ALT 5+
CHOLESTATIC: normal ALT, raised ALP, ALT/ALP<2
Mixed: both raised, ratio 2-5
acute liver failure: best measurement
Prothrombin time is the most accurate determinate of acute liver failure as it is a measurement of the liver’s synthetic function.
Diarrhoea acid-base balance
The answer is a normal anion gap metabolic acidosis. This woman has increased gastrointestinal loss of bicarbonate from prolonged diarrhoea. The increased loss of bicarbonate results in the loss of alkalotic ions, leaving the blood in an acidotic state. This is a metabolic acidosis as carbon dioxide plays no role in the pH state. It is a normal anion gap as acidosis is not a result of acidotic ion production, such as lactate, ketosis, or salicylate acid.
prolactin casues
pregnancy
prolactinoma
physiological
polycystic ovarian syndrome
primary hypothyroidism
phenothiazines, metoclopramide, domperidone
Phaeochromocytoma management
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)
PHaeochromocytoma - give PHenoxybenzamine before beta-blockers
HbA1c should not be sued to diagnose in
acute pancreatic damage
HIB infection
end stage renal disease
medication causes hyperglycaemia (corticosteroids)
acutely ill
Sx for <2 months
prengnanct
children <18yrs
Interpret with caution in:
haemoglobinopathy
severe anaemia
altered redc cell span
recent transfusion
milk alkali syndrome
slow onset hypercalaemia
–> renal failure and metabolic acidosis
(due to milk and antacids (alkali) being used for epigastric pain)
best test for acromegaly
IGF-1. (not GH)
Acrus seniles
whitish grey opaque ring in corneal margin
?cushing disease investigations
OVERNIGHT dexamethasone suppression test
(or the 24hr urinary free cortisol)
Conns syndrome
INCREASED aldosterone
–> HTN and hypokalaemia
(think of it as the OPPOSITE to spirolactone)
cirrhosis, diabetes, skin pigmentations
Haemachromatosis
(Wilsons is just liver problems)
low sodium serum
normal urine osmolality
small cell lung carcinoma
SIADH
excess hair in eating disorders
lanugo
sitagliptin is what type of drug? how does it work?
DPP-4 inhibitor (glisten)
increased peripheral breakdown of incretins
Side effects thyorixine therapy
hyperthyroisim
reduced bone mineral density
worsening angina
AF
Interacts with
iron
calcium
tender goitre, hyperthyroid, raised ESR
subacute thyroiditis / viral thyoriditis/ de Quervain’s thyoriditis
phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
phase 2 (1-3 weeks): euthyroid
phase 3 (weeks - months): hypothyroidism
phase 4: thyroid structure and function goes back to normal
reduced hypoglycaemic awareness in which drug…
beta blocker
1st line management peripheral neuropathy
amitriptyline, duloxetine, gabapentin or pregabalin
CONSIDER BPH in amitrpytiline
steroids and MSK problems
osteoporosis
proximal myopathy
avascular necrosis of the femoral head
brain mets- what type of steroid
DEXAMETHASONE
GORD and wheeze
you CAN get wheeze due to aspiration of contents
PROBLEMS Swallowing acelasia vs cancer
cancer= SOLIDS then liquids
acalasia= LIQUIDS then solids , regurgitation of food
Primary Biliary cirrhosis
AUTOIMMUNE
undercooked poultry
watery, bloody diarrhoea
crampy abdo pain
linked to reactive arthritis and Guillian-Barre syndrome
Campylobacter
single most appropriate investigation to exclude exarcerbation of Crohns
Faecal calprotectin
most common cause of lower GI bleeding in adults requiring hospitalization
diverticular disease
gen unwell
run down
loss of appetitte
raise billirubin
gilberts syndrome
abdo pain
jaundice
ascieties
hepatomegaly
CT abdo shows caudate lobe hypertrophy and occluded hepatic veins
Budd-Chiari syndrome
jaundice, weight loss, palpable fall bladder
carcinoma of pancreas
toxic megacolon investigations
XR - dilated >6cm
Couvoisiers law
present of palpable galls bladder and no pain, it is unlikely to be gallstones
(Pancreatic malignancy)
35 M - 2 day Hx of anal pain when defecating.
blood on toilet pape.r
red/purpilish pea sized lump on anal margin
perianal haematoma
25 M crohns disease
extreme pain
defecation on blood toilet paper
anal fissure
INCREASED risk of colorectal cancer
polyps
IBD
FH
high fat diet high red meat
low physical activity
smoking
alcohol
When to do ERCP for cholecystitis
recent cholangitis
recent acute pancreatitis
abnormal LFTs (ALP >2x normal)
dilated CBD >10mm
what type of anti-diabetic is gliclazide
SULFONYLUREA
coeliac disease - what type of anaemia
microcytic (iron def anaemia)
B12 deficiency (pernicious anaemia) investigaton
Intrinsic factor antibodies
(autoimmune destruction of gastric parietal cells)
severe UC
> 6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
H pylori is associated with what cancer
MALT lymphoma
Coeliac disease associated with what cancer
enteropathy associated T cell lymphoma
HbA1c target for T2DM on metformin
48
HbA1c target for T2DM on 2 agents
53 (or if on hypoglycaemic med)
1st line management microprolactinoma
Bromocriptine
2nd line= trans=sphenoidal hypophysectomy
diabetes: what to co if triple therapy stops
TD2M: if a triple combination of drugs has failed to reduce HbA1c then switching one of the drugs for a GLP-1 mimetic is recommended, particularly if the BMI > 35
carcinoid syndrome- flushing, diarrhoea, bronchospasm, hypotension, and weight loss. - investigation
Urinary 5-HIAA
higher hba1c levels - causes
Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy
thyroid storm - 1st line treatment (1)
Sx (4)
IV propranolol
hyperthyroid crisis - hyperthermia, tachycardia, jaundice, and altered mental status, fever >38.5oC
haemochormatosis inheritance
recessive (METABOLIC)
PTH primary - high Ca - what is the level of PTH?
can be HIGH or NORMAL (inappropriate)
IBD and smoking
STOP in Crohns
HYPERTENSIOn and hypokalaemia
Conns (primary hyperaldosteronism)
Causes
bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases
adrenal adenoma: 20-30% of cases
management Conns
(primary hyperaldosteronism)
BILATERAL= spirolactone
SINGLE ADENOMA= surgery
acromegaly medical treatment if not suitable for trans-sphenoidal surgery
octreotide
