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MSRA > Gastro + Endo + Nephro > Flashcards

Gastro + Endo + Nephro Flashcards

1
Q

H pylori post eradication therapy

A

NICE guidance advises that we should not routinely offer H. pylori re-testing, however we can consider re-testing if:
There has been poor compliance to eradication therapy
Aspirin or NSAID is indicated
There is a family history 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.

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2
Q

GI bleed scoring system

A

blatchford bleeding risk
rockall rebleeding risk

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3
Q

1st-3rd line therapy c diff

A

first-line therapy is oral vancomycin for 10 days

second-line therapy: oral fidaxomicin

third-line therapy: oral vancomycin +/- IV metronidazole

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4
Q

C peptide and type 1 vs type 2 diabetes?

A

C peptides raised in type 2

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5
Q

Prolactinoma treatment

A

Dopamine agonist (e.g cabergoline, bromocriptine)

surgery if fail to respond

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6
Q

acromegaly and elevated IGF-1 (insulin growth factor) investigations

A

OGTT and serial GH levels

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7
Q

acromegaly how to diagnose

A

1st = serum IGF-1
2nd= OGTT+ serial GH

in normal patients if hyperglycaemic then GH reduced, but in acromegaly GH still high

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8
Q

what marker monitors disease In acromegaly

A

IGF-1

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9
Q

crushing syndrome metabolic disturbance

A

hypokalaemia metabolic alkalosis

Bicarbonate resorption is increased in the tubules with potassium depletion causing metabolic alkalosis.

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10
Q

Gynaecomastia causes: drugs

A

spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids

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11
Q

Treatment for galactorrhoea

A

bromocriptine (dopamine agonist)

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12
Q

how do thiazides impact Ca level

A

HYPERcalacemia

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13
Q

what is subclinical hypothyroid

A

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

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14
Q

what medication interacts with thyroxine absorption

A

iron

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15
Q

Kallman’s syndrome hormone level

A

low LH & FSH and testosterone (failure of GnRH secreting neurones in hypothalamus)

Kallman = Fallman

Poor Kall the man cannot smell

chromosome = X linked drecessive

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16
Q

Klinefelter Sx

A

High FSH and high LH. But low testosterone. Tall, no secondary sexual characteristics. Small firm testes + gynecomastia.

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17
Q

Addisons and hyperpigmentation

A

primary Addison’s is associated with hyperpigmentation whereas secondary adrenal insufficiency is not

secondary causes= tumours, irradiation, infiltration, exogenous steroids

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18
Q

Diabetes-specific autoantiboits T2DM vs T1DM

A

in type 1 C peptide LOW but others present

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19
Q

OGTT test: imaired glucose tolerance

A

Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

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20
Q

drug causes raised prolactin (and –> galacctoreoa)

A

metoclopramide, domperidone
phenothiazines
haloperidol
very rare: SSRIs, opioids

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21
Q

non drug causes raised prolactin

A

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)

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22
Q

T1DM with bloating, vomiting and erratic CGMs? what med to try

A

metoclopramide

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23
Q

tender goitre, hyperthyroidism and raised ESR. The globally reduced uptake on technetium thyroid scan is also typical

A

Sub acute (De Quervains) thyroiditis

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24
Q

diabetes medicaition and BMI>35 - what to consider?

A

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.

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25
Q

Who avoids SGLT-2?

A

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).

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26
Q

T2DM triple therapy not worked.. what to do?

A

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

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27
Q

most common cause of cushings SYDNROME

A

pituitary adeoma (aka cushings DISEASE) - ACTH

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28
Q

Thiazolinediones - what is the the side effects?

A

e.g. Pioglitazone

T2DM medication

weight gain
liver impairment
fluid retention –. CONTRAINDICATED in hearty failure
increased fractures
bladder cancer

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29
Q

which diabetic meds cause weight gain

A

gliclazide and prioglitazone

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30
Q

thyrotoxicosis with tender goitre

A

de Quervains thyroiditis

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31
Q

Addisons and vomiting

A

take IM hydrocortisone until vomiting stops

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32
Q

hypoglycaemia - what two things to measure to investigate cause? (2)
What does this show? (2)

A

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

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33
Q

a HbAlc value of less than 48 mmol/mol (6.5%)

A

does not exclude diabetes (i.e. it is not as sensitive as fasting samples for detecting diabetes) –> consider fasting glucose sample

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34
Q

T4 vs T3

A

T4 is the synthetic form

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35
Q

raised ESR

A

AUTOIMMUNE CONDITIONS e.g. hashimotos thyroiditis

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36
Q

Addisons - high or low aldosteronism

A

PRIMARY HYPOaldosteronism

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37
Q

hypercalacemia- two most common causes

A

malignancy and PTH

-> PTH best test for confimin diagnosis

e.g. if PTH raised or normal = Primary hyperparathyroidism

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38
Q

PTHrP tumour

A

squamous cell lung cancer

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39
Q

how do sulfonyluyrea work

A

bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells

–> insulin release

(hence why you get weight gain)

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40
Q

Crohns:
how to induce remission (3)
fistulating disease (1)
peri-anal disease (1)
what diet? (1)

A

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)

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41
Q

Crohns:
maintaining remission? (1)
smoking: what to do? (1)
perianal disease (3)

A

azathioprine or mercatopurine

stop smoking

peri-anal disease: MRI
metronidazole
anti-TNF (infliximab)
draining seton for complex

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42
Q

Crohns:
common complications (3)

A

small bowel cancer
colorectal cancer
osteoporosis

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43
Q

Diarrhoea:
acid-base balance seen on arterial blood gas?

A

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.

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44
Q

Causes of anion gap metabolic acidosis

A

lactate (shock, sepsis, hypoxia)
ketones: diabetic ketoacidosis
alcohol
urate: renal failure
acid poisoning: salicylates, methanol

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45
Q

Iron studies:
how to tell difference between deficiency anaemia vs. anaemia of chronic disease (1)

A

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.
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46
Q

Transferrin: how does it change in iron deficiency

A
  • 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.
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47
Q

Iron studies:
when is ferritin high/low? (2)

A

high= inflammatory disorders
low= IDA

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48
Q

Which Abx causes C diff? (1)
what other drug linked to it? (1)

A

Clindamycin

PPI !

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49
Q

C diff:
distinguishing features for severe/ life threatening? (2)

A

severe:
increased WCC, temperature

life threatening:
hypotension, partial/complete ileus, toxic megacolon

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50
Q

C diff:
diagnosis (1)

A

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

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51
Q

C diff: 1st/2nd/3rd management (3)
if recurrent (2)
life-threatening (1)

A

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

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52
Q

flushing, diarrhoea, bronchospasm, hypotension, and weight loss.

A

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

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53
Q

Coagulopathy:
all clotting factors are low except for factor VIII. Both PT and APTT prolonged.

A

liver failure

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54
Q

Coagulopathy:
VIII low only (1)
IX low only (1)

A

Haemophilia A
Haemophilia B

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55
Q

Diabsts insipidus: causes

A

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

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56
Q

Pernicious anaemia:
which Vitamin? (1)
other causes of deficiency (3)
diagnosis (1)

A

B12

Other causes include atrophic gastritis (e.g. secondary to H. pylori infection), gastrectomy, malnutrition (e.g. alcoholism)

Anti intrinsic factor antibodies

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57
Q

Pernicious anemaia: feature

A

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

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58
Q

Pernicious anaemia management

A

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

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59
Q

A BMI >30 kg/m², increased hepatic echogenicity on liver ultrasound, and an ALT:AST ratio >2

A

NAFLD

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60
Q

Barretts:
management

A

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

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61
Q

Haemochromatosis:
how inherited?
how to monitor (1)
why is serum iron useless (1)

A

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.

62
Q

CKD on haemodialysis:
most likely cause of death (1)
causes (5)

A

IHD

diabetes
chronic glomerulonephritis
chronic pyelonephritis
HTN
adult PCKD

63
Q

Granulomas: Crohns vs UC

A

Crohns

64
Q

Pseudopolyps: Crohns vs UC

A

UC

65
Q

Skip lesions: Crohns vs UC

A

Crohns

66
Q

Goblet cells + granulomas: Crohns vs US

A

Crohns

67
Q

Primary sclerosing cholangitis more common: C vs UC

A

UC

68
Q

Gallstones are more common secondary to reduced bile acid reabsorption

Oxalate renal stones*: Crohns Vs UC

A

CrohnsWidespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)

69
Q

Widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)

A

UC

70
Q

Radiology results UC vs Crohns

A

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’

71
Q

Mild/ moderate/ severe UC: diarrhoea

A

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)

72
Q

UC: mild-moderate disease
how to induce remission

A

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

73
Q

UC: severe disease remission

A

HOSPITAL for IV steroids 1st line

74
Q

UC: maintenance

A

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

75
Q

Diagnosis of non-alcoholic fatty liver diseases

A

Enhanced liver fibrosis blood test

76
Q

H pylori test:
when to stop meds before urea breath test

A

4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)

77
Q

peritonitis post dialysis organism

A

Staphylococcus epidermidis.

78
Q

UC most common site

A

rectum

79
Q

triad of normocytic anaemia, thrombocytopenia and acute kidney injury.

A

Haemolytic uraemia syndrome

80
Q

HUS most common cause (1)
treatment (1)

A

E coli

supporitive (no Abx)

81
Q

cancer Sx in coeliac disease

A

enteropathy-associated T cell lymphoma (EATL),

82
Q

acute interstitial nephritis:
features? (1)
causes (4)
ffeawtures (4)

A

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

83
Q

Acute interstitial nephritis
histology (1)
investigations (2)

A

histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

Investigations
sterile pyuria
white cell casts

84
Q

CKD stage 1 and 2 diagnosis needs..

A

Some Sx/ features other than low eGFR

85
Q

Oesophageal bleeding:
prophylaxis? (1)
acute management drug (1)

A

NS BB e.g. propranolol

Terlipressin is a vasopressin analogue that is indicated in the acute management of variceal bleeding.
(+ prophylactic Abx)

86
Q

primary biliary cholangitis: Management (1)
associations (4)

A

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

87
Q

primary biliary cholagitis:
features (5)

A

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

88
Q

primary biliary cholangitis: complications (3)

A

Complications
cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)

89
Q

Coeliac disese: WHAT biopsy?

A

JEJUNAL biopsy

90
Q

Liver Hepatitis bloods

A

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

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

91
Q

Hepatic encepalopathy:
grading (4)
precipitating factors (5)
management (2)

A

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

92
Q

Size of kidneys: CKD in diabetes?
AKI vs CKD?
other features differentiating CKD and AKI? (1)

A

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

93
Q

visible haematuria following a recent URTI

A

IgA nephropathy (Bergers disease)

Associated conditions
alcoholic cirrhosis
coeliac disease/dermatitis herpetiformis
Henoch-Schonlein purpura

94
Q

IgA nephropathy and post-streptococcal glomerulonephritis
time difference?
protein and haematuria?

A

IgA= 1-2 days after URTI, PSGN= 1-2 weeks after
IgA= haematuria, PSGN= proteiuira AND haematuria
IgA= macroscopic haematuia, PSGN= low complement

95
Q

Cholestatis +/ hepatitis: which drugs cause it?

A

combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine

96
Q

which drugs cause liver cirrhosis

A

methotrexate
methyldopa
amiodarone

97
Q

SBP:
most common organism? (1)
how to diagnose (1)
treatment (1)
prohplayxis? 91)

A

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’

98
Q

Primary biliary cholangitis - what rule

A

the M rule

IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females

99
Q

dyspepsia, abdominal pain, nausea and anorexia

A

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

100
Q

live screening for hepatocellular carcinoma is for who

A

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

101
Q

Risk factors for HCC

A

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

102
Q

diagnosis post-streptococcal glomerulonephritis

A

raised anti-streptolysin O titre

103
Q

most common nephrotic syndrome in kids

A

minimal change disease
(IgA nephropathy and post streptococcal glomerulonephritis are nephrITICs syndrome)

104
Q

abdominal pain, arthritis, haematuria and a purpuric rash over the buttocks and extensor surfaces of arms and legs

A

HSP

105
Q

The risk of which one of the following cancers is he most at risk of following renal transplantation?

A

squamous cell carcinoma

106
Q

Rhabdomyolysis:
features - electrolytes? (3)

A

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

107
Q

Rhabdomyolysis
management (1)

A

IV fluids to maintain good urine output
urinary alkalinization is sometimes used

108
Q

Triad: haematuria, loin pain, abdominal mass

A

renal cell carcinoma

109
Q

Renal cell carincoma:
features

A

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

110
Q

young person, dysuria. Treated for UTI already. Urine dipstick is positive for blood + and leucocytes +. A MSSU shows no organism.

A

chlamydia

111
Q

Hypokalaemia:
management if <2.5? (1)
management if 2.5-3.4? (1)

A

The infusion rate should not exceed 20mmol/hr. In this case, 3 bags of 0.9% Saline with 40mmol KCL

IV +/- oral replacement

112
Q

U waves
T wave flattening
ST segment changes

A

hypokalaemia

113
Q

Glucose requirement when prescribing fluids

A

50-100g /day irrespective of weight

114
Q

0.9% salie- if large volumes used then concerns RE….

A

hyperCHLORAEMIC metabolic acidosis

115
Q

how to calculate anion gap

A

(sodium + potassium) - (bicarbonate + chloride)

116
Q

loss of P waves
broad QRS complexes
sinusoidal wave pattern

A

(and tented T waves)

HYPERkalaemia

117
Q

Diagnosis of AKI:
Creatine % (1) and amount (1)
urine output (1)

A

↑ creatinine > 26µmol/L in 48 hours
↑ creatinine > 50% in 7 days
↓ urine output < 0.5ml/kg/hr for more than 6 hours

118
Q

AKI: when to refer? (10)

A

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)

119
Q

AKI:
when stage 2 and 3?

A

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.

120
Q

tachycardia, fatigue, pallor and an aortic flow murmur.

A

anaemia

(murmur due to increased blood flow through the valves/ chambers –> turbulence –> soft murmur)

121
Q

SBP:
Abx management? (1)
who gets it? (1)

A

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.

122
Q

Metabolic ketoacidosis with normal or low glucose

A

Alcohol ketoacidosis

123
Q

Haemochromatosis:
how to monitor treatment? (2)

A

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.

124
Q

‘double duct’ sign on MRCP

A

pancreatic cancer

125
Q

Achalasia:
management (1)

A

pneumatic (balloon) dilation

surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms

126
Q

Hepatitis:
IgG vs IgM

A

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

127
Q

Crohns - most common site affected

A

ileum

128
Q

watery travellers diarrhoea

A

E coli

129
Q

Bile acid malabsopriton management (1)

A

cholestyamine

130
Q

Creon

A

replace pancreatic enzymes, for example in cystic fibrosis where there is a reduction in pancreatic enzymes reaching the intestine.

131
Q

most common extra-intestinal feature in both Crohn’s and UC

A

arthritis

132
Q

Melanosis coli

A

laxative abuse

133
Q

numerous hamartomatous polyps in the GI tract and pigmented freckles on lips/ face/ palms/ soles

A

Peutz-Jeghers syndrome

134
Q

Oesophageal cancer: SCC vs adenocarcinoma
location? (1)
risk factors adenocarinoma (4)
risk factors SCC? (5)

A

lower 1/3 = adenocinoma

GORD
barretts
smoking
obesity

smoking
alcoohl
achalasia
Plummer vinson syndrome
nitrosamine rich diet

135
Q
A
136
Q
A
137
Q

Crohns:
with extra-intestinal Sx related to disease activity

A

erythema nodosum

138
Q

Which TB therapy causes B6 deficiency

A

Isoniazid

139
Q

IBS: laxative

A

isphagula husk (bulk forming)

140
Q

High ferritin:
what to look at first in iron studies (1)

A

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

141
Q

diarrhoea, floating stool greasy, swimming pools

A

Giardia lamblia

142
Q

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.

A

gallstone ileus

143
Q

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

A

cholangiocarcinoma

144
Q

Typical symptoms are malaise, anorexia and weight loss. The associated RUQ pain tends to be mild and jaundice is uncommon.

A

amoebic liver abscess

145
Q

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.

A

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.

146
Q

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

A

diffuse erosive gastritis

147
Q

Glasgow-Blatchford

A

outpatient vs not for UGI bleed

148
Q

Rockhall

A

AFTER endoscopy - risk of Rebleed and mortality

includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage

149
Q

AST/ALT ration 2:1

A

Alcohol hepatitis

150
Q
A

MSRA (9 decks)

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