Gastro + Endo + Nephro Flashcards

1
Q

H pylori post eradication therapy

A

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.

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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: IMPAIRED glucose tolerance

A

Fasting plasma glucose < 7.0 mmol/l
OGTT 2-hour value: 7.8 to 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
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).
26
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
27
most common cause of cushings SYDNROME
pituitary adeoma (aka cushings DISEASE) - ACTH
28
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
29
which diabetic meds cause weight gain
gliclazide and prioglitazone
30
thyrotoxicosis with tender goitre
de Quervains thyroiditis
31
Addisons and vomiting
take IM hydrocortisone until vomiting stops
32
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
33
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
34
T4 vs T3
T4 is the synthetic form
35
raised ESR
AUTOIMMUNE CONDITIONS e.g. hashimotos thyroiditis
36
Addisons - high or low aldosteronism
PRIMARY HYPOaldosteronism
37
hypercalacemia- two most common causes
malignancy and PTH -> PTH best test for confimin diagnosis e.g. if PTH raised or normal = Primary hyperparathyroidism
38
PTHrP tumour
squamous cell lung cancer
39
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)
40
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)
41
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
42
Crohns: common complications (3)
small bowel cancer colorectal cancer osteoporosis
43
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.
44
Causes of anion gap metabolic acidosis
lactate (shock, sepsis, hypoxia) ketones: diabetic ketoacidosis alcohol urate: renal failure acid poisoning: salicylates, methanol
45
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.
46
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.
47
Iron studies: when is ferritin high/low? (2)
high= inflammatory disorders low= IDA
48
Which Abx causes C diff? (1) what other drug linked to it? (1)
Clindamycin PPI !
49
C diff: distinguishing features for severe/ life threatening? (2)
severe: increased WCC, temperature life threatening: hypotension, partial/complete ileus, toxic megacolon
50
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
51
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
52
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
53
Coagulopathy: all clotting factors are low except for factor VIII. Both PT and APTT prolonged.
liver failure
54
Coagulopathy: VIII low only (1) IX low only (1)
Haemophilia A Haemophilia B
55
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
56
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
57
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
58
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
59
A BMI >30 kg/m², increased hepatic echogenicity on liver ultrasound, and an ALT:AST ratio >2
NAFLD
60
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
61
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.
62
CKD on haemodialysis: most likely cause of death (1) causes (5)
IHD diabetes chronic glomerulonephritis chronic pyelonephritis HTN adult PCKD
63
Granulomas: Crohns vs UC
Crohns
64
Pseudopolyps: Crohns vs UC
UC
65
Skip lesions: Crohns vs UC
Crohns
66
Goblet cells + granulomas: Crohns vs US
Crohns
67
Primary sclerosing cholangitis more common: C vs UC
UC
68
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')
69
Widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps ('pseudopolyps')
UC
70
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'
71
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)
72
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
73
UC: severe disease remission
HOSPITAL for IV steroids 1st line
74
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
75
Diagnosis of non-alcoholic fatty liver diseases
Enhanced liver fibrosis blood test
76
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)
77
peritonitis post dialysis organism
Staphylococcus epidermidis.
78
UC most common site
rectum
79
triad of normocytic anaemia, thrombocytopenia and acute kidney injury.
Haemolytic uraemia syndrome
80
HUS most common cause (what bacteria) (1) treatment (1)
E coli supporitive (no Abx)
81
cancer Sx in coeliac disease
enteropathy-associated T cell lymphoma (EATL),
82
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
83
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
84
CKD stage 1 and 2 diagnosis needs..
Some Sx/ features other than low eGFR
85
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)
86
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
87
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
88
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)
89
Coeliac disese: WHAT biopsy?
JEJUNAL biopsy
90
Liver Hepatitis bloods
HBsAg = ongoing infection, either acute or chronic if present > 6 months anti-HBc = caught, i.e. negative if immunized
91
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
92
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
93
visible haematuria following a recent URTI
IgA nephropathy (Bergers disease) Associated conditions alcoholic cirrhosis coeliac disease/dermatitis herpetiformis Henoch-Schonlein purpura
94
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
95
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
96
which drugs cause liver cirrhosis
methotrexate methyldopa amiodarone
97
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'
98
Primary biliary cholangitis - what rule
the M rule IgM anti-Mitochondrial antibodies, M2 subtype Middle aged females
99
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
100
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
101
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
102
diagnosis post-streptococcal glomerulonephritis
raised anti-streptolysin O titre
103
most common nephrotic syndrome in kids
minimal change disease (IgA nephropathy and post streptococcal glomerulonephritis are nephrITICs syndrome)
104
abdominal pain, arthritis, haematuria and a purpuric rash over the buttocks and extensor surfaces of arms and legs
HSP
105
The risk of which one of the following cancers is he most at risk of following renal transplantation?
squamous cell carcinoma
106
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
107
Rhabdomyolysis management (1)
IV fluids to maintain good urine output urinary alkalinization is sometimes used
108
Triad: haematuria, loin pain, abdominal mass
renal cell carcinoma
109
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
110
young person, dysuria. Treated for UTI already. Urine dipstick is positive for blood + and leucocytes +. A MSSU shows no organism.
chlamydia
111
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
112
U waves T wave flattening ST segment changes
hypokalaemia
113
Glucose requirement when prescribing fluids
50-100g /day irrespective of weight
114
0.9% salie- if large volumes used then concerns RE....
hyperCHLORAEMIC metabolic acidosis
115
how to calculate anion gap
(sodium + potassium) - (bicarbonate + chloride)
116
loss of P waves broad QRS complexes sinusoidal wave pattern
(and tented T waves) HYPERkalaemia
117
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
118
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)
119
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.
120
tachycardia, fatigue, pallor and an aortic flow murmur.
anaemia (murmur due to increased blood flow through the valves/ chambers --> turbulence --> soft murmur)
121
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.
122
Metabolic ketoacidosis with normal or low glucose
Alcohol ketoacidosis
123
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.
124
'double duct' sign on MRCP
pancreatic cancer
125
Achalasia: management (1)
pneumatic (balloon) dilation surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
126
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
127
Crohns - most common site affected
ileum
128
watery travellers diarrhoea
E coli
129
Bile acid malabsopriton management (1)
cholestyamine
130
Creon
replace pancreatic enzymes, for example in cystic fibrosis where there is a reduction in pancreatic enzymes reaching the intestine.
131
most common extra-intestinal feature in both Crohn's and UC
arthritis
132
Melanosis coli
laxative abuse
133
numerous hamartomatous polyps in the GI tract and pigmented freckles on lips/ face/ palms/ soles
Peutz-Jeghers syndrome
134
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
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136
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Crohns: with extra-intestinal Sx related to disease activity
erythema nodosum
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Which TB therapy causes B6 deficiency
Isoniazid
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IBS: laxative
isphagula husk (bulk forming)
140
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
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diarrhoea, floating stool greasy, swimming pools
Giardia lamblia
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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
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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
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Typical symptoms are malaise, anorexia and weight loss. The associated RUQ pain tends to be mild and jaundice is uncommon.
amoebic liver abscess
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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.
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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
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Glasgow-Blatchford
outpatient vs not for UGI bleed
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Rockhall
AFTER endoscopy - risk of Rebleed and mortality includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage
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AST/ALT ration 2:1
Alcohol hepatitis
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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.
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Typical symptoms are malaise, anorexia and weight loss. The associated RUQ pain tends to be mild and jaundice is uncommon.
amoebic liver disease
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Common symptoms include: nausea and vomiting, anorexia myalgia lethargy right upper quadrant (RUQ) pain forge in travel/ IVDU
viral hepatitis
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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
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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
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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)
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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
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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
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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
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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
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Cyclical vomiting syndrome: management (3)
Avoidance of triggers Prophylactic treatments include amitriptyline, propranolol and topiramate. Ondansetron, prochlorperazine and triptans in acute episodes.
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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
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There may be a history of heartburn Odynophagia but no weight loss and systemically well
oesophagi's
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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)
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Dysphagia_ There may be a history of HIV or other risk factors such as steroid inhaler use
oesophageal candidacies
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Dysphagia of both liquids and solids from the start Heartburn Regurgitation of food - may lead to cough, aspiration pneumonia etc
achalasia
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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
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Other symptoms may include extraocular muscle weakness or ptosis Dysphagia with liquids as well as solids
myasthenia travis
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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.
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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.
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A combination of liver and neurological disease points towards .....
Wilsons disease
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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
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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
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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
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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=
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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
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urea breath test; when to stop drugs
no antibiotics in past 4 weeks, no antisecretory drugs (e.g. PPI) in past 2 weeks
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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
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UC most common site
rectum
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prophylaxis of oesophageal bleeding
propanolol
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coeliac disease - how to diagnose? (gold standard)
jejunal biopsy
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haemochromatosis treatment: how to monitor
Ferritin and transferrin saturation are used to monitor treatment in haemochromatosis
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IgG
Golly its chronic
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Chrons most common site
ilieium
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Bile-acid malabsorption may be treated with
cholestyramine
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most common extra-intestinal feature in both Crohn's and UC
Arthritis
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Clindamycin important GI side effect
C diff
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used to monitor treatment in haemochromatosis
What is Ferritin and transferrin saturation ferritin= stored iron transferrin= transferring iron
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Liver problems + amenorrohoea
AUTOIMMUNE
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severe UC
IV steroids and ADMIT (less severe you can give aminosalicylate)i
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in liver cirrhosis liver enzymes are..
relatively normal
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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
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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
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Ispaghula husk
bulk forming laxative used in IBS
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lansoprazole vs omeprazole
lansoprazole apparently has less impact on CYP2c19 enzyme --> better for preventing drug interactions
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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
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adequate response to immunisation heptitis
Anti-HBc = cirrhosis (previous or current infection) Anti-HBs = safe (you are safe because of your immunisations)
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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
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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.
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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.
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prolactin casues
pregnancy prolactinoma physiological polycystic ovarian syndrome primary hypothyroidism phenothiazines, metoclopramide, domperidone
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Phaeochromocytoma management
alpha-blocker (e.g. phenoxybenzamine), given before a beta-blocker (e.g. propranolol) PHaeochromocytoma - give PHenoxybenzamine before beta-blockers
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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
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milk alkali syndrome
slow onset hypercalaemia --> renal failure and metabolic acidosis (due to milk and antacids (alkali) being used for epigastric pain)
200
best test for acromegaly
IGF-1. (not GH)
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Acrus seniles
whitish grey opaque ring in corneal margin
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?cushing disease investigations
OVERNIGHT dexamethasone suppression test (or the 24hr urinary free cortisol)
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Conns syndrome
INCREASED aldosterone --> HTN and hypokalaemia (think of it as the OPPOSITE to spirolactone)
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cirrhosis, diabetes, skin pigmentations
Haemachromatosis (Wilsons is just liver problems)
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low sodium serum normal urine osmolality small cell lung carcinoma
SIADH
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excess hair in eating disorders
lanugo
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sitagliptin is what type of drug? how does it work?
DPP-4 inhibitor (glisten) increased peripheral breakdown of incretins
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Side effects thyorixine therapy
hyperthyroisim reduced bone mineral density worsening angina AF Interacts with iron calcium
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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
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reduced hypoglycaemic awareness in which drug...
beta blocker
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1st line management peripheral neuropathy
amitriptyline, duloxetine, gabapentin or pregabalin CONSIDER BPH in amitrpytiline
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steroids and MSK problems
osteoporosis proximal myopathy avascular necrosis of the femoral head
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brain mets- what type of steroid
DEXAMETHASONE
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GORD and wheeze
you CAN get wheeze due to aspiration of contents
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PROBLEMS Swallowing acelasia vs cancer
cancer= SOLIDS then liquids acalasia= LIQUIDS then solids , regurgitation of food
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Primary Biliary cirrhosis
AUTOIMMUNE
217
undercooked poultry watery, bloody diarrhoea crampy abdo pain linked to reactive arthritis and Guillian-Barre syndrome
Campylobacter
218
single most appropriate investigation to exclude exarcerbation of Crohns
Faecal calprotectin
219
most common cause of lower GI bleeding in adults requiring hospitalization
diverticular disease
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gen unwell run down loss of appetitte raise billirubin
gilberts syndrome
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abdo pain jaundice ascieties hepatomegaly CT abdo shows caudate lobe hypertrophy and occluded hepatic veins
Budd-Chiari syndrome
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jaundice, weight loss, palpable fall bladder
carcinoma of pancreas
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toxic megacolon investigations
XR - dilated >6cm
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Couvoisiers law
present of palpable galls bladder and no pain, it is unlikely to be gallstones (Pancreatic malignancy)
225
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
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25 M crohns disease extreme pain defecation on blood toilet paper
anal fissure
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INCREASED risk of colorectal cancer
polyps IBD FH high fat diet high red meat low physical activity smoking alcohol
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When to do ERCP for cholecystitis
recent cholangitis recent acute pancreatitis abnormal LFTs (ALP >2x normal) dilated CBD >10mm
229
what type of anti-diabetic is gliclazide
SULFONYLUREA
230
coeliac disease - what type of anaemia
microcytic (iron def anaemia)
231
B12 deficiency (pernicious anaemia) investigaton
Intrinsic factor antibodies (autoimmune destruction of gastric parietal cells)
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severe UC
>6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
233
H pylori is associated with what cancer
MALT lymphoma
234
Coeliac disease associated with what cancer
enteropathy associated T cell lymphoma
235
HbA1c target for T2DM on metformin
48
236
HbA1c target for T2DM on 2 agents
53 (or if on hypoglycaemic med)
237
1st line management microprolactinoma
Bromocriptine 2nd line= trans=sphenoidal hypophysectomy
238
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
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carcinoid syndrome- flushing, diarrhoea, bronchospasm, hypotension, and weight loss. - investigation
Urinary 5-HIAA
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higher hba1c levels - causes
Vitamin B12/folic acid deficiency Iron-deficiency anaemia Splenectomy
241
thyroid storm - 1st line treatment (1) Sx (4)
IV propranolol hyperthyroid crisis - hyperthermia, tachycardia, jaundice, and altered mental status, fever >38.5oC
242
haemochormatosis inheritance
recessive (METABOLIC)
243
PTH primary - high Ca - what is the level of PTH?
can be HIGH or NORMAL (inappropriate)
244
IBD and smoking
STOP in Crohns
245
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
246
management Conns
(primary hyperaldosteronism) BILATERAL= spirolactone SINGLE ADENOMA= surgery
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acromegaly medical treatment if not suitable for trans-sphenoidal surgery
octreotide
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