Gastroenterology Flashcards
1
Q
Girotra’s trait: what does it indicate?
A
Clostridium difficille infection
2
Q
C. diff: what does it cause?
A
Pseudomembranous colitis
3
Q
C. diff: what bacteria is it?
A
gram +ve
4
Q
Girotra’s triad of c.diff: features
A
increased pain/distention and diarrhoea
leukocytosis >18k
haemodynamic instability
5
Q
C. diff infection treamtment
A
stop causative abx
metronidazole or vancomycin for up to 10d
urgent colectomy for toxic megacolon
6
Q
Acute severe diarrhoea: management
A
treat cause
rehydrate: IV saline + 20 mmol K+
codeine phosphate (antimotility drug/opioid receptor)
loperamide (antimotility/ opioid r. but doesn’t cross BBB)
avoid abx unless injective
7
Q
CIrrhosis: define
A
irreversive liver damage
loss of architecture with bridging fibrosis and nodular regeneration
8
Q
Cirrohosis: complications:
A
liver failure
portal hypertension
hepatocellular carcinoma (HCC) increased risk
9
Q
Hereditary Haemochromatosis define
A
disorder of iron metabolism
increased iron absorption
causes liver deposition in the joints, liver, heart, pancreas, pituitary, adrenals and skin
10
Q
Hereditary Haemochromatosis: signs
A
early: none or tiredness, arthralgia (pseudo-gout)
later: slate-grey pigmentation of the skin, chronic liver disease signs, osteoporosis
Endocrinopathies: DM, hypogonadism (putuitary deposits)
11
Q
alpha-1 antitripsin deficiency: cause and effects
A
inherited disease in serine protease inhibitor, mechanism unclear
it controls inflammation
affects the lungs (emphysema) and liver (cirrhosis and HCC)
causes liver disease in children (cholestatic jaundice)
12
Q
WIlson’s disease: define
A
autosomal recessive inherited disorder of biliary copper excretion (problem with copper incorporation in hepatocytes and its excretion into bile)
- > too much copper in liver and CNS (basal ganglia)
- > screen young in cirrhosis
13
Q
Cirrhosis: signs
A
leuconychia (hypoalbuminaemia), Terry’s nails (Talangectesia distally),clubbing
palmar erythema, Dupuryen’s circulation
hyperdynamic circulation
spider naevi, xanthelasma,
hepato- and spleno- megally/small liver
Portal HTN: astices, splenomeg, varices, caput metusae
14
Q
Cirrhosis: management
A
nutrition, avoid alcohol, NSAIDs, sedatives and opiates colestyramine for pruritus consider USS +/- alpha fetoprotein varicies-> banding recurrent encephalopathy-> rifaximin
15
Q
Cirrhosis: diagnosis
A
transient elastography in pt’s at risk
biopsy if unsuitable
caution in obese or T2DM
re-test high risk patients every 2 yrs
16
Q
Recurrent encephalopathy management
A
rifaximin
17
Q
Primary biliary cirrhosis: define
A
interlobular bile ducts damage by chronic autoimmune gronulomatous inflammation (genetic and environmental influence)
-> cholestasis
-> fibrosis, cirrhosis and portal HTN
hallmark: antimitochondial antibodies (AMAs)
malabsorption of fat soluble vitamins (due to cholestasis and inc bilirubin)
18
Q
Primary sclerosing cholangitis: define
A
progressive cholestatis with bile duct inflammation and strictures (outside of liver)
-> pruritis +/- fatigue
-> ascending cholangitis, cirrhosis and end-stage liver failure
primary or secondary to infections, thrombosis or trauma
19
Q
Liver failure: signs
A
jaundice, encephalopathy
pear drop smell
liver flap (asterixis)
constructional apraxia (Star)
20
Q
Liver failure: investigations
A
FBC, U&E (use creatine for renal func.), LFT, clotting (inc. prothrombin, INR), paracetamol levels
blood/urine culture, ascitic tap (MC&S)-> spontaneous bacterial peritonitis
CXR, abdo USS, Doppler portal v. (Budd-Chiari synd)
21
Q
Budd-Chirari syndrome: define
A
hepatic vein obstruction by thrombosis or tumour
- > ischaemia and hepatocyte damage
- > abdo pain, hepatomegaly, ascites and inc. ALT
- > portal HTN in chronic cases
22
Q
Liver failure management
A
ITU bed 20* head up tilt
Protect airway (intubation + NG to for aspiration risk and remove blood from stomach)
Fluid status (urinary and central venous catheters)
Obs + daily weights
FBC, U&E, LFT and INR daily
avoid hypoglycaemia (frequent BMs +/- 10% dextrose IVI)
Nutrition (thiamine and folate supplements)
Lorazepam for seizures
Consider liver transplant
23
Q
Hepatic encephalopathy: pathophysiology
A
liver failing -> amonia waste builds up in curculation
- > passess to the brain
- > cleared by astrocytes (glutamate-> glutamine)
- > glutamine builds up
- > osmotic imbalance
- > cerebral oedema
24
Q
Hepatic encephalopathy: stages
A
- altered mood/behaviour (sleep disturbance, dyspraxia (star), no liver flap)
- Increased drowsiness, confusion, slurred speech, liver flap, inappropriate behaviour and personality change
- Incoherent, restless, liver flap, stupor
- coma
25
Liver transplant indications
end stage liver failure (acute or chronic)
| primary liver cancers
26
Liver transplant donation options
living donor: right lobe (for critically ill)
| cadeveric donor
27
Hepatorenal syndrome: define and pathophysiology
cirrhosis, ascites and renal failure (abnormal haemodynamics)
bacterial translocation cytokines and mesenteric autoregulation
-> splanchnic and systemic vasodilatation
-> renal vasoconstrictio
28
Hepatorenal syndrome: types
1. rapidly progressive, <2wks median survival -> Terlipressin and haemodialysis may be needed
2. steady deterioration, survival around 6 months. Transjugular intrahepatic potrosystemic shunt
29
Jaundice: pathophysiology (from haemoglobin breakdown)
Hb broken down to Heme and globin.
Heme is converted to UCB by heme oxygenase (bound to Albumin as water insoluble)
Enters the liver where it gets unbound
UCB+ glucoronic acid -> CB excreted in bile enters the intestine
bacteria cleave glucoronic acid off and CB -> Urobilinogen
Excteted in urine (10%) and in faeces (90%- steobilin)
30
What happends to globin after Hb breakdown?
Broken down by macrophages of the reticuloendothelial system (Kupffer cells)
31
Pre- hepatic jaundice UCB and CB levels, urine and stool colour
UCB- increased
CB- normal
urine- normal
stool- normal
32
Hepatic jaundice UCB and CB levels, urine and stool colour
UCB- increased
CB- increased
urine- dark
stool- normal
33
Post- hepatic UCB and CB levels, urine and stool colour
UCB- normal
CB- increased
urine- dark
stool- pale (low levels reach the intestine due to an obstruction)
34
Kernicterus: define
unbound bilirubin deposited in infant basal ganglia
| -> bilirubin induced brain dysfunction
35
Causes of acute jaundice in cirrhosis patient
sepsis
malignancy
alcohol and drugs
GI bleeding
36
Hereditary Haemochromatosis: management
venesection
| consider vitamin supplements
37
Primary sclerosing cholangitis: associated cancers
increased risk of bile duct, GB, liver and colon cancer
| -> yearly colonoscopy and USS
38
Hepatitis A: pathogen type and course
RNA virus
| self limiting and not chronic
39
Hepatitis A: incubation time and symptoms
2-6 wks
| fever,malaise, anorexia nausea, arthralgia, jaundice, hepato and splenomegaly and adenopathy
40
Hepatitis A: investigations
ALT ^^
AST ^
IgG detectable for life
IgM for 20d to 20wks
41
Hepatitis A: management
immunization (harvix monodose)-> for 1 year
| usually self- limiting
42
Hepatitis B: pathogen type
DNA virus
43
Hepatitis A: spread
faecal-oral route
44
Hepatitis B: spread
blood products, IV drug use, sexual, direct
45
Hepatitis B: incubation time and symptoms
1-6 months
| fever, malaise, anorexia, nausea, arthralgia and uratica, jaundice
46
Hepatitis B: investigations
HBsAg (surface antigen, if +ve over 6m -> carrier)
| HBeAg (antigen, +ve during acute phase and up to 3 m after) -> implies increased infectivity
47
Hepatitis B: management
vaccination (specific anti-HBV immuniglobulin) for high risk exposure individuals
avoid alcohol
antivirals: PEG intaferon alpha 2a, lamivudine, entecavir, adefovir
48
Hepatitis C: pathogen type
RNA flavivirus
49
Hepatitis C: spread
blood transfusion, IV drug use, sexual, acupuncture
50
Hepatitis C: course
early infection often mild or asymptomatic
- > 85% silent chronic infection
- > 25% cirrhosis -> 4% HCC
51
What's the commonest cause of liver transplant?
Hep C
52
Hepatitis C: investigations
LFT- AST:ALT <1:1 until cirrhosis develops
HCV PCR confirms diagnosis, if +ve:
-biopsy to check liver damage and need for Rx
-HCV genotype
- viral load
53
Hepatitis C: management
boceprevir
telaprevir (both serine protease inhibitors)
PEG interferon alpha 2a
54
Autoimmune hepatitis: define
liver inflammation without a known cause
| characterised by T-cell defects with autoantibodies against hepatocyte surface agents
55
Autoimmune hepatitis: investigations
increased bilirubin, alk phos, ALT, AST
inc. IgG
+ve antibodies: ANA, ASMA, LKM1, SLA (variable depending on the type)
56
Autoimmune hepatitis: management
immunosuppression (prednisolone min. 2yrs and/or Azathrioprine)
liver transplant for decompensated cirrhosis or unsuccesful medical treatment
57
Wilson's disease: clinical features
liver disease (Esp. in young)
CNS signs: tremor, dyarthria etc
mood: depression/mania, personality change
cognition: memory loss, IQ deterioration, delusions, mutism, irritability
Kayser-Fleischer rings (iris)
haemolysis
58
Wilson's disease: investigations
```
24h urine copper collection
non specific LFT increase
decreased serum copper
decreased coeruplasmin (but can be low in low protein states)
molecular genetic testing
liver biopsy: inc. copper
MRI: basal ganglia deterioration
```
59
Wilson's disease: management
diet: avoid copper high meals
panicillamine (chelating agent) lifelong
liver transplant
screen siblings
60
Chronic liver disease pt: Haemochromatosis screen
iron studies (increased iron, inc ferrin, inc total iron binding capacity
61
Chronic liver disease pt: alpha 1 antitrypsin def. screen
A1AT levels + genotyping
62
Chronic liver disease pt: Wilson's disease
low copper and caeruloplasmin
63
Chronic liver disease pt: Primary biliary cirrhosis
AMA antibodies
64
Chronic liver disease pt: Primary sclerosing cholangitis
ANA, SMA and ANCA may be increased (but AMA negative)
65
Chronic liver disease pt: autoimmune hep
increased ANA, ASMA, IgG
66
Chronic liver disease pt: HCC
alpha fetoprotein
67
Chronic liver disease pt: Gilbert's disease
increased bilirubin concentration with normal LFTs
68
IBS management: constipation
bisacodyl, sodium picosulfate and ispaghula
69
IBS management: diarrhoea
bulking agents +/- loperamide
| avoid sorbitrol in sweateners
70
IBS management: colic/bloating
mebeverine, alverine citrate, dicycloverine
71
IBS management: psychological symptoms meds
anticyclics: amitryptyline
72
Pt with diarrhoea and weight loss/anorexia; suspect
coeliac disease
73
Coeliac disease: define
t-cell mediated autoimmune disease of the small bowel
prolamin (gluten- alcohol soluble proteins in wheat, barley, rye +/- oats) intolerance
-> villous artophy and malabsorption (inc bile acids)
74
Coeliac disease: investiagtions
low Hb, ferrin, B12
increased RCDW (Red cell distribution width)
serological testing: inc total IgA and IgA tissue transglutaminase. if inconclusive -> IgA EMA
75
Coeliac disease: biopsy results
duodenal biopsy
subtotal villous atrophy
intra epithelial WBC
crypt hyperplasia
76
Coeliac disease: complications
```
anaemia
2* lactate intolerance
GI t-cell lymphom a
increased risk of malignancy
myopathies
hyposplenism
osteoporosis
```
77
Coeliac disease: associated skin condition
dermatitis hypetiformis
78
Diabetes: cardiovascular risk assessment
QRISK2
- age, gender, smoking, diabetes, angina/MI/1st degree relative, HTN Rx, postcode, BMI, systolic BP, total and HDL cholesterol, ethnicity
79
Diabetes: diagnosis
symptoms of hypergylcaemia (polyuria, polydipsia, unexplained weight loss, visual blurring) and
increased venous glucose (7+ fasting or 11.1+ random)
or increased on 2 separate occasions
or HbA1C 6.5% +
80
Diabetes: treatment options
```
Metformin
Sulfonylurea
Glitazone
GLP1 analogues and DPP4
Insulin
```
81
Diabetic ketoacidosis: define
acidaemia, hyperglycaemia, ketoanaemia
life-threatening.
venous XS glucose due to lack of insulin
82
Diabetic ketoacidosis: management
IV fluids
insulin infusion: atrapid
K+ status: low -> potassium phosphate/chloride
or high -> calcium gluconate, salbutamol
83
Diabetes: HONK diagnosis
hyperglycaemic hyperosmolar non-ketotitc coma
| +/- decreased conscious level and mental confusion
84
Diabetes: HONK management
```
slow rehydration (6-12 l may be required)
insulin infusion (actrapid)
NG tube (unconscious)
LMWH
```
85
Causes of hypoglycaemia
ExPLAIN
Exogenous drugs (insulin, hypoglycaemic drugs)
Pituitary insufficiency
Liver failure
Addison's disease
Islet cell tumours/ Immune hypoglycaemia (Hodgkin's disease(
Non-pancreatic neoplasms
86
Hypoglycaemia: management
20-30g glucose IV or
glucagon (not in drunks)
if conscious: sugary drink and a meal
87
Microvascular complications of diabetes
retinopathy
nephropathy
neuropathy
88
Diabetic retinopathy stages and features
background retinopathy: microaneurysms, haemorrhages and hard exudates
pre-proliferative: cotton wool spots, haemorrhages, venous bleeding (Retinal ischaemia)
proliferative: new vessel formation
maculopathy: reduced acuity (changes as above)
89
Diabetic retinopathy: pathogenesis
capillary basement membrane thickening -> leaky vessels, lipid deposids
90
Diabetic retinopathy: when to refer
pre-proliferative stage
changes near the macula
(annual eye checks)
91
Diabetic nephopathy: pathophysiology
glomerular hyperfiltration initially
GBM thickening -> eGFR decreases
microalbuminaemia
-> HRN, oedema and uraemia
92
Diabetic neuropathy: pathophysiology
damage to small blood vessels supplying the nerves and abnormal sugar metabolism
-> peripheral sensory neuropathy (loss of vibration sense and glove and stocking distribution of neuropathy)
93
Diabetic neuropathy: deformities
```
pes cavus, claw toes, loss of transverse arch, rocker-bottom sole
bony deformity- Charcot's deformity
foot ulceration (punched out painless)
```
94
Diabetes: macrovascular complications
atherosclerosis
| foot disease -> ulceration, gangrene
95
Cause of primary hyperlipidaemia
Account for 70% of cases
| - familial primary hyperlipidaemia (multiple phenotypes)
96
Causes of secondary hyperlipidaemia
```
Cushing's syndrome
hypothyrodism
nephrotic syndrome
cholestasis
Mixed hyperlipidaemias: T2DM, metabolic syndrome, alcohol abuse, CKD
```
97
Hyperlipidaemia: managmenet
Diet (reduce saturated fats), weight loss
treat known CVD, DM and 10 year risk of CVD >20%
(target plasma cholesterol 4 mmol/l or less)
-> statins
-> fibrates
98
Posterior pituitary: features
collection of axonal (large diameter) projections from the hypothylamus containing nerve endings (Start in the supraopic and paraventricular nuclei)
99
Posterior pituitary: hormones produced and function
ADH-> water balance regulation, increased water permeability in the distal convoluted tubule (Aquaporin 2 insertion in the basolateral membrane)
OXYTOCIN -> uterine contraction and lactation
100
Anterior pituitary: features
glandular tissue synthesis and secretes 5 peptide hormones
| under the control of hypothylamic releasing hormones transported in the hypophyseal portal veins
101
Anterior pituitary: hormones produced
```
ACTH
TSH
FHS
LH
Growth hormone
Prolactin
```
102
Test for primary adrenal failure
syntacthen test
- no response -> adrenal problem
- normal response excludes Addison's
103
Test for hypopituatarism
insulin tolerance test
- tests ACTH and growth hormone reserve
differentiates between normal individual from ACTH deficiency
(Stress -> cortisol needed, ACTH should be released)
104
Test for acromegaly
glucose tolerance test
stress/hypoglycaema -> growth hormone
bolus glucose -? suppression of growth hormne in a normal person
acromegaly- failure to suppress
105
Test for Cushing's syndrome
Dexamthasone suppression test
Potent supressor of cortisol release
no suppression- ectopic ACTH/Cortisol release
suppression- confirms Cushing's syndrome
106
Pituitary tumours: clinical features (local)
visual loss- bitemporal heminopia (optic chiasm compression) + red. visual acuity
pituitary failure/hypopituatirism
general: headaches, diplopia
107
Pituitary tumours: types
micoadenomas vs macroadenomas
| functioning vs non-functioning
108
Hypopituatirism: hormone levels
all decrease except for prolactin, which increases (under inhibatory control from dopamine)
panhypopituitarism if all hormones affected
109
Hypopituitarism: causes
hypothalamus: kallman's synd, tumour, inflamm., infection, ischaemia
pituitary stalk: trauma, surgery, mass, menangioma, carotid artery aneurysm
pituitary gland: tumour, irradiation, inflammation, autoimmune, infiltration (Amyloid, haemochromatosis, mets) or ischaemia
110
Hypothalamus- thyroid axis
Hypothalamus -> TRH
Anterior pituitary -> TSH
Thyroid gland -> T3 and T4 (negative feedback)
111
Hypothyrodism: differentiation between primary and secondary
primary: increased TSH and decreased T4
secondary: low or normal TSH (problem in the pituitary)
112
Hypothyrodism: treatment
levothyroxine
113
Hyperthyrodism: causes
Grave's disease (2/3 cases)
toxic multinodular goitre (15%)- in eldery and iodine deficient -> xs secretion w/o stimulation
Toxic adenoma producting T3/4 with the rest of the gland suppressed by XS TSH
Ectopic thyroid tissue
114
Hyperthyrodism: management
B-blockers for symptoms
carbimazole
radioiodine
thyroidectomy
115
Cushing's syndrome; ACTH dependant causes (3)
Cushing's disease: bilateral adrenal hyperplasia from ACTH secreating pituitary adenoma
Ectopic ACTH production (non-pituitary, eg small cell carcenoma)
Ectopic CRH production (rare) from thyroid and prostate cancers
116
Cushing's syndrome: ACTH independent cause
ACTH is low due to -ve feedback
adrenal adenoma/cancer
Iatrogenic- steroids
Adrenal nodular hyperplasia
117
Metabolic syndrome: define
central obesity (BMI >30 or increased weist) + 2 of the following:
- BP 130/85 or higher
- trygliccerides 1.7mmol/l or more
- HDL low
- fasting glucose 5.6mmol or more or DM
118
Craniopharyngioma: define
Rathke's pouch tumout (not pituitary)
commonest childhood intracranial tumour
-> growth failure
adults -> ammenorrhoea, reduced libido, hypothalamic symptoms or tumour mass effect
119
Adrenal gland structure and hormones produced
```
Cortex:
- z. glomerulosa -> mineralocorticoids
- z. fasciculata -> glucocorticoids
- z. reticularis -> adrogens
Medulla -> catecholamines (Na and adrenaline)
```
120
Addison's disease: define
Primary adrenocortical failure
121
Addison's disease: treatment
replace steroids
mineralocorticoids to correct postural HTN
avoid abrupt stopping of steroids
122
Endocrine HTN: causes
hyperaldosteronism (primary: Conn's syndrome or secondary to adrenal hyperplasia )
phaeochromocytoma
123
AKI stages
1. creatine 1.5x baseline or <0.5 ml/kg/h urine output in 6 hours
2. C 2x baseline or <0.5 ml/kg/h urine output in 12h
3. X 3x baseline (or >354micromol/l) or <0.3 ml.kg.h output in 24 h or anuria for 12
124
Uteric calculi treatment
```
nephrostomy tube placement, insertion of ureteric catheters or ureteric stent placement.
shock wave lithotripsy,
percutaneous nephrolithotomy,
ureteroscopy,
open surgery
```
125
What type of anaemia is present in Haemolytic uraemic syndrome and Thrombotic Thrombocytopenic purpura?
Microangiopathic haemolytic anaemia (MAHA)
