General Medicine Review Flashcards
1
Q
name given to the type of breathing pattern a patient may develop when close to end of life, and describe the characteristics of this breathing
A
Cheyne-Stokes breathing: periods of shallow breathing alternate with periods of deeper, rapid breathing. The latter may be followed by a pause before breathing begins again. rapid, irregular.
Patient’s breathing may also make a rattling sound due to mucus accumulation due to patient not coughing mucus up-can give antimuscarinic e.g. glycopyrronium SC infusion-1.0mg/24hr to reduce resp secretions.
2
Q
what type of heart murmur might you expect a patient with PKD to have?
A
late systolic murmur heard loudest over the apex of the heart
3
Q
what sign of thyrotoxicosis is not directly due to the presence of excess thyroid hormones?
A
exophthalmos
4
Q
most important potentially treatable variable in autosomal dominant PKD?
A
HTN
but treatment has little effect on disease progression
5
Q
extra-renal manifestations of PKD?
A
liver cysts, and pancreatic cysts-rarely can cause recurrent pancreatitis
intracranial (berry) aneurysm, which can cause a SAH if rupture-sudden onset thunderclap headache
aneurysms elsewhere e.g. thoracic aorta, and can cause dissections
mitral valve prolapse-end systolic heart murmur heard loudest over apex. (?mid systolic click)
diverticulosis-formation of diverticula
male infertility-rarely, result of cyst deposition in seminal vesicles and defective sperm motility
symptoms from mass effect e.g. early satiety, GORD, low back pain, ascites, oesophageal varices, dyspnoea
6
Q
signs of PKD due to effect on kidneys?
A
abdominal pain due to renal enlargement-chronic dull ache in loin
haematuria with haemorrhage into a cyst
cyst infection
UTIs
renal calculi
HTN-retinopathy identified on fundoscopy, renal bruits, carotid bruits where HTN complicated by atherosclerosis, forceful apex beat, displaced apex with bibasal crackles and ankle oedema if HF is complication of HTN, pulse-irregularly irregular if HTN has caused AF
progressive renal failure
7
Q
a Dieulafoy lesion may present as both upper and lower GI bleeding. describe what the lesion is.
A
an ectatic (dilated) submucosal artery in the GIT, most commonly the stomach, but may also occur in small or large bowel and oesophagus.
8
Q
drugs known to aggravate C.difficile toxin infection?
A
PPIs e.g. lansoprazole and omeprazole
9
Q
meropenem is an example of what class of antibiotics?
A
beta-lactam (carbapenem)
very broad spectrum
can only be given IV
10
Q
if a CXR shows a gastric bubble to be present underneath the diaphragm, what might be the cause?
A
hiatus hernia
11
Q
how is a patient with a neuropathic foot at risk of ulcers with respect to pressure point development?
A
neuropathic foot-motor and sensory dysfunction, toe clawing results in more pressure put through the metatarsal heads and heels, predisposing to callus and ulcers.
12
Q
a patient with COPD is cyanosed. what term may be used to describe the picture of this pt?
A
a blue bloater:
CO2 is being retained by the patient due to inadequate ventilation, so the choroid plexus cells will increase the amount of HCO3- in response to the lowered pH in order to normalise it, so their breathing will be driven by hypoxia and not CO2 concentration.
13
Q
why is a patient with chronic alcoholism at risk of diabetes?
A
likely to develop chronic pancreatitis
14
Q
why might H pylori NOT be tested for in a pt with an actively bleeding duodenal ulcer?
A
test more likely to be -ve if bleeding
15
Q
confusion screen components?
A
MMSE bloods: LFTS-hepatic encephalopathy, Ca2+-hypercalcaemia, FBC-WCC, blood cultures, TFTs-hypo urine dipstick CXR CT head
16
Q
what does percussion myotonia indicate?
A
nutritional deficiency
17
Q
causes of an isolated raised bilirubin in seemingly otherwise well patient?
A
Gilbert’s syndrome: inherited disorder where problem with UDP-glucuronosyltransferase enzyme required for bilirubin conjugation by the liver. Pts have mildly elevated bilirubin. Patients have intermittent episodes of jaundice due to unconjugated hyperbilirubinaemia, but often don’t need medical help for this. Triggers to episodes of jaundice include stress, infection, dehydration, sleep deprived and surgery.
haemolysis: unconjugated hyperbilirubinaemia, haeolytic anaemia- may be noromocytic or macrocytic if many young RBCs and reticuocytes, rasied reticulocyte count , decrease haptoglobin-an acute phase reactant protein prod. by liver which binds rbc, raised bilirubin, increase urobilinogen as increased bilirubin being produced from rbc breakdown, splenomegaly, blood film, direct coombs test (DCT) for AI haemolytic anaemia- Abs to human IgG added to rbc sample and if red cells coated by Abs, they will agglutinate-+ve test.
18
Q
most common manifestation of autonomic neuropathy in pts with DM?
A
postural hypotension*
19
Q
why should bloods NOT be taken from the same arm as an IV drip is going through?
A
will show erroneus results-electrolytes which are in the fluid being infused will be higher than their concentration in the peripheral blood.
20
Q
hypernatraemia causes?
A
poor water intake e.g. in elderly patients-may have poor access if bed bound or unable to ask
diabetes insipidus
IV fluids with sodium e.g. excessive use of 0.9% sodium chloride- espec. important if given to patients with high fluid losses e.g. burns, high output stoma.
drugs with high sodium concentration
21
Q
what combination of features identified with a FBC and Us and Es are suggestive of GI bleeding?
A
low Hb raised WCC (in absence of infection) raised PLTs raised urea (with normal creatinine)
22
Q
11 diagnostic criteria for SLE?
A
A RASH POINts Medical Diagnosis
ANA-titre greater than or equal to 1:160
Renal-proteinuria, cellular casts (but pts also get haematuria, HTN, raised Us and Es, glomerulonephritis common)
Arthritis-non-erosive 2 or more peripheral joints
Serositis-pleuritis or pericarditis
Haem abnormalities-haemolytic anaemia or thrombocytopenia or leucopenia or lymphopenia
Photosensitivity
Oral ulcers-painless
Immunological abnormalities-+ve anti-dsDNA or anti-smith or antiphospholipid
Neurolog abnormalities e.g. seziures, psychosis, depression
Malar rash
Discoid rash
23
Q
features suggesting giant cell arteritis diagnosis?
A
GIANT:
granulomatous inflammation-biopsy of temporal artery
increase CRP/ESR-?more than 40/PV
age over 50 yrs
new headache
temporal tenderness/more powerful temporal arterial pulse
24
Q
causes of erythema nodosum?
A
NODOSUM: NO cause (60% of the time) drugs e.g. sulfonamides OCP sarcoidosis UC (IBD) malignancy/microbial e.g. TB, strep throat-group A streptococcus-?does pt have a sore throat
25
investigations used to confirm a diagnosis of primary biliary cirrhosis (PBC)?
bloods: LFTs-raised ALP, raised GGT, poss. mildy raised ALT/AST
late disease:increase blilrubin-liver cirrhosis, reduce albumin and increase PT as reduced liver synthetic function with irreversible fibrosis
AMA-antimitochondrial antibody +ve M2 subtype in 98% of cases
high Igs, espec. IgM
TSH and cholesterol may be raised
imaging: US-exclude extrahepatic cholestasis
Liver BIOPSY-granulomas around bile duct, progressing to cirrhosis
26
complications of PBC (primary biliary cirrhosis)?
```
osteoporosis
osteomalacia and coagulopathy as malabsorption of fat soluble vitamins
portal hypertension
ascites
variceal haemorrhage
hepatic encephalopathy
HCC
```
27
what diseases is PBC associated with?
```
RA
Sjogrens
thyroid disease
systemic sclerosis
renal tubular acidosis
keratoconjunctivitis sicca
membranous glomerulonephritis
```
28
symptomatic tment of PBC?
pruritis-give cholestyramine, or naltrexone or rifampicin
cholestyramine-bile salt sequestrant-binds bile acids in the small bowel to form an insoluble complex which is excreted in the faeces, hence reduces bile acid levels in the serum and their deposition under the skin that causes itching.
diarrhoea-codeine
OP prevention-Ca2+ and Vit D, bisphosphonates
29
drugs likely to cause acid reflux?**
```
NSAIDs
steroids
Ca2+ channel blockers, nitrates
bisphosphonates e.g. alendronate
antichoinergics
```
30
which LFT can be used to screen for alcohol abuse?
GGT-gamma glutamyltransferase
| this will be raised in 75% of life-long alcohol drinkers
31
cardiac problems associated with hypothyroidism?
bradycardia
pericardial effusion
congestive cardiac failure
32
causes of pt presenting with a tremor?
parkinson's disease-pill rolling tremor at rest, disappears with movement
parkinsonism
drug ADRs e.g. EP side effects of antipsychotic medication, beta 2 agonists in the tment of asthma
benign essential tremor
hyperthyroidism
phaeochromocytoma-problems with life threat. HTN and cardiac arrhythmias
anxiety
33
why must TFTs be viewed with caution in a patients who is acutely unwell?
TFTs often deranged (sick euthyroid syndrome)
common for all to be low (TSH and T3 and T4)
should rpt after recovery
pituitary disease would also produce these results
34
causes of a raised or lowered thyroxine binding globulin that may result in abnormal T4 measurement but normal TSH?
raised: high oestrogen states e.g. pregnancy, OCP
hypothyroidism
lowered: protein deficiency: malnutrition, chronic liver disease, nephrotic syndrome
high corticosteroid levels
thyrotoxicosis
35
how is a diagnosis of phaeochromocytoma made?
demonstrate raised metanephrines in the plasma and 3 24hr urine samples
if borderline, can measure free plasma metanephrines after giving clonidine, would expect metanephrines to be suppressed in those without the tumour.
36
A patient presents with true polycythaemia (raised packed cell volume due to raised red cell mass). What renal differentials could be responsible for this?
Polycystic kidney disease
Renal cell carcinoma
both of which will raise erythropoietin stimulating increase in rbc production.
37
common causes of neutrophilia?
```
bacterial infection
inflammation
necrosis e.g. post MI
corticosteroid tment
metabolic disorder e.g. renal failure
myeloproliferative disorder
malignancy
```
38
common causes of neutropenia?
```
post-chemo
post-radio
ADRs e.g. clozapine, carbimazole
viral infection
Felty syndrome (RA, splenomegaly and reduced WCC, with rpt infections)
```
39
common causes of lymphocytosis?
viral infections
chronic infections e.g. TB
chronic lymphocytic leukaemia
lymphomas
40
what test can be used to distinguish between the different causes of Vit B12 deficiency?
Schilling test: oral radioactively labelled vitB12 and normal IM vitB12 given, urine collected over 24hrs, with vitB12 malabsorption urinary vitB12 will be reduced as less absorbed, when test rpted with oral intrinsic factor given at same time as oral dose of vit B12, if now normal test then know inadequate intrinsic factor, if abnormal problem most likely in ileum e.g. bacterial overgrowth-can test by giving Abx or do hydrogen breath test giving oral carbohydrate.
41
investigation to confirm thalassaemia diagnosis?
Hb electrophoresis
42
when does the formation of multiple cysts in the kidney which enlarge with time, known as cystic degeneration, occur regularly?
in patients with end stage renal disease treated by dialysis and/or transplantation
malignant tumour formation more common in such kidneys
43
USS diagnostic criteria for testing individuals at risk of autosomal dominant PKD?
15-39 yrs: 3 or more cysts (unilateral or bilateral)
40-59 yrs: 2 or more cysts in each kidney
60 yrs or older: 4 or more cysts in each kidney
below age of 30, -ve renal USS does not exclude ADPKD diagnosis, so CT and MRI may also be useful, and may need molecular genetic testing-PKD1 and 2 genes.
once established in 1 family member, good to screen others-can then maybe protect themselves against the complications of the disease e.g. ensure good diet and adequate BP control.
can also determine whether a young memeber of family can safely donate a kidney to a parent affected.
44
why is bruising more common in pts with CKD?
platelet abnormality*
45
genetic abnormalities in autosomal dominant PKD?
PKD1 on chromosome 16-polycystin 1 protein encoded-regulates PKD2 channel activity-Ca2+ ion channel.
PKD2 gene chromosome 4
46
what causes renal function loss in PKD?
compression by cysts
reactive fibrosis
apoptosis of healthy tissue
renal function declines more rapidly if rapid growth in cyst size, can be slowed down e.g. vasopressin V2 receptor inhibitor
47
what is Felty's syndrome?
combination of RA, splenomegaly and neutropenia
48
if a patient presents with an acutely inflamed joint, what condition MUST be ruled out and what investigation is required in order to do this?
SEPTIC ARTHRITIS
as can causes irreparable joint destruction in less than 24hr. consider that inflammation may be less in IC pt e.g. on corticosteroids, or if underlying joint disease e.g. OA.
must do a joint aspiration- synovial fluid then sent off for analysis-synovial fluid microscopy-gram stain and CULTURE essential to rule out/in septic arthritis-turbid yellow, reduced viscosity, 10-10,000 WBC, neutrophils more than 90%, polarised light microscopy-presence of negatively birefringent crystals diagnostic of gout (monosodium urate crystals).
49
in a patient presenting with joint pain, why might the doctor want to palpate the heel and Achilles tendon?
identify plantar fasciitis (like walking on pebbles?*) and Achilles tendonitis (enthesitis) often associated with seronegative rheumatological conditions.
50
blood tests to be performed in presentation of a patient with an acutely swollen and painful joint?
FBC-raised WCC, neutrophilia in septic arthritis, RA, gout?, anaemia-trauma causing haemarthrosis?, assess for anaemia and neutropenia before starting allopurinol for gout*
ESR
CRP-maybe slightly elevated in OA
clotting studies-haemophilia being responsible for haemarthrosis?
Us and Es-renal function prior to medication starting e.g. NSAIDs for gout
blood culture-for septic arthritis, can guide later Abx choice, at least 2
lactate-isoenzymes in septic arthritis
serum urate-gout
RF, ANA, other autoantibodies, HLA-B27 guided by presentation
viral serology, HIV serology, hepatitis serology, urine chlamydia PCR in suspected reactive arthritis. gonococcal swabs-urethral, rectal, cervical, pharyngeal.
51
presentation of chronic pancreatitis?
this is 1 of the common causes of GI malabsorption in the UK, along with coeliac disease and crohn's disease.
symptoms of GI malabsorption=diarrhoea, steatorrhoea, lethargy, weight loss.
specific to chronic pancreatitis=epigastric pain 'bores' through to back, relieved by sitting forward or hot water bottles on epigastrium/back-look for erythema ab igne-mottled dusky greyness
pt may also have bloating and brittle diabetes
symptoms relapse and worsen
pancreatic calcifications confirm diagnosis on CT
52
causes of chronic pancreatitis?
```
alcohol
more rarely:
familial
cystic fibrosis
haemachromatosis
pancreatic duct obstruction e.g. gallstones/tumour
hyperparathyroidism
congenital
```
53
complications of chronic pancreatitis?
```
pancreatic carcinoma
diabetes
pseudocyst
biliary obstruction
gastric varices
local arterial aneurysm
splenic vein thrombosis
```
54
what features would you want to know about in the hx of a patient with an isolated raised ALT?
```
age
gender
alcohol
IV drug abuse
risky travel
contacts
DM
BMI, lipids
autoimmunity
fever
pregnant
FH of autoimmunity, unexplained cirrhosis
```
55
abnormal LFTs in patients who are asymptomatic occur most commonly due to what causes?
```
DM and metabolic syndrome-increased likelihodd of non alcoholic fatty liver disease (NAFLD)
chronic hepatitis B
chronic hepatitis C
excessive alcohol intake
drugs
```
56
what condition has the worst prognosis out of all the complications of liver cirrhosis?
hepatorenal syndrome
57
pathophysiology of hepatorenal syndrome?
splanchnic vasodilation
activation of RAAS, SNS, ADH
results in renal vasoconstriction
no histological damage to kidney
58
why is oesophageal Ca unlikely if a pt complains of odynophagia?
implies mucosal sensation is intact
59
systemic manifestations of IBD?
skin: erythema nodoum (NODOSUM-NO known cause, drugs e.g. sulfonamide Abx, OCP, sarcoidosis, UC (IBD), malignancy and microbial-TB.
eyes: anterior uveitis, episcleritis
joints: enteropathic arthritis-seronegative spondyloarthropathy, sacroileitis, spondylitis, peripheral arthritis
mouth:aphthous ulcers
liver: steatosis, GSs, primary sclerosing cholangitis
kidneys: UTIs, nephrolithiasis (stones), fistulae, hydronephrosis
phlebitis, thrombi
60
advice to patients with wilson's disease when started on medical treatment?
treatment=penicillamine
must warn pt to present if develop sore throat, fever or bruising as drug can cause decrease WCC and PLTs.
drug can also cause lupus
61
ADRs of 5-ASAs?
```
dangerous:
hepatitis
pulmonary toxicity
pericarditis
pancreatitis
aplastic anemia
thrombocytopenia
leukopenia
```
62
chronic liver disease complications?
portal hypertension-opening up of portosystemic anastamoses, varices-oesophageal, caput medusae, rectal varcies, ascites, oedema, splenomegaly
ascites and oedema
jaundice
hepatic encephalopathy and dementia
bleeding-reduced clotting factor production
SBP, infections-reduced Ig production, reduced removal of bacteria from blood via detoxifying action of liver
hepatocellular carcinoma-Hep B most common cause
GSs and bile duct stones
malnutrition
osteoporosis-less vitamin and mineral storage, vit D malabsoprtion as impaired bile production with bile salts necessary for fat absorption and subsequent absorption of fat soluble vitamins.
63
what classification can be used to assess severity of liver cirrhosis, and so help in determining requirement of liver transplant?*
```
Child-Pugh classification
scoring based on bilirubin, albumin, PT, presence of encephalopathy and ascites, each scored either 1, 2 or 3
total score less than 7=A
7-9=B
more than 9=C=worst severity.
```
64
why should a patient with Crohn's disease be asked about urinary symptoms?
may present with pneumaturia-gas bubbles in the urine, if there is a fistula formed due to the transmural inflammtion of the disease, between the colon and the bladder.
may also be faecuria.
65
most common presenting symptom in PBC (primary biliary cirrhosis?
fatigue
66
what conditions should be suspected if a urine dipstick for protein is negative but other tests suggest proteinuria?
multiple myeloma
chronic lymphocytic leukaemia
amyloidosis
as in these conditions, proteinuria predominated by globulins and Ig light chains, rather than albumin and stick-reagents are albumin-specific.
67
when might proteinuria occur in normal patients?
when febrile illness
68
causes of haematuria?
```
note whether painless or with pain
painless: glomerulonephritis
tumour-kidney, prostate, bladder, ureter
TB
schistosomiasis
interstitial nephrits
ATN
renal ischaemia
coagulation disorders
```
pain:
UTI
renal stones with obstruction
loin pain-haematuria syndrome
```
either:
adult PKD
UTI
renal stones without obstruction
reflux nephropathy and renal scarring
```
69
causes of proteinuria?
```
diabetes mellitus
glomerulonephritis
amyloidosis
SLE
drugs e.g. gold, penicillamine
multiple myeloma
infection
fever
severe HTN
burns
HF
```
transient in fever, severe exertion and HTN, burns, HF and orthostatic proteinuria.
70
in renal hx, what is it important to ask about in terms of PMH?
HTN-may be causative or result of renal disease
DM-diabetic nephropathy-CKD, and renovascular disease
vascular disease e.g. intermittent claudication-PAD, CAD-angina, prev MIs, as renovascular disease then more likely
past hx of urinary tract stones or surgery
recurrent infections-UTIs may be assoc with renal scarring, and URTIs may be assoc. with glomerularnephritis and/or vasculitis e.g. wegener's granulomatosis
anaemia
71
why would illicit drug use e.g. cocaine and ecstasy, be important to know about in suspected kidney failure?
they can cause rhabdomyolysis and myoglobinuria leading to AKI (intrinsic)
72
why might we want to know about death form intracranial bleeds in the FH of someone with suspected PKD?
because PKD is inherited in autosomal dominance pattern, and is assoc. with IC berry aneurysms which can cause SA haemorrhages.
73
extra-renal assoc. of alport's syndrome-a glomerulonephropathy that can cause nephritic syndrome?
sensorineural deafness
74
important components to SH of renal patient?
ICE-espec. with RRT in end-stage renal disease, and incontinence
smoking
alcohol
diet-renal stones-H20, calcium, oxalate-choc, rhubarb. ensure not excessive protein intake in CKD-won't be able to excrete urea adequately, and salt intake in HTN and CKD.
75
causes of polyuria?
```
psychogenic
diabetes insipidus-cranial and nephrogenic
diabetes mellitus
hypercalcaemia
SVT-release of ANP
```
76
drug with benefit on mortality of patients with type 2 DM who develop microalbuminuria?
ACEI
77
in the management of a UTI, why might a patient be advised to drink cranberry juice, and why must the DH of this patient be checked carefully?
cranberry juice may inhibit the adherence of bacteria to the bladder uroepithelial cells
BUT it is a CYP450 inhibitor, so caution with patients on warfarin-can significantly increase bleeding risk.
78
why might a patient with crohn's disease NOT be given azathioprine or mercaptopurine as maintenance treatment?
```
deficient TPMT (thiopurine methyltransferase) activity
other contraindications e.g. previous episodes of pancreatitis
```
instead might be maintained on methotrexate-*RISK OF ACUTE INTERSTITIAL PNEUMONITIS- this is an emergency!
79
when might monitoring for changes in bone mineral density be considered in patients with crohn's disease?
consider monitoring in children and young people with RFs e.g. low BMI, low trauma fracture or continued or repeated glucocorticosteroid use.
80
only cure for primary biliary cirrhosis?
liver transplant
| BUT not always curative as disease can recur in the transplanted liver.
81
how does CKD affect PLTs?
CKD causes platelet function disorder
| *look for bruising o/e of patients with CKD
82
treatment of acutely bleeding oesophageal varices?
IV terlipressin-vasconstrictor, also used in tment of hepatorenal syndrome
OGD with injection sclerotherapy and banding?*
83
test for AI haemolytic anaemia?
direct antibody test (DAT) test/ Coombs' test:
antibodies directed against human Ig are added to a sample of the patient's red cells. if the red cells are coated in Abs (so pt has an AI haemolytic anemia) the rec cells will agglutinate.
84
how does diabetes mellitus affect the kidneys and how can nephropathy in this case be managed?
renal hyperperfusion due to hyperglycaemia increase GFR and causes hypertrophy and increased renal size. Mesangial hypertrophy and focal glomerulosclerosis (kimmelsteil-wilson lesion) occur later due to raised glomerular pressure. causes microalbuminuria, which progresses to proteinuria and ESRF.
Tx: good glycaemic control-delays onset and progression
BP control-ACEIs or AngII RBs, even if normotensive in patients with microalbuminuria, slow renal disease progression by reducing intraglomerular pressure.
smoking cessation.
85
nephropathies associated with infection?
glomerulonephritis e.g. post streptococcal, Hep B/C, HIV, syphilis.
vasculitis e.g. Hep B or C, post strep or staph septicaemia
interstitial nephritis e.g. HIV, CMV, Hep B, bacterial pyelonephritis.
86
effects of myeloma on the kidneys?
light chains block renal tubules and have direct toxic effect on tubular cells, causing ATN.
AKI
CKD
amyloidosis-may cause proteinuria and nephrotic syndrome
hypercalcaemic nephropathy
87
methotrexate ADRs?
```
myelosuppression
mouth ulcers
hepatotoxicity, liver cirrhosis
nephrotoxicity
pulmonary fibrosis
acute interstitial pneumonitis-life threatening complication often presents subacutely with cough, dyspnoea and fever over a few weeks, can rapidly progress to resp failure with fluid filling the alveoli causing hypoxia, requires MTX stopping and administering corticosteroids or cyclophosphamide.
```
88
sulfasalazine ADRs?
```
reversible azoospermia
nausea and vomiting, GI upset
hepatitis
rash
myelosuppression
```
89
why should we test Us and Es and LFTs in patient with supsected RA?
check function before prescribing drugs-MTX and sulfasalazine can cause hepatotoxicity, and MTX can cause nephrotoxicity
renal function can be impaired in RA with secondary amyloidosis causing proteinuria and nephrotic syndrome.
90
empirical Abx treatment septic arthritis?
IV flucloxacillin 4-6weeks
91
why might you examine the soles of the feet of a patient with suspected reactive arthritis?
look for keratoderma blennorrhagica- a sign of reactive arthritis
disease can also manifest with circinate balanitis
92
pharmacological agent of choice in wegener's granuloamtosis?
cyclophosphamide, given in comb with high dose corticosteroids
93
what important qns should you ask to rule out another co-existing disease in suspected PMR?
unilateral headache?
scalp tenderness?
visual problems?
tongue and jaw claudication?
ensure no coexisting GCA that can cause blindness
94
how is clinical response to treatment in polymyositis measured?
measure creatine kinase levels
| these should decrease in response to active treatment
95
complications of paget's disease and who is affected?
```
male, middle aged, FH, caucasian
bone pain
bone deformity and enlargement
increaed temp over affected bones
pathological fractures
secondary OA
hearing loss and tinnitus
```
affects skull, pelvis, femur, tibia and lumbar spine commonly
96
Ab to aid diagnosis and prognosis of wegener's granulomatosis?
c-ANCA
97
pathophysiology of grave's disease?
antibodies produced which mimic TSH. antibodies known as TSH receptor antibodies or thyroid-stimulating immunoglobulins (TSIs). act on TSH receptors in the thyroid gland to simulate increased production and release of T3 and T4. cause thyroid follicular cell hyperplasia.
98
what monitoring is required when initially starting an ACEI?
require renal function and electrolyte monitoring with each dose change until max. tolerated dose is determined, as risk of renal failure and hyperkalaemia, especially in patients with co-existing PVD and CAD as may also have silent renovascular disease.
99
what criteria should be met for CKD to be diagnosed?
eGFR less than 60ml/min on 2 separate occasions at least 3 months apart
100
complications of cholestasis-halting of bile flow between the gallbladder and the duodenum?
hepatic fibrosis-retention of bile salts damages membranes of hepatocytes
metabolic bone disease-osteopenia, osteoporosis and occasionally osteomalacia (?due to Vit D malabsorption)
bleeding tendencies, part. nosebleeds
asthma-type wheeze
complications from investigative procedures e.g. cholangitis or acute pancreatitis from ERCP, and bleeding from BIOPSY.
101
indications and MOA of ursodeoxycholic acid?
used to dissolve gallstones in a patient with a functioning gallbladder
acts by reducing cholesterol content of bile, either by inhibiting hepatic cholesterol synthesis or reducing cholesterol absorption
102
in which people can diabetes mellitus be reversed?
in those who lose weight and the cause of their DM was obesity
103
how can patients be further investigated for type 1 DM if atypical presentation e.g. patient 50yrs of age or over or BMI 25 or more?
measure C peptide or diabetes specific AI antibodies, or both
104
what features constitute a diagnosis of type 1 DM in adults?
```
ketosis, but be wary that type 2 DM can present in DKA aswell!
rapid weight loss
age of onset below 50 years
BMI below 25
hx or FH of AI disease
```
105
what biochemical values are diagnostic of DKA?
```
blood ketones 3mmol/L or more,
or more than 2+ ketonuria on strip testing
venous HCO3- less than 15mmol/L,
or venous pH less than 7.3
or a combination thereof
```
106
examples of structured education programme for flexible insulin therapy in type 1 DM management that should be offered to all 6-12 mnths after diagnosis?
DAFNE-dose adjustment for normal eating
as part of structured education programmes, carbohydrate counting training should also be offered
107
how can impaired awareness of hypoglycameia in type 1 DM patients be treated?
1st reinforce principles of structured education
then off insulin pump therapy
then offer real time SC glucose monitoring if impaired awareness persists
this should be annually assessed using a scoring system
108
what is the risk with having frequent DKAs?
increased risk of cardiac arrest
109
components to an annual diabetic r/v?
advice on diet and lifestyle e.g. carbohydrate counting, recognising carbohydrate as store in body for releasing glucose
refer to retinal screening on 1st visit-should be checked annually
education sessions-DAFNE 1 week programme for type 1 DM, and DESMOND for type 2 DM (diabetes education and self management for ongoing and newly diagnosed)
glucose diary-look at their reading, compare to HbA1c, and look at site of finger pricking, look at insulin doses as matching blood sugar
check weight, BMI, BP, smoking status
check foot pulses and vibration sensation-tuning fork
check urine for protein, sugar and ketones, and send for ACR
blood test r/v-FBC-anaemia with renal disease, Us and Es-eGFR-stop metformin if less than 40, LFTs-drug metabolism, lipids, HbA1c, TFTs-endocrine
check injection sites, needle lenghts
med r/v and compliance, explain taking med. with food e.g. metformin, as metabolised when food taken
dementia screening
110
routes of transmission of hepatitis B and C?
Hep B=blood and body fluids, Hep C=blood
blood to blood transmission: IV drug use-equipment sharing between users, needlestick injury, blood transfusion
sexual transmission-vaginal or anal intercourse
infected tattoo equipment-less than 1% Hep C transmission through sex but likelihood increases if person also infected with HIV.
vertical transmission from infected mother to child
haemodialysis also for Hep C
111
viral hepatitis vaccinations?
available for Hep A and Hep B
112
hepatitis types of viruses?
Hep A and C= enveloped RNA viruses
| Hep B=dsDNA enveloped virus
113
benefit of Hep B vaccine in addition to protecting against Hep B infection?
reduces risk of developing hepatocellular carcinoma
114
presentation of hepatitis B infection?
often vague presentation
new infection may present with a flu like illness
usually insidious illness onset with nausea, anorexia and right upper abdomen ache
some patients develop jaundice, with progressive darkening of urine and lightening of stools
fever usually mild if present
profound malaise, don't want to smoke or drink alcohol
acute infection can present in fulminant hepatic failure
can cause decompensated liver disease with ascites, encephalopathy and GI bleeding
115
what is chronic hepatitis B defined by?
presence of Hep B surface antigen (HBsAg) in blood or serum for more than 6 months
can be divided into Hep B e antigen (HBeAg) positive or negative, with e antigen presence associated with higher rates of viral replication and so increased infectivity
116
symptoms of chronic Hep B?
fatigue, nausea, anorexia, RUQ pain
with liver disease progression-clubbing, asterixis, spider naevi, gyaecomastia, jaundice, ascites, hepatomegaly, splenomegaly, bleeding varices, caput medusae, testicular atrophy, oedema
117
the progression of liver disease due to Hep B is associated with what blood marker?
Hep B virus DNA levels in the blood
118
investigations for Hep B infection?
specific to Hep B:
HBsAg-only serological marker detectable in 1st 3-5 wks, usually 30days for detection, persistence for more than 6mnths defines carrier status, and follows 5-10% of infections
HBeAg-usually present for 1.5-3mnths post acute illness, anti-HBs-antibodies to HepBsurfaceantigen alone implies vaccination, anti-HBe, anti-HB core-this implies past infection (antibodies), but also raised in acute infection
quantitative Hep B virus DNA
HBV genotype (for those considered for interferon)
HDV serology
FBC
Us and Es
LFTs-bilirubin, ALT/AST-ALT likely raised more so than ALP, GGT
ferritin
clotting-PT, APTT, fibrinogen
AI screen-anti-liver and kidney microsomal-1 Abs, ANA, anti-smooth muscle Ab
caeruloplasmin
lipid profile
Hep C screen
USS and alpha fetoprotein-screening for liver Ca
disease staging in secondary care-transient elastography and liver biopsy
119
relevance of being HBeAg positive aswell as HBsAg positive?
individuals are more infectious
120
tment of acute Hep B infection?
admit to hosp if ser unwell, or mange in primary care
notify health protection unit-faciliate approp. surveillence e.g. contact tracing
hep serology to confirm diagnosis
refer to approp specialist
supportive symptom tment-analgesia, fluids, anti-emetics
avoid alcohol
r/v med.s, stop non-essentials
antivirals only in fulminant hepatitis when acute pres.
121
tment of adults with HBeAg-positive chronic hep B and compensated liver disease?
offer 48wk course of peginterferon alfa-2a as 1st line, tenofovir 2nd line
offer tenofovir in pregnancy or if breast feeding
122
complications of Hep B infection?
```
fulminant hepatic failure
prolonged cholestasis
relapse
chronic hepatitis
liver cirrhosis
HCC
glomerulonephritis
cryoglobulinaemia
```
123
HCC screening in patients with chronic Hep B infection?
6mnthly US and alpha-fetoprotein measurement in those with significant cirrhosis or fibrosis
124
pathology of AI hepatitis?
thought environmental trigger e.g. virus in genetically predisposed individual e.g. HLA-DR4, type 1 disease assoc. with other AI disease e.g. coeliac disease, thyroiditis and pernicious anaemia- Abs against intrinsic factor and parietal cells?, causes a T cell mediated immune response producing necroinflammation, and progressing to cirrhosis and fibrosis.
125
clinical features of AI hepatitis?
2 presentation peaks:
teens and early 20s-acute hepatitis with jaundice and very high aminotransferases which remain high, and often features of cirrhosis with hepatosplenomegaly, cutaneous striae, acne, hirsutes, bruises and sometimes ascites
can also be features of an AI disease e.g. pleurisy, lung fibrosis, fever, polyarthritis and glomerulnephritis
peri and post menopausal: asymptomatic or fatigue, picked up on blood tests
rare overlap syndromes with PBC and PSC
126
results of investigations into AI hepatitis?
FBC-normochromic normocytic anaemia, leucopenia, thrombocytopenia
clotting-raised PT
LFTs-raised ALT/AST with lesser elevations in ALP and bilirubin, serum gamma-globulins high, part. IgG
type 1 disease with antibodies=ANA, anti-smooth muscle(anti-actin), soluble liver antigen (anti-SLA/LP), this presents in adults of any age and gender
type 2 disease with antibodies=anti-liver/kidney microsomal (anti-LKM1), more commonly progresses to cirrhosis, mainly affects girls and young women
liver biopsy-plasma cell infiltration, lymphocyte infiltration, fibrosis
127
most common cause of hepatocellular carcinoma worldwide?
chronic hepatitis B infection
128
AI hepatitis tment?
budesonide 3mg BD or TDS
alternatively, oral pred 30mg daily for at least 2 wks, then slow reduction and maintenance 10-15mg daily.
azathioprine added as steroid sparing, and can be used as sole maintenance tment in some pts, ensure measure TPMT activity
remission achieved in more than 80% of cases
liver transplant if tment fails, but disease may recur
HCC less frequent than with viral-induced cirrhosis
129
clinical features of multiple myeloma?*
pt typically aged between 45 and 65
presents with: weakness
bone pain
backache
pathological fracture, osteoporosis-vertebral compression fractures
symptoms of hypercalcaemia due to marrow cell proliferation and increased osteoclast activity-abdo pain, polyuria, nausea, depression, thirst
130
results of investigations in multiple myeloma?
FBC: macrocytic anaemia
CRP/ESR-ESR raised due to raised plasma viscosity due to Ab light chains
Us and Es-deranged with renal disease-renal tubular blockage by light chains, AKI, CKD, amyloidosis-nephrotic syndrome and proteinuria, damage from hypercalcaemia
urine dip-proteinuria-may be -ve as test for albumin but protein mainly light chain Abs, test for bence-jones proteins=Ab light chains
serum protein electrophoresis-characteristic abnormal band
X-ray-multiple punched-out defects-pepper pot skull, also pelvis and prox femur, crushed vertebra, or a solitary lytic tumour in a large bone metaphysis. osteoporosis.
131
management of mutliple myeloma?
```
analgesia
correct fluid balance and hypercalcaemia
treat pathological fractures
chemotherapy-alkylating toxic agents
corticosteroids
radiotherapy for solitary plasmacytomas
```
132
what is multiple myeloma?
a monoclonal malignant proliferation of plasma cells producing diffuse bone marrow destruction and failure. overproduction of monoclonal Ab-detected in plasma-serum protein electrophoresis and raised ESR, and urine-bence-jones proteins-light chain part of Ab. osteolytic bone lesions, renal disease and immune deficiency.
133
factors assoc. with more rapid progression of Hep C infection to severe liver disease?
```
over 40 years at time of infection
male
high alcohol intake
co-infection with HIV or Hep B-leads to earlier and more severe liver disease
immunosuppressive therapy
```
134
how is ongoing infection with Hep C in those with positive Hep C serology confirmed?
testing for HCV RNA
there is loss of this within the 1st 2 months of infection if the acute hepatitis spontaneously resolves (occurs in 25%)
Abs stay in the blood lifelong regardless of treatment
135
what other viruses should be tested for in those with Hep C?
Hep A, B and HIV
| immunise against Hep A and B if no evidence of previous infection-antibodies
136
drug tment for chronic hep c?
peginterferon alfa-2a or 2b weekly SC injections and daily oral ribavirin
this can treat genotypes 2 and 3, and requires 24 weeks
137
defects in which gene assoc. with most cases of hereditary haemochromatosis?
HFE
138
main investigation used in monitoring patients with hereditary haemochromatosis?
serum ferritin, as corresponds with symptoms and risks of complications
139
management of hereditary haemochromatosis?
Venesection should be carried out by removing 400-500 ml of blood (200-250 mg iron) weekly or every two weeks. Adequate hydration before and after treatment and avoidance of vigorous physical activity for 24 hours after phlebotomy are recommended.
C282Y homozygotes without evidence for iron overload could be monitored annually and treatment instituted when the ferritin rises above normal.
Before starting venesection, pts should be assessed for complications (including diabetes mellitus, joint disease, endocrine deficiency (hypothyroidism), heart failure, porphyria cutanea tarda and osteoporosis), which should be managed regardless of whether or not HC is the underlying cause and whether there is symptomatic relief or improvement during phlebotomy.
To minimise the risk of additional complications, patients could be immunised against hepatitis A and B while iron-overloaded.
Liver transplantation:
Hepatic decompensation with ascites, spontaneous bacterial peritonitis, encephalopathy, variceal haemorrhage and early small tumour formation may require assessment for liver transplantation.
140
how does osteomalacia occur?
due to Vit D deficiency- causes low Ca2+ and PO43-, and secondary hyperparathyroidism.
osteomalacia occurs with loss of skeletal mass caused by inadequate bone osteoid mineralisation after closure of the growth plates.
90% vit D from sunlight, rest from dietary intake-oily fish, cod liver oil, egg yolks, fortified breakfast cereals
141
recommended daily Vit D intake in adults in UK?
400IU (10 micrograms/day)
142
presentation of vit d deficiency in adults?
pain and proximal muscle weakness, general lack of well being
rib, hip, pelvis, thigh and foot pain typical
more diffuse muscular aches and pains also typical e.g. limbs and back
fatigue
differentials: PMR, RA, polymyositis, multiple myeloma, hypothyroidism
143
associations of minimal change disease?
most common cause of nephrotic syndrome in children, often follows an URTI
clinically nephrotic syndrome with proteinuria,increased risk of UTIs and pneumococcal peritonitis, so give prophylactic penicillin if oedematous
assoc. with atopy in children
electron microscopy-fusion of podocyte foot processes so loss of filtration slit diaphragm-filter leak
may be related to underlying Hodgkin's disease in adults
144
prognosis in focal segmental glomerulosclerosis?
up to 50% of patients progress to end stage kidney disease over several yrs, although progression may be halted by corticosteroid tment
a variant collapsing glomerulonephropathy assoc. with HIV
disease involves collagen deposition causing glomeular scarring, and fusion of podocyte foot processes
145
most common cause of nephrotic syndrome in adults?
membranous glomerulonephropathy:
immune complex deposition, IgG autoantibodies destroy podocytes
may respond to alternating treatment with corticosteroids and cyclophosphamide
can be secondary to SLE, chronic hep B, use of gold or penicillamine e.g. rheumatological diseases and wilson's disease.
146
what is concerning about crescenteric glomerulonephritis?
e.g. which occurs with systemic vasculitis e.g. wegener's granulomatosis, assoc. with ANCA-abnormally activates neutrophils which cause endothelial damage
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS-progresses to end stage renal disease within a a few months without tment.
prednisolone and cyclophosphamide generally effective before severe renal damage occurs
may require plasma exchange
goodpastures syndrome another example, due to autoantibodies directed against type IV collagen-component to both glomerular and pulmonary BM
147
ADRs of ACEIs?
```
persistent dry cough
renal impairment, AKI
hyperkalaemia
rash
hepatitis
angioedema
```
148
define nephrotic syndrome?
proteinuria with more than 3.5g/24hr protein loss in the urine, plus hypoalbuminaemia and oedema
149
characteristics of nephritic syndrome?
haematuria
proteinuria-less than in nephrotic syndrome
HTN
decrease urine output due to poor renal function, eGFR reduced, increased creatinine and renal failure
*PHAROAH
150
if a patient has an eGFR of 75, and this is the same at 3 mnths, would the patient be classed as having CKD?
patient would only be classified as CKD stage 2 if other evidence of chronic kidney damage:
persistent microalbuminuria
persistent proteinuria
persistent haematuria (after exclusion of other causes e.g. urological disease)
kidney structural abnormalities as demonstrated on US or other radiological tests e.g. PKD, reflux nephropathy
biopsy-proven chronic glomerulonephritis
151
investigations in CKD?
renal function?-eGFR-often given if request serum creatinine
Us and Es: Na+ usually normal, may be low, K+ raised, HCO3- low, high phosphate, Ca2+ may be normal, low or high, serum albumin low if nephrotic syndrome or malnourished
BC continued: ALP raised when bone disease develops e.g. osteitis fibrosa cystica, rising PTH as renal function declines, serum lipid profile-often dyslipidaemia, plasma glucose-detect undiagnosed DM or assess control
haem: normochromic normocytic anemia-decrease erythropoietin prod., BM dysfunction
serology: autoantibodies e.g. c-ANCA-wegener's, ANA-SLE, serum complement, Hep serology-esnure not infected and vaccinate against Hep B, HIV-performed before dialysis or transplantation
urine: urinalysis-proteinuria, haematuria and red cell casts
pyuria and/or white cell casts suggests interstitial nephritis or UTI, spot urine for total protein:creatinine, 24 hr urine collection for total protein and creatinine clearance, urine ACR
serum and urine protein electrophoresis-?multiple myeloma
ECG and echo-LV hypertrophy and ischaemia? assess function
renal USS-small kidneys advanced CKD, initially large in diabetic nephropathy
retrograde pyelogram if suggestion of obstrcution despite normal US
CT with IV contrast-define renal masses and cysts, most sensitive for renal stones
micturating cystourethrogram: for vesicoureteric reflux diagnosis
RENAL BIOPSY
152
in a pt newly diagnosed with eGFR less than 60, how can rapid progression be assessed?
rpt serum creatinine measurement within 5 days
153
role of statins in patients with CKD?
atorvastatin 20mg should be offered for primary or secondary prevention of CVD to those with CKD, increase dose if more than 40% reduction in non-HDL cholesterol is not achieved and eGFR is 30 or more
consult renal specialist to agree higher doses when eGFR less than 30
154
why might ACEIs have to be stopped in patients with CKD?
if plasma K+ reaches 6mmol/L or more and other drugs known to promote hyperkalaemia have been stopped
155
how are mineral and bone disorders managed in CKD?
if vit d deficient, offer colecalciferol or ergocalciferol
if vit d defic corrected and mineral and bone disorders persist, offer alfacalcidol or calcitriol if GFR less than 30
offer bisphosphonates for OP prevention and tment if indicated in those with eGFR 30 or more
156
what should be assessed before renal transplantation and give some contraindications?
virology status: CMV, Hep B and C, HIV, EBV, varicella-zoster-all may cause severe disease when immunocompromised
existing urine ouput, and CVD?
previous TB?-may reactivate, so proven cases and high risk groups given isoniazid and pyridoxine (vit B6)
ABO blood group and tissue typing for HLA
ensure pre-op K+ controlled or may need dialysis
CIs:
active infection
Ca
severe heart disease
157
complications of renal transplantation?
post-op: bleeding, infection, oliguria, urinary leaks, thrombosis
acute rejection (less than 6mnths)-rising serum creatinine with/without fever and graft pain. graft biopsy=immune cell infiltrate and tubular damage. tx-high dose methylprednisolone IV, resistant cases require anti-thymocyte globulin (ATG)
chronic rejection (more than 6mnths)- interstitial fibrosis and tubular atrophy. present with gradual rise in creatinine and proteinuria. graft biospy shows vascular changes, fibrosis and tubular atrophy. not responsive to increase immunosuppression.
ciclosporin/tacrolimus toxicity-afferent arteriole vasoconstriction acutely, chronc-tubular atrophy and fibrosis.
INFECTION
malignancy e.g. skin Ca, lymphoma (EBV)
atheromatous vascular disease
HTN
158
why is haemofiltration used for critically ill pts?
less haemodynamic instability
159
why is risk of obesity with peritoneal dialysis?
glucose contained in dialysis fluid as osmotic agent to achieve ultrafiltration across peritoneal membrane
160
characteristic biochemical features of HONK, distinguishing it from DKA?
hypovolaemia
marked hyperglycaemia (30mmol/L or more) without significant hyperketonaemia (blood ketones less than 3mmol/L) or acidosis (pH more than 7.3, venous HCO3- more than 15mmol/L)
osmolality usually 320mOsm/kg or more
161
complications of HONK?
cerebral oedema
arterial and venous thrombosis, MI, stroke, DVT, PE
foot ulceration
ARDS
rhabdomyolysis
multi-organ failure
central pontine myelinolysis-nerve demyelination in the brainstem, often complication in patients with profound life threatening hyponatraemia.
162
why should Hartmann's solution NOT be prescribed in a patient with DKA?
K+ component, and risk of hyperkalaemia due to metabolic acidosis*
also fixed IV insulin so glucose isn't brought down too quickly*
163
why would we be concerned about chest pain in a patient with nephrotic syndrome?
may be indication of PE due to hypercoagulable state as loss of antithrombin III protein in the urine so inability to inactivate clotting factors
164
causes of restless legs syndrome?
primary (idiopathic), thought to be in someway related to dysfunction in dopaminergic system, with relation to Fe as Fe important for dopamine metabolism, and Fe deficiency known to be a cause.
secondary: stage 5 CKD
Fe deficiency anaemia
pregnancy
adverse reaction to drugs e.g. beta blockers, ADs, lithium and dopamine antagonsits e.g. antipsychotics and metoclopramide.
165
criteria for restless legs syndrome diagnosis?
Essential:
urge to move the legs, usually (but not always) accompanied by uncomfortable or unpleasant (and difficult to describe) sensations in the legs.
urge to move and any accompanying unpleasant sensations begin or worsen during periods of rest or inactivity such as lying or sitting.
urge to move and any accompanying unpleasant sensations are partly or totally relieved by movement such as walking, bending, stretching, etc, at least for as long as the activity continues.
urge to move and any accompanying unpleasant sensations are worse in the evening or at night rather than during the day, or only occur in the evening or night.
The above symptoms cannot be accounted for as symptoms primary to another medical or a behavioural condition. Examples given in the criteria are myalgia, venous stasis, leg oedema, arthritis, leg cramps, positional discomfort, or habitual foot tapping.
Supportive criteria:
Positive response to dopaminergic treatment.
Periodic limb movements during wakefulness or sleep.
Positive family history of RLS amongst first-degree relatives.
Lack of profound daytime sleepiness
166
symptoms of iron deficiency anaemia?
```
fatigue
SOBOE
headaches
dizziness
faintness
tinnitus
palpitations
angina if pre-existing CAD
anorexia
sore tongue and taste disturbance
hair loss
```
167
signs on examination of a patient with Fe deficiency aneamia?
pallor-look at palmar creases and conjunctivae
koilonychia-spooning of nails with Fe deficiency
angular cheilitis-ulceration at corners of mouth
atrophic glossitis
tachycardia, flow murmur, cardiac enlargement, ankle oedema, heart failure-raised JVP, bibasal crackles, S3 gallop rhythm, displaced apex beat
168
when might a ferritin level be less useful in diagnosing a patient with Fe deficiency anaemia?
if the patient has some sort of chronic inflammatory disease e.g. RA, as ferritin can be raised when infection or inflammation present, but would expect low in Fe deficiency anaemia as is a representation of Fe stores in the body.
169
complications of acid reflux?
```
oesophagitis
benign oeseophageal stricture
barrett's oesophagus and subsequent increased risk of oesophageal adenocarcinoma
ulcers
Fe deficiency anaemia-rare
```
170
predisposing factors to pathological acid reflux?
smoking
alcohol
overeating
surgery in achalasia
drugs e.g. anticholinergics, nitrates, TCAs
H.pylori?-role in GORD not yet established, although major role in gastric and duodenal ulcers, gastritis and gastric Ca
hiatus hernia
systemic sclerosis
pregnancy
gastric acid hypersecretion, ?zollinger-ellison syndrome*
171
symptoms of GORD?
```
heartburn-retrosternal discomfort related to meals, lying down, stooping, and straining, relieved by antacids e.g. gaviscon and rennie-neutralise stomach acid
belching
acid brash
waterbrash-excessive salivation
odynophagia-due to oesophagitis or ulceration
nocturnal asthma
chronic cough
laryngitis-hoarseness, throat clearing
sinusitis
```
172
should treatment for H pylori infection always be given in cases of recurrence?
shouldn't treat +ve cases more than twice
| if still +ve, do upper GI endoscopy, ?Ca
173
importance of smoking cessation in PUD?
smoking reduces healing rates of gastric ulcers and increases recurrence of duodenal ulcers
174
complications of PUD?
perforation
bleeding
malignancy
reduced gastric outflow
175
how is H pylori tested for and its eradication confirmed?
can be tested for with urease breath test or stool antigen test
retesting should be done with urease breath test
176
PPI treatment of GORD?
offer PPI at full dose for 4 or 8 weeks
then if symptoms recur, offer at lowest dose possible to control symptoms
for univestigated dyspepsia, offer full dose PPI therapy for 4 weeks, then leave 2 wk washout period before H pylori testing
in PUD, and tested negative for H pylori and not on NSAIDs, offer full dose PPI for 4-8 weeks.
177
H pylori eradication therapy?
7 day twice daily course of PPI plus amoxicillin and either clarithromycin or metronidazole
if pen allergic, clarithromycin and metronidazole
if pen allergic and previous clarithromycin, give metronidazole and bismuth and tetracycline
178
new diet recommendation for IBS sufferers?
low FODMAP diet-fermentable oligo-, di-, mono-sacchardies and polyols=poorly absorbed sugars and sugar alcohols
foods high in FODMAPs include milk products containing lactose, wheat, stone fruits, fruit juice concentrates
179
why does a high urea:creatinine ratio occur in pre-renal AKI?
as pre-renal AKI=inadequate kidney perfusion, so glomerulus filters less and so filtrate more slowly moved through renal tubules allowing more time for urea absorption so increase urea in bloodstream
contrast to intrinsic renal failure where ratio close to 1 as urea unable to be absorbed.
180
problems associated with erythropoietin treatment in CKD patients with anaemia?
HTN
| stroke
181
what needs to be excluded in cases of a non-healing peptic ulcer?
```
malignancy
treatment non-adherence
continued NSAID use
zollinger-ellison syndrome
crohn's disease
failure to detect h.pylori
```
182
how is remission induced in Crohn's disease?
monotherapy: glucocorticosteroid-prednisolone, methylprednisolone or IV hydrocortisone if 1st presentation or single inflammatory exacerbation in 1 year. alternatives: enteral nutrition in young people, budesonine or 5 ASA treatment.
if 2 or more inflammatory exacerbations in 1 year, or steroid dose cannot be tapered, consider adding azathioprine or mercaptopurine, alternative=methotrexate addition if azathioprine not tolerated or low/absent TPMT activity.
infliximab and adalimumab are considered tment options in those with severe active crohn's not responding or intolerant to conventional therapy, continued until failure/need for surgery/or for 1 year-then r/v.
remission then maintained with azathioprine or mercaptopurine, or MTX if induced remission, others not tolerated or contraindications to others e.g. low TPMT activity or prev. pancreatitis.
post surgery consider remission maintenance with azathioprine or mercaptopurine if prev. severe disease with stricturing/fistulae, or more than 1 resection. can consider 5-ASA tment in remission maintenance post surgery.
183
raised mortality in acromegaly is primarily due to what, and why does this happen?
cardiovascular disease
cardiomyopathy-LV hypertrophy due to the effects of the GH/IGF-1 axis, causing diastolic dysfunction
remodelling enhanced due to DM and HTN
atherosclerosis and IHD due to HTN and DM, and GH and IGF-1 directly causing endothelial cell dysfunction and reduced vasodilating ability.
disease manifestations result of excess GH effect on liver increasing insulin like growth factor-1 (IGF-1) secretion
184
investigation results in grave's disease?
```
raised T3 and T4
lowered TSH
raised antibodies-TSH receptor antibody
isotope scan increased
opthalmopathy
```
in hashimotos, may find anti-thyroid peroxidase antibodies (anti-TPO)
note hypothyroidism-abnormal bloods include anaemia-normocytic or macrocytic, raised lipid profile-triglycerides and cholesterol, and raised CK
185
why might a CXR be requested in suspected addison's disease?
look for TB-cavity-commonest cause worldwide
186
how is remission induced in UC?
mild to moderate proctitis and proctosigmoiditis: topical 5-ASA e.g. olsalazine, or add oral or oral alone, topical steroid or oral pred if 5-ASA not tolerated or CI.
L sided or extensive: oral 5-ASA, and consider adding topical or oral beclometasone. oral pred if not.
if on ASA and no improvement within 1mnth, then add oral pred. if response inadequate, consider adding oral tacrolimus
acute severe: IV steroids, add IV ciclosporin if little improvement or worsening.
oral azathioprine or mercaptopurine to maintain remission if 2 or more inflammatory exacerbations in last year that required systemic steroid tment, or remission not maintained by aminosalicylates, or after single acute severe episode.
187
define acute liver failure
potentially reversible condition that is the result of severe liver injury, with onset of encephalopathy within 8 weeks of appearance of 1st symptoms-usually jaundice, and in absence of pre-existing liver disease.
188
what treatment should be given to all patients on acute liver failure, regardless of aetiology?
N-acetylcysteine-this should be given in 5% glucose by IVI
| importance=increase hepatic availability of glutathione which protects against ROS.
189
general investigations and management in acute liver failure?
FBC-thrombocytopenia
Us and Es, creatinine-AKI
PT-coagulopathy
LFTs-bilirubin
Phosphate, magnesium
ABGs, including lactate
USS abdomen with Doppler of hepatic veins
2hr monitoring of blood gluocse for hypoglycaemia
urinary catheter, and monitor output hourly
N-acetylcysteine in 5% glucose IVI for all
monitor for encephalopathy and conscious state
avoid all sedating agents where possible (unless intubated), NSAIDs and BZDs.
190
specific management in acute liver failure?
CVS: colloid resuscitation initially, then 0.9% sodium chloride maintenance and concentrated glucose (50%) infusions, avoid lots of 5% glucose as can cause hyponatraemia and cerebral oedema-precipitate encephalopathy?
Neur: grade 3 or 4 encep need ITU and intubation. elevate head to 30 degrees, maintain sodium, monitory for bradycardia/HTN suggesting raised ICP, sustained ICP rise manage with 20% mannitol, and increase sedation with propofol
Renal: if pre-renal AKI and ATN require RRT, continuous veno-venous haemofiltration with a dialysis catheter into a vein is preferred, with bicarb buffered solution.
Haem: give PLT if less than 50 and bleeding, Vit K
GI: sucralfate or H2RA for stress ulcers, OGD if major bleed, enteral nutrition caution with protein-encephalopathy, may need NJ as gastric stasis occurs.
Resp: ABGs, early intubation
Micro: once ventilated on ITU, give fluconazole and BS eg. co-amoxiclav
191
why are liver failure patients intravascularly deplete?
low peripheral vascular resistance
| previous vomiting
192
how is decision about liver transplantation made in acute liver failure?
use of king criteria:
Paracetamol OD: pH less than 7.3, OR PT more than 100s and serum creatinine more than 300 in those with grade 3 or 4 encephalopathy
Non paracetamol: PT more than 100s OR any 3 of age under 10 or over 40, PT 50s, serum bilirubin more than 300, jaundice more than 7 days before encephalopathy, aetiology-hepatitis non-A, non-B, halothane, idiosyncratic drug reactions.
193
when does well localised pain from the liver in the RUQ occur?
when there is stretching of the liver capsule which receives somatic innervation form the lower intercostal nerves
194
what is livedo reticularis? what causes it?
reticular mottled reddish blue skin discolouration surrounding pale central skin, result of altered b.flow in small vessels to upper skin, so other vessels dilate to compensate.
can be idiopathic
can occur secondary to antiphospholipid syndrome, TB, polycythaemia rubra vera, buerger disease, SLE, RA, dermatomyositis, lymphoma.
195
what autoantibody screen would be used to aid pernicious anaemia diagnosis (Vit B12 deficiency thought related to AI destruction of gastric parietal cells)?
intrinsic factor antibodies (100% specific) and gastric parietal cell antibodies
196
before treating a patient's folate deficiency, what vitamin would we want to know the patient's level of and why?
Vit B12
if vit B12 deficient, need to treat this 1st as giving folate can lower vit B12 levels further and cause subacute degeneration of the SC.
197
severe consequences of Vit B3 (niacin) deficiency?
dermatitis (eczema), diarrhoea and dementia-pt may initially be depressed, then progress through anxiety, confusion, irritability, and eventually coma and death.
198
disease which is most commonly the cause of Raynaud's?
systemic sclerosis
199
causes of colitis?*
```
microscopic
IBD
radiation
ischaemia
drugs e.g. ABx
```
200
most common extra intestinal manifestation of IBD?
arthritis
201
ICD-10 criteria for alcohol dependence?
3 or more needed from the following:
compulsion to drink
continued drinking despite evidence of harm
neglect of alternative activities to drinking
physiological withdrawal
difficulties controlling alcohol consumption
tolerance to alcohol
202
what is the most effective screening tool for harmful alcohol drinking and alcohol dependence?
AUDIT-10 item questionnaire, 15 or more in men, 13 or more in women likely alcohol dependence
203
causes of jaundice that result from reduced conjugation of bilirubin?
result of hepatocyte damage e.g. alcohol, NAFLD, viral hep, alpha 1 antitrypsin def, HH, wilsons, sarcoidosis, drugs e.g. MTX
or reduced hepatic uptake of unconjugated bilirubin e.g. portosystemic shunts bypassing a cirrhotic liver
or congenital enzymatic problems:
gilberts syndrome and crigler-najjar syndrome-jaundice in 1st few days of life due to no activity of UDP-glucuronosyltransferase
204
causes of jaundice specific to pregnancy?
intrahepatic cholestasis of pregnancy
pre-eclampsia with HELLP syndrome (seen only in pregs more than 20wks)
acute fatty liver of pregnancy
205
management of pt with acute viral hepatitis B?
```
supportive tx
minimise alcohol consumption during acute phase
barrier contraception
avoid sharing toothbrushes or razors
vaccination of current sexual partners and children
contact tracing
GP-notifiable disease
r/f to specialist hepatologist
```
206
why does the body want to have a limit on Fe absorption (achieved by hepcidin)?
as Fe used by bacteria to replicate**
207
how is H pylori eradication confirmed?
urea breath test
note H pylori serology can remain positive for up to 1 year post successful H pylori eradication
208
causes of Vit B12 deficiency?
inadequate dietary intake (rare) e.g. vegans
MALABSORPTION-pernicious anaemia (atrophic gastritis-auto Abs against intrinsic factor), GI disease e.g. crohns, coeliac, or drug induced e.g. metformin, long term PPI treatment-causes achlorydia-lack HCL to digest food adequately for vit B12 release.
genetic disorders-transcobalamin deficiency
infection
pregnancy
209
classic triad for perinicious anemia?
sore tongue
weakness
paraesthesia
210
causes of raised vit B12?
excess dietary intake
solid tumour e.g. HCC-increased hepatocyte degradation releases vit B12, and reduced hepatic clearance of vit B12 complex
myeloproliferative disorders e.g. CML, myelofibrosis-increased granulocytes and transcobalamin is produced by granulocytes so B12 uptake out of blood, + transport and uptake by cells increased, and transcobalamin I protects vit B12 from HCL in stomach.
liver disease
renal failure-serum accumulation of TCBs
AI conditions-SLE, RA
inflammatory conditions-increased release of TCB II
211
causes of anaemia in patients with chronic liver disease?
inadequate nutrition-inadequate Fe, folate, vit B12 intake
acute and chronic GI bleeding-clotting factor deficiency and thrombocytopenia-portal HTN and reduced TP production
portal HTN-splenomegaly-increased breakdown of rbc by the spleen.
212
4 phases of subacute thyroiditis?
1: hyperthyroidism, raised ESR, painful goitre, 3-6wks
2: euthyroid, 1-3wks
3: hypothyroid, wks to months
4: return of thyroid structure and function to normal
