General Medicine Review Flashcards
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
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.
what type of heart murmur might you expect a patient with PKD to have?
late systolic murmur heard loudest over the apex of the heart
what sign of thyrotoxicosis is not directly due to the presence of excess thyroid hormones?
exophthalmos
most important potentially treatable variable in autosomal dominant PKD?
HTN
but treatment has little effect on disease progression
extra-renal manifestations of PKD?
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
signs of PKD due to effect on kidneys?
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
a Dieulafoy lesion may present as both upper and lower GI bleeding. describe what the lesion is.
an ectatic (dilated) submucosal artery in the GIT, most commonly the stomach, but may also occur in small or large bowel and oesophagus.
drugs known to aggravate C.difficile toxin infection?
PPIs e.g. lansoprazole and omeprazole
meropenem is an example of what class of antibiotics?
beta-lactam (carbapenem)
very broad spectrum
can only be given IV
if a CXR shows a gastric bubble to be present underneath the diaphragm, what might be the cause?
hiatus hernia
how is a patient with a neuropathic foot at risk of ulcers with respect to pressure point development?
neuropathic foot-motor and sensory dysfunction, toe clawing results in more pressure put through the metatarsal heads and heels, predisposing to callus and ulcers.
a patient with COPD is cyanosed. what term may be used to describe the picture of this pt?
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.
why is a patient with chronic alcoholism at risk of diabetes?
likely to develop chronic pancreatitis
why might H pylori NOT be tested for in a pt with an actively bleeding duodenal ulcer?
test more likely to be -ve if bleeding
confusion screen components?
MMSE bloods: LFTS-hepatic encephalopathy, Ca2+-hypercalcaemia, FBC-WCC, blood cultures, TFTs-hypo urine dipstick CXR CT head
what does percussion myotonia indicate?
nutritional deficiency
causes of an isolated raised bilirubin in seemingly otherwise well patient?
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.
most common manifestation of autonomic neuropathy in pts with DM?
postural hypotension*
why should bloods NOT be taken from the same arm as an IV drip is going through?
will show erroneus results-electrolytes which are in the fluid being infused will be higher than their concentration in the peripheral blood.
hypernatraemia causes?
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
what combination of features identified with a FBC and Us and Es are suggestive of GI bleeding?
low Hb raised WCC (in absence of infection) raised PLTs raised urea (with normal creatinine)
11 diagnostic criteria for SLE?
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
features suggesting giant cell arteritis diagnosis?
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
causes of erythema nodosum?
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
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
complications of PBC (primary biliary cirrhosis)?
osteoporosis osteomalacia and coagulopathy as malabsorption of fat soluble vitamins portal hypertension ascites variceal haemorrhage hepatic encephalopathy HCC
what diseases is PBC associated with?
RA Sjogrens thyroid disease systemic sclerosis renal tubular acidosis keratoconjunctivitis sicca membranous glomerulonephritis
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
drugs likely to cause acid reflux?**
NSAIDs steroids Ca2+ channel blockers, nitrates bisphosphonates e.g. alendronate antichoinergics
which LFT can be used to screen for alcohol abuse?
GGT-gamma glutamyltransferase
this will be raised in 75% of life-long alcohol drinkers
cardiac problems associated with hypothyroidism?
bradycardia
pericardial effusion
congestive cardiac failure
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
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
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
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.
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.
common causes of neutrophilia?
bacterial infection inflammation necrosis e.g. post MI corticosteroid tment metabolic disorder e.g. renal failure myeloproliferative disorder malignancy
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)
common causes of lymphocytosis?
viral infections
chronic infections e.g. TB
chronic lymphocytic leukaemia
lymphomas
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.
investigation to confirm thalassaemia diagnosis?
Hb electrophoresis
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
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.
why is bruising more common in pts with CKD?
platelet abnormality*
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
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
what is Felty’s syndrome?
combination of RA, splenomegaly and neutropenia
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).
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.
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.
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
causes of chronic pancreatitis?
alcohol more rarely: familial cystic fibrosis haemachromatosis pancreatic duct obstruction e.g. gallstones/tumour hyperparathyroidism congenital
complications of chronic pancreatitis?
pancreatic carcinoma diabetes pseudocyst biliary obstruction gastric varices local arterial aneurysm splenic vein thrombosis
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
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
what condition has the worst prognosis out of all the complications of liver cirrhosis?
hepatorenal syndrome
pathophysiology of hepatorenal syndrome?
splanchnic vasodilation
activation of RAAS, SNS, ADH
results in renal vasoconstriction
no histological damage to kidney
why is oesophageal Ca unlikely if a pt complains of odynophagia?
implies mucosal sensation is intact
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
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
ADRs of 5-ASAs?
dangerous: hepatitis pulmonary toxicity pericarditis pancreatitis aplastic anemia thrombocytopenia leukopenia
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.
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.
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.
most common presenting symptom in PBC (primary biliary cirrhosis?
fatigue
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.
when might proteinuria occur in normal patients?
when febrile illness
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
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.
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
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)
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.
extra-renal assoc. of alport’s syndrome-a glomerulonephropathy that can cause nephritic syndrome?
sensorineural deafness
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.
causes of polyuria?
psychogenic diabetes insipidus-cranial and nephrogenic diabetes mellitus hypercalcaemia SVT-release of ANP
drug with benefit on mortality of patients with type 2 DM who develop microalbuminuria?
ACEI
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.
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!
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.
only cure for primary biliary cirrhosis?
liver transplant
BUT not always curative as disease can recur in the transplanted liver.
how does CKD affect PLTs?
CKD causes platelet function disorder
*look for bruising o/e of patients with CKD
treatment of acutely bleeding oesophageal varices?
IV terlipressin-vasconstrictor, also used in tment of hepatorenal syndrome
OGD with injection sclerotherapy and banding?*
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.
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.
