Day 6 Flashcards
Loss of Haustra
ulcerative colitis
drainpipe colon
ulcerative colitis
rose thorn ulcers
chrons
coble stone appearance
chrons
granulomas and increased goblet cells
chrons
crypt abscesses
ulcerative colitis
Features of DKA
Abdominal pain
Polyuria, polydipsia, dehydration
Kussmaul respiration (deeo hyperventilation)
Acetone-smelling breath
Management of DKA
fluid replacement- isotonic saline
insulin- IV infusion at -0.1unit/kg/hour
once blood glucose is <15mmol/l an infusion of 5% dextrose started
Long acting insulin continues, short-acting insulin stopped
COPD stages
Stage 1 (Mild) as his FEV1 is >80% of what is expected.
Stage 2 (Moderate) is an FEV1 which is 50-79% of the predicted value.
Stage 3 (Severe) is an FEV1 which is 30-49% of the predicted value.
Stage 4 (Very severe) is an FEV1 <30% of the predicted value.
Stage 5 is not an option in COPD staging.
COPD initial management
- smoking cessation
- annual influenza vaccine
- pneumococcal vaccine
- pulmonary rehab
Bronchodilator therapy (SABA or SAMA) if still struggling check for steroid responsiveness...
Signs of asthmatic/steroid responsive features
> any previous, secure diagnosis of asthma or of atopy
a higher blood eosinophil count - note that NICE recommend a full blood count for all patients as part of the work-up
substantial variation in FEV1 over time (at least 400 ml)
substantial diurnal variation in peak expiratory flow (at least 20%)
Management of COPD with no asthmatic features
add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA)
if already taking a SAMA, discontinue and switch to a SABA
Management of COPD with asthmatic features
LABA + inhaled corticosteroid (ICS)
if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS
if already taking a SAMA, discontinue and switch to a SABA
NICE recommend the use of combined inhalers where possible
When is oral theophylline recommended in COPD
when inhaled therapy can’t be used
When is antibiotic prophylaxis recommended in COPD
> azithromycin prophylaxis
patients should not smoke, > have optimised standard treatments
continue to have exacerbations
other prerequisites include;
:a CT thorax (to exclude bronchiectasis)
: sputum culture (to exclude atypical infections and tuberculosis)
:LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval
When should mucolytics be considered in COPD
patients with a chronic productive cough and continued if symptoms improve
Features of cor pulmonale
peripheral oedema, raised jugular venous pressure, systolic parasternal heave, loud P2
Management of cor pulmonale
use a loop diuretic for oedema, consider long-term oxygen therapy
ACE-inhibitors, calcium channel blockers and alpha blockers are not recommended by NICE
tear drop cells on blood film
myelofibrosis
thalassaemia
megaloblastic anaemia
What is myelofibrosis
> myeloproliferative disorder
hyperplasia of abnormal megakaryocytes
resultant release of platelet derived growth factor is thought to stimulate fibroblasts
haematopoiesis in liver and spleen
Features of myelofibrosis
- elderly person with anaemia
- massive splenomegaly
- hypermetabolic symptoms: weight loss, night sweats
Lab findings in myelofibrosis
> anaemia
high WBC and platelet count early in the disease
‘tear-drop’ poikilocytes on blood film
unobtainable bone marrow biopsy - ‘dry tap’ therefore trephine biopsy needed
high urate and LDH (reflect increased cell turnover)
Death in HOCM
Ventricular arrythmia
COPD - still breathless despite using SABA/SAMA and asthma/steroid responsive feature
LABA + ICS
Types of transfusion reaction
- non-haemolytic febrile reaction
- minor allergic reaction
- anaphylaxis
- acute haemolytic reaction
- transfer associated circulatory overload (TACO)
- transfusion-related acute lung injury (TRALI)
Cause of non-haemolytic febrile reaction
due to white blood cell HLA antibodies
often result of sensitisation by previous pregnancies or transfusions
management of non-haemolytic febrile reaction
paracetamol
Cause of minor allergic reaction
hypersensitivity reactions to components within the transfusion
Symptoms of allergic/anaphylaxis reaction
> Symptoms typically arise within minutes of starting the transfusion and severity can range from urticaria to anaphylaxis with hypotension, dyspnoea, wheezing, and stridor, or angioedema.
Management of simple urticaria
discontinuing transfusion and give antihistamine
Once the symptoms resolve, the transfusion may be continued with no need for further workup.
Management of anaphylaxis
transfusion should be permanently discontinued, intramuscular adrenaline should be administered and supportive care. Antihistamine, corticosteroids and bronchodilators should also be considered for these patients.
Features of TRALI
> development of hypoxaemia/acute respiratory distress syndrome within 6 hours of transfusion.
Features include: hypoxia pulmonary infiltrates on chest x-ray fever hypotension
Features of TACO
common reaction due to fluid overload resulting in pulmonary oedema. As well as features of pulmonary oedema the patient may also by hypertensive, a key difference from patients with TRALI.
Infective transfusion reaction cause
Transmission of vCJD
although the absolute risk is very small, vCJD may be transmitted via blood transfusion
rapid hyponatraemia correction
osmotic demyelination syndrome
rapid hypernatraemia correction
cerebral oedema
Symptoms of osmotic demyelination syndrome
brainstem damage- spastic quadriparesis, pseudobulbar palsy, emotional lability
Signs of cerebral oedema
bradycardia
gaze paresis
medications to be stopped in AKI
NSAIDs (except aspirin at cardiac dose 75mg) aminoglycosides ACE inhibitors A2RB diuretics metformin lithium digoxin
medications to be continued in AKI
> paracetamol > warfarin > statins > aspirin > clopidogrel > beta-blockers
Plucking of clothes, smacking of lips, aura and feelings of de-ja-vu
temporal lobe seizures
sensory abnormalities seizure
parietal
Most common cause of thyrotoxicosis
grave’s
MOA of orlistat
inhibiting gastric and pancreatic lipase to reduce the digestion of fat
Who is eligible for orlistat?
> BMI of 28 or more with associated risks
BMI of 30 or more
continued weight loss e.g. 5% at 3 months
orlistat used for <1 year
Post-eradication test of cure H.pylori
urea breath test
Features of anaplastic carcinoma
local invasion common
features of medullary carcinoma
serum calcitonin raised
features of follicular carcinoma
macroscopically encapsulated, microscopically capsular invasion seen- > without this it is follicular adenoma
vascular invasion predominates
how does follicular adenoma present
solitary thyroid nodule
features of papillary carcinoma
> Histologically tumour has papillary projections and pale empty nuclei
Seldom encapsulated
Lymph node metastasis predominate
Haematogenous metastasis rare
features of chronic lymphocytic leukaemia
often none: incidental finding of lymphocytosis
constitutional: anorexia, weight loss
bleeding, infections
lymphadenopathy more marked than chronic myeloid leukaemia
Investigations for CLL
FBC: lymphocytosis, leukaemia
blood film: smudge cells
immunophenotyping is key
Endocrine complication of SCLC
SIADH
Management of SIADH
slow correction
fluid restriction
demeclocycline: reduces responsiveness of the collecting tubule cells to ADH
ADH (vasopressin receptor antagonists) have been developed
screening for haemochromatosis
gen population: transferrin saturation > ferritin
family members: HFE genetic testing
Most common cause of peritonitis secondary to peritoneal dialysis
staphylococcus epidermidis
what do patients who’ve had catheter ablation for AF require
lifelong anticoagulation
patients with cellulitis who are penicillin allegic
clarithromycin, erythromycin (pregnancy), or doxycycline
Common trigger for cluster headaches
alcohol
charts acronym
fibrosis of upper lobes C- coal workers pneumoconiosis H- histiocytosis/hypersensitivity pneumonitis A- ankylosing spondylitis R- radiation T- tuberculosis S- silicosis/sarcoidosis
What can result in a lower HbA1c reading
lower average blood glucose concentration and a shorter red cell life span.
What causes reduced RBC lifespan?
hereditary spherocytosis
sickle cell
G6PD
multiple endocrine neoplasia type IIa
Medullary thyroid cancer, hypercalcaemia, phaeochromocytoma
