Community health and GP Flashcards
What is anaphylaxis?
rapid onset of type 1 IgE hypersensitivity reaction that develops after pt is exposed to something - life threatening emergency
Causes of anaphylaxis?
insect stings, nuts, other food, abx, IV contrast, other medications
Clinical features of anaphylaxis?
skin reactions: widespread urticaria, itching, flushed skin
Resp: swollen tongue/lips, sneezing, wheeze
GI: abdo pain, nausea, vomiting, diarrhoea
Tachycardia
hypotension
serum levels of mast cell tryptase can be measured to confirm dx
Management of anaphylaxis?
remove trigger
call for help
ABCDE assessment
Administer O2
Lie pt flat, raise legs
Administer adrenaline - adult dose 500mg IM
admisiter chlorophenamine and hydrocortisone
IV fluid if hypotensive
Mechanism of action of donepezil and rivastigmine?
Acetylcholinesterase inhibitor - increases the availability of the neurotransmitter acetylcholine
What is mechanism action of memantine and when is it used?
Glutamate receptor antagonist - used in severe alzheimer’s disease
Which drug classes commonly cause delerium in the elderly?
benzodiazepines, opiaes, antiparkinsonian agents, tricyclic antidepressants, digoxin, beta blockers, steroids, antihistamines (chlorphenamine)
What is predominant toxic protein in alzheimer’s disease?
beta-amyloid
Which form of dementia is seen frequently in motor neuron disease?
frontotemporal dementia
What is semantic memory and in which dementia is this most affected?
the ability to associate meaning to objects presented via visual or auditory modalities - frontotemporal dementia
How does normal pressure hydrocephalus present?
urinary incontinence, gait instability, cognitive chnage
definitive treatment options for normal pressure hydrocephalus
ventriculoperitoneal shunt
Mechanism of action of tricyclic antidepressants
mixture of serotonin reuptake inhibition, noradrenaline reuptake inhibition, antimuscarinic activity and anti-histamine activity
What kind of drug is paroxetine?
SSRI
Sedation is most strongly associated with which type of antipsychotic?
typical
Name 3 atypical anti-psychotics
olanzapine, clozapine, risperidone
name 3 side effects of atypical anti-psychotics
weight gain, metabolic syndrome, agranulocytosis
Cautions with tricyclics
CI in those with previous heart disease, exacerbate schizophrenia, may exacerbate long QT syndrome
use in caution in pregnancy and breastfeeding
may alter blood sugar in T1 and T2 diabetes
may precipitae urinary retention - avoid in men with enlarged prostates
side effects of tricyclic anti depressants
2nd line medication
urinary retention, drowsiness, blurred vision, constipation, dry mouth
What kind of drug is amitryptiline
tricyclic antidepressant
What is iron deficient anaemia
caused by an increased loss of iron, reduced intake or malabsorption
Causes of iron deficient anaemia
increased loss: menorrhagia, GI bleeding, hookworm
Reduced intake: poor diet
Malabsorption: coeliac, IBD
Clinical features of iron deficient anaemia
lethargy, tiredness, weakness, jaundice, heavy periods, change in bowel habit
Dx of iron deficient anaemia
clinical sx
hypochromic, microcytic red cells
total iron binding capacity (TIBC) and ferritin may confirm dx
Mx of iron deficient anaemia
unexplained - investigation for underlying cause
Ferrous sulfate supplements
What is pernicious anaemia?
deficiency in red blood cells caused by lack of vit b12 in blood
autoimmune condition caused by autoantibodies to gastric parietal cells which leads to gastric intrinsic factor secretion. Results in poor vit B12 absorption which leads to anaemia.
Causes of B12 deficiency
gastric causes - pernicious anaemia, chronic severe atrophic gastritis
pancreatic - any cause of pancreatic insuffiency
small bowel bacterial overgrowth, terminal ileal resection, severe ileal disease (Crohn’s disease)
TB
Metformin therapy
Zollinger-Ellison syndrome
thyroid disease
Haematological features of pernicious anaemia
low hb
high MCV
high mean corpuscular haemoglobin (MCH)
normal mean corpuscular haem concentration (MCHC)
abnormally large and oval shaped RBCs in blood smear
Low vitB12
Low or normal folic acid
low reticulyte count
Mx of pernicious anaemia
life-long replacement treatment with cobalamin
Features of pernicious anaemia
lethargy
fatigue
chronic condition
red beefy tongue
erythema or ulcers in mouth
What confirms dx of pernicious anaemia
Anti-intrinsic factor antibodies
What causes anaemia of chronic disease
malignancy
chronic infections - TB
connective tissues disease - RA
Pathophysiology of anaemia caused by chronic disease
chronic disease causes formation of inflammatory cytokines such as IL-1 and IL-6. high levels of LH-6 stimulates hepcidin release from liver, which inhibitory in iron absorption, decreasing activity of ferropotin- iron export channel of basolateral surface of gut enterocytes and plasma membrane of reticuloendothelial cells (macrophages), so haemo production decreases.
Investigations of anaemia of chronic disease
normocytic type, but eventually progresses to microcytic.
Low total iron binding capacity, and high ferritin.
What is thalassaemia
group of inherited disorders characterised by abnormal haemoglobin production
alpha globin and beta globin - whichever is defective results in alpha thalassaemia or beta thalassaemia
What genetic pattern if alpha thalassaemia
autosomal recessive inheritence
clinical features of alpha thalassaemia
jaundice
fatigue
facial bone deformities
dx of alpha thalassaemia
genetic testing
FBC - microcytic anaemia
mx of alpha thalassaemia
blood transfusions and stem cell transplantation
splenectomy
what pattern of inheritence is beta thalassaemia
autosomal recessive
Clinical features of beta thalassaemia minor
isolated microcytosis and mild anaemia
pts usually asymptomatic
Clinical features of beta thalassaemia major
severe symptomatic anaemia at 3-9months age when foetal haemoglobin levels fall.
frontal bossing
maxillary overgrowth
extramedullary haematopoiesis (hepatosplenomegaly)
prognosis - death by heart failure if undiagnosed
mx of beta thalassaemia
regular blood transfusions
– reduce risk of iron overload toxicity; affects heart, joints, liver, endocrine glands
prevented by iron chelating agents (desferrioxamine)
Definition of haemorrhoids
occurs when cushoins within the anal canal expand and protrude outside the anal canal
Clinical features of haemorrhoids
bright red PR bleeding associated with defecation
no pain usually
anal itching or a mass may be felt
o/e: palpable anal mass present in prolapsing haemorrhoids
Risk factors for haemorrhoids
constipation, pregnancy, space occupying lesion
mx of grade 1 haemorrhoids
no prolapse
conservatively +/- topical corticosteroid to alleviate itching
mx of grade 2 haemorrhoids
prolapse on straining
rubber band ligation, sclerotherapy or infrared photocoagulation
mx grade 3haemorrhoids
prolapse on straining and require manual reduction
rubber band ligation
mx of grade 4 haemorrhoids
prolapse on straining and can’t be manually reduced
surgical haemorrhoidectomy
pts advised to eat high fibre diet and high intake of fluids
What’s GORD
dyspepsia, heartburn, acid reflux
reflux of gastric contents into oesophagus caused by defective lower oesophageal sphincter
dx of GORD
typical sx:
dyspepsia
sensation of acid regurgitation
can trial PPI to see if improves sx
Alarm sx of GORD - may be differential
weight loss
anaemia
dysphagia
haematemesis
melana
persistant vomiting
Risk factors for GORD
obesity
alcohol use
smoking
intake of specific foods; coffee, citrus food, spicy foods, fat
Investigations of GORD
trial PPI therapy
oesophagogastroduodenoscopy (OGD) if alarm features or atypical sx or relapsing sx
oesophageal manometry
Mx of GORD
lifestyle interventions - weight loss, dietary changes, elevation of head in bed at night, avoidance of late night eating
PPI therapy - pts <40 standard dose PPI for 8 weeks in combination of lifestyle changes
antacids for symptomatic relief
anti-reflux surgery for refractory cases
Complications for GORD
oesophageal ulcer
barrett’s oesophagus
oesophageal stricture
adenocarcionma of oesophagus
What is chronic kidney disease (CKD)
gradual, irreversible decline in kidney function. Criteria:
either decreased GFR (below 60ml/min/1.73m2) or markers of kidney damage (albuminuria, electrolyte abnormality, structural or histological renal abrnomalities) present for >3months
Staging of chronic kidney disease (CKD)
stage 1: eGFR >90ml/min/1.73m2 with demonstatable kidney damage (haematuria or proteinuria)
stage 2: eGFR 60-89 with haematuria, proteinuria, or raised albumin/creatinine ration
stage 3: eGFR 30-59
stage 4: 15-30
stage 5: <15
Causes of chronic kidney disease (CKD)
glomerular causes: primary (IgA nephropathy) or secondary (SLE (lupus))
vascular: vasculitis, renal artery stenosis
Tubulointerstitial: amyloidosis, myeloma
Congenital: Polycystic kidney disease and Alport syndrome
Systemic: diabetes, hypertension
Developmental: vesico-uteric reflux causing chronic pyelonephritis
Complications of chronic kidney disease (CKD) ((CRF HEALS)
Cardiovascular disease
renal osteodystrophy
fluid (oedema)
hypertension
electrolyte disturbance (hyperkalaemia, acidosis)
anaemia
leg restlessness
sensory neuropathy
features of renal osteodystrophy
reduce bone density (osteoporosis)
reduce bone mineralisation (osteomalacia)
secondary/tertiary hyperparathyroidism
Rugger Jersey spine
Mx of chronic kidney disease (CKD)
oedema: fluid and salt restriction - diuretics: furesomide
anaema: monthly subcut erythropoeitin
hypocalacaemia and hyperphosphataemia: restrict dietary potassium
What is COPD
irreversible obstruction of airways. Comprises of both chronic bronchitis (hypertrophy and hyperplasia of mucus glands in bronchi) and emphysema (enlargement of air spaces and destruction of alveolar walls)
Pathophysiology of chronic bronchitis
chronic exposure to noxious particles; smoking, air pollutants cause hypersectretions of mucus in large and small bronchi
airway inflammation and fibrotic changes result in narrowing of airways and subsequent;y airway obstruction
Clinical features of chronic bronchitis
chronic productive cough at least 3 months in at least 2 consequetive years without other identifiable causes
purulent sputum production
hypoxia
hypercapnia
exertional dyspnoea
cyanosis (blue bloaters)
peripheral oedema secondary to cor pulmonae
pathophysiology of emphysema
abnormal irreversible enlargement in airspaces distal to terminal bronchioles due to destruction of walls
reduce alveolar surface area thus impeding effiecient gaseous exchange
Types of emphysema and aetiology
centriacinar - cigarette smoking
panacinar - alpha1 antitrypsin deficiency
distal acinar - fibrosis, atelectasis
clinical features of emphysema
carbon dioxide retention
pursed lip breathing exertional dyspnoea
use of acessory muscles in breathing
barrel chest (hyperextended)
hyperresonant chest on percussion
sits forward in hunch over position
Symptoms of COPD
productive cough
wheeze
dyspnoea
reduced exercise tolerance