Gen Med MD3 Flashcards
how to prevent refeeding syndrome?
Measure serum electrolytes (including potassium, phosphate, calcium and magnesium) before commencing feeding, then daily for the first week.
Give thiamine (vitamin B1) at least 30 minutes before feeding (100 mg/day).
Consider phosphate supplementation in the first 2 weeks of refeeding.
Start slowly (eg 30% to 50% of estimated caloric requirement) and increase gradually over a week to the patient’s estimated needs.
Monitor vital signs and look for signs of oedema, congestive cardiac failure and deteriorating mental state in the first week of refeeding.
what are some causes you need to screen for in a patient presenting with erectile dysfunction?
- mental illness e.g. depression
- hx of cardiovascular disease including diabetes, metabolic syndrome
- medications such as SSRIs
- previous prostate surgery
- Lifestyle- alcohol abuse, recreational drugs, smoking
- other medical conditions like MS
why do male patients with cardiovascular risk factors e.g. dyslipidaemia, obesity, diabetes often present with erectile dysfunction?
because these metabolic factors causes endothelial dysfunction–> vascular disease process
(essentially atherosclerosis)
Secondary preventative measures for stroke?
- reduce risk factors= lower BP, lipids pharmacologically; cease smoking/improve diet + increase physical activity
- optimise other medical comorbidities e.g. diabetes
- carotid endarectomy/PFO mx if relevant
- proper management of AF
- stop HRT if relevant
- consider different types of contraception other than COCP
a 55 year old male patient comes in with crushing central chest pain, feeling sweaty and clammy. There is some nausea and abdo pain as well. Obviously you would think AMI. where do you think the infarct is, and why?
you would think it would be an inferior infarct, due to vagal stimulation resulting in symptoms like sweaty and clammy, and the fact the pain is difficult to localise
you suspect a patient who has just arrived in the ED has a stroke. what is your acute medical management?
- call code stroke
- ABCDE (e.g. ensure airway patent)
- get as much collateral history as possible and try and ascertain time period since onset of symptoms
- CT brain to rule out haemorrhage
- if ischaemic, DWI/MRI may also be performed
- if confirmed ischaemic stroke, admit under stroke unit
- If less than 4.5 hrs since onset of symptoms, thrombolyse patient
- manage other medical comorbidities such as hyperglycaemia, pyrexia, hypoxia, airway obstruction and frequently monitor pt
- with-hold aspirin for at least 24-48 hrs and then administer 300mg
- find cause- echo, ecg, carotid u/s
- once patient is stable, plan rehabilitation with relevant allied health staff and organise a secondary prevention plan of action
define anaphylaxis
potentially life threatening systemic allergic response that either has cardiac and or respiratory involvement AND skin and or GIT involvement
dose of adrenaline for adult with anaphylaxis?
0.5mg
what are some common triggers for anaphylaxis?
food- peanuts/shellfish/treenuts/eggs/cows milk etc
bites and stings
drugs- antibiotics/anaethestics
other- e.g. latex/exercise
what are some signs of symptoms of anaphylaxis?
urticaria/pruritus angioedema stridor/increased work of breathing/inability to talk swollen tongue tachycardia/hypotension flushed appearance floppy infant cough/wheeze loss of consciousness abdominal pain/N+V
what are some risk factors for osteoporosis?
post menopause/ 60 yrs and over for men smoking low body weight hypogonadism malabsorption prolonged steroid use recurrent falls hyperthyroidism, hyperparathyroidism
what cancers are usually associated with hypercalcemia of malignancy, and what is the usual mechanism of action for this?
breast cancer, lung cancer and multiple myeloma are the usual suspects but any cancer can cause hypercalcemia.
There are three major mechanisms by which hypercalcemia of malignancy can occur: osteolytic metastases with local release of cytokines (including osteoclast activating factors); tumor secretion of parathyroid hormone-related protein (PTHrP); and tumor production of 1,25-dihydroxyvitamin D (calcitriol)
describe alcohol withdrawal syndrome
The alcohol withdrawal syndrome is characterised by anxiety, tremor, sweating, nausea and vomiting, agitation, headache and perceptual disturbances. Seizures are occasionally observed.
Some highly dependent patients will progress to an alcohol withdrawal delirium- delirium tremens
Symptoms usually appear within 6 to 24 hours of the last consumption of alcohol and typically persist for up to 72 hours, but may last for several weeks.
treatment is diazepam
what are some symptoms of hypoglycaemia
Adrenergic symptoms- palpitations, sweatiness, tremor, tachycardia
Neuroglycopenic symptoms later- dizziness, visual disturbances, mental dullness, seizures
what are the symptoms of hyponatremia?
Moderate hyponatremia–> confusion, muscle cramps
Severe hyponatremia–> coma, convulsions
what is the general approach to treating hyponatremia?
• Treat the underlying cause
• Fluid restriction- because usual suspects are SIADH and inappropriate fluid resuscitation
• However if GI losses apparent, normal saline
If Na
for emergency cases of hyperkalemia- what drug do we give acutely?
what are some other alternative treatments for hyperkalemia?
IV calcium gluconate + fluid replacement if required
other therapies include:
insulin + glucose (in renal failure)
sodium bicarbonate (in metabolic acidosis)
dialysis (last resort)
corticosteroids (in adrenal insufficiency)
how might we assess the severity of hyperkalemia?
ECG changes-
Typically, peaked T-waves, prolongation of the PR interval, flattening or absence of the P-wave, widening of the QRS interval, ‘sine-wave’ appearance,
ventricular fibrillation, and asystole are the sequential changes that occur as hyperkalaemia-related cardiotoxicity evolves
what are the electrolyte disturbances apparent in SIADH
hyponatremia
euvolemia
low serum osmolarity
highly concentrate Na+ in urine
Describe some symptoms/signs which may suggest a left mca stroke
Right face and arm upper-motor weakness due to damage to motor cortex, nonfluent (Broca’s) aphasia due to damage to Broca’s area.
There may also be right face and arm cortical type sensory loss if the infarct involves the sensory cortex.
Other deficits include a fluent (Wernicke’s) aphasia due to damage to Wernicke’s area.
Describe some symptoms/signs which may suggest a RIGHT mca stroke
Left face and arm upper-motor weakness due to damage to motor cortex.
Left hemineglect (variable) due to damage to non-dominant association areas.
There may also be left face and arm cortical type sensory loss if the infarct involves the sensory cortex.
what cerebral arteries are affected if you have a patient complaining of homomynous hemianopia?
contralateral posterior cerebral artery to the homomynous hemianopia
describe some symptoms/signs which may suggest a left ACA stroke
Left leg upper-motor neuron weakness due to damage to motor cortex and left leg cortical type sensory loss due to damage to sensory cortex.
Grasp reflex, frontal lobe behavioural abnormalities and left hemineglect can also be seen if the prefrontal cortex and non-dominant association cortex are involved.
describe some symptoms/signs which may suggest a right ACA stroke
Right leg upper-motor neuron weakness due to damage to motor cortex and right leg cortical sensory loss due to damage to sensory cortex.
Grasp reflex, frontal lobe behavioral abnormalities, and transcortical aphasia can also be seen if the prefrontal cortex and supplemental motor areas are involved.
how might we differentiate between red eye caused by iritis versus red eye caused by acute closed angle glaucoma?
iritis- associated with photosensitivity and tenderness to the globe; constricted pupil
acute closed angle glaucoma- more nausea and vomiting, less photosensitivity and fixed dilated pupil
what are the main causes of lower limb amputation in western societies?
PVD with Diabetes +/- non healing foot ulcers
Trauma
Tumour
Infection
what are some functional impairments associated with MS?
decreased mobility decreased continence altered cognition communication difficulties difficulties driving and returning to work difficulties with sexual function dysphagia
what anatomical changes cause spinal canal stenosis?
disc bulge
ligamentum flavum hypertrophy
OA of facet joints
What pharmacological treatments would you initiate in CKD?
- In Stage 1,2 disease: mainly BP control using Ace inhibitor or ARBs (Ca2+ channel blockers are 2nd line)
- Also manage co-morbidities such as CVD, diabetes
• In Stage 3-4 disease, begin synthetic EPO, phosphate binders, calcium, vitamin D3 replacement and sodium bicarbonate (for metabolic acidosis)
Stage 5 CKD= dialysis + renal transplant
what are the metabolic changes for Ca and PO4 with CKD? and what about PTH?
Calcium: Decreases because as the kidney fails, vitamin D activation does not occur and thus leads to low calcium
Phosphate: increases as it is no longer excreted by the failing kidney. Binds Calcium, further decreasing calcium levels.
PTH: increases because of low calcium
define CKD?
estimated or measured GFR less than 60 for greater than 3 months +/- evidence of kidney damage
dose of adrenaline for child?
0.01mls/kg
pathophysiology of anaphylaxis?
• Prior sensitisation to allergen
• IgE antibodies specific to allergen bound to mast cells
• Upon re-exposure to allergen, allergen binds IgE on mast cells and mast cells degranulate
• Mast cells release histamine, leukotrines and cytokines that initiate a widespread inflammatory response
• Vasodilation, increased vasopermeability, bronchoconstriction and mucus hypersecretion occurs
• Myocardial dysfunction, tachycardia and increased platelet aggregation can occur
Eosinophils are recruited and enhance the response
