Gen Med MD3

Question 1

how to prevent refeeding syndrome?

Answer 1

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.

Question 2

what are some causes you need to screen for in a patient presenting with erectile dysfunction?

Answer 2

1. mental illness e.g. depression
2. hx of cardiovascular disease including diabetes, metabolic syndrome
3. medications such as SSRIs
4. previous prostate surgery
5. Lifestyle- alcohol abuse, recreational drugs, smoking
6. other medical conditions like MS

Question 3

why do male patients with cardiovascular risk factors e.g. dyslipidaemia, obesity, diabetes often present with erectile dysfunction?

Answer 3

because these metabolic factors causes endothelial dysfunction–> vascular disease process

(essentially atherosclerosis)

Question 4

Secondary preventative measures for stroke?

Answer 4

• 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

Question 5

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?

Answer 5

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

Question 6

you suspect a patient who has just arrived in the ED has a stroke. what is your acute medical management?

Answer 6

1. call code stroke
2. ABCDE (e.g. ensure airway patent)
3. get as much collateral history as possible and try and ascertain time period since onset of symptoms
4. CT brain to rule out haemorrhage
5. if ischaemic, DWI/MRI may also be performed
6. if confirmed ischaemic stroke, admit under stroke unit
7. If less than 4.5 hrs since onset of symptoms, thrombolyse patient
8. manage other medical comorbidities such as hyperglycaemia, pyrexia, hypoxia, airway obstruction and frequently monitor pt
9. with-hold aspirin for at least 24-48 hrs and then administer 300mg
10. find cause- echo, ecg, carotid u/s
11. once patient is stable, plan rehabilitation with relevant allied health staff and organise a secondary prevention plan of action

Question 7

define anaphylaxis

Answer 7

potentially life threatening systemic allergic response that either has cardiac and or respiratory involvement AND skin and or GIT involvement

Question 8

dose of adrenaline for adult with anaphylaxis?

Answer 8

0.5mg

Question 9

what are some common triggers for anaphylaxis?

Answer 9

food- peanuts/shellfish/treenuts/eggs/cows milk etc
bites and stings
drugs- antibiotics/anaethestics
other- e.g. latex/exercise

Question 10

what are some signs of symptoms of anaphylaxis?

Answer 10

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

Question 11

what are some risk factors for osteoporosis?

Answer 11

post menopause/ 60 yrs and over for men
smoking
low body weight
hypogonadism
malabsorption
prolonged steroid use
recurrent falls
hyperthyroidism, hyperparathyroidism

Question 12

what cancers are usually associated with hypercalcemia of malignancy, and what is the usual mechanism of action for this?

Answer 12

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)

Question 13

describe alcohol withdrawal syndrome

Answer 13

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

Question 14

what are some symptoms of hypoglycaemia

Answer 14

Adrenergic symptoms- palpitations, sweatiness, tremor, tachycardia

Neuroglycopenic symptoms later- dizziness, visual disturbances, mental dullness, seizures

Question 15

what are the symptoms of hyponatremia?

Answer 15

Moderate hyponatremia–> confusion, muscle cramps

Severe hyponatremia–> coma, convulsions

Question 16

what is the general approach to treating hyponatremia?

Answer 16

• Treat the underlying cause
• Fluid restriction- because usual suspects are SIADH and inappropriate fluid resuscitation
• However if GI losses apparent, normal saline
If Na

Question 17

for emergency cases of hyperkalemia- what drug do we give acutely?

what are some other alternative treatments for hyperkalemia?

Answer 17

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)

Question 18

how might we assess the severity of hyperkalemia?

Answer 18

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

Question 19

what are the electrolyte disturbances apparent in SIADH

Answer 19

hyponatremia
euvolemia
low serum osmolarity
highly concentrate Na+ in urine

Question 20

Describe some symptoms/signs which may suggest a left mca stroke

Answer 20

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.

Question 21

Describe some symptoms/signs which may suggest a RIGHT mca stroke

Answer 21

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.

Question 22

what cerebral arteries are affected if you have a patient complaining of homomynous hemianopia?

Answer 22

contralateral posterior cerebral artery to the homomynous hemianopia

Question 23

describe some symptoms/signs which may suggest a left ACA stroke

Answer 23

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.

Question 24

describe some symptoms/signs which may suggest a right ACA stroke

Answer 24

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.

Question 25

how might we differentiate between red eye caused by iritis versus red eye caused by acute closed angle glaucoma?

Answer 25

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

Question 26

what are the main causes of lower limb amputation in western societies?

Answer 26

PVD with Diabetes +/- non healing foot ulcers
Trauma
Tumour
Infection

Question 27

what are some functional impairments associated with MS?

Answer 27

decreased mobility
decreased continence
altered cognition
communication difficulties
difficulties driving and returning to work
difficulties with sexual function
dysphagia

Question 28

what anatomical changes cause spinal canal stenosis?

Answer 28

disc bulge
ligamentum flavum hypertrophy
OA of facet joints

Question 29

What pharmacological treatments would you initiate in CKD?

Answer 29

• 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

Question 30

what are the metabolic changes for Ca and PO4 with CKD? and what about PTH?

Answer 30

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

Question 31

define CKD?

Answer 31

estimated or measured GFR less than 60 for greater than 3 months +/- evidence of kidney damage

Question 32

dose of adrenaline for child?

Answer 32

0.01mls/kg

Question 33

pathophysiology of anaphylaxis?

Answer 33

• 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