General medicine knowledge Flashcards
What are normal CBC values?
What are normal clotting profile values?
What are normal electrolyte profile
What is normal LFT?
What is normal renal function test?
What is normal arterial blood gas values?
What is normal blood total protein, globulin, CK, LDH ESR?
What is the classification of gram+ve bacteria (cocci, bacilli –> aerobic, anaerobic)
What is the classification of gram-ve bacteria (cocci, bacilli, coccobacilli)?
How to differentiate gram+ve cocci?
How to differentiate gram+ve bacilli?
Differentiating aerobic gram-ve bacilli
Differentiating gram-ve coccobacilli
What can the groups of penicillins be used for?
What can the groups of cephalosporins be used for?
What pathogens can macrolides be used against?
What are its AE?
What pathogens can tetracyclines be used against?
What pathogens can aminoglycosides be used against?
AE?
What pathogens resistant against aminoglycosides?
What pathogens can fluoroquinolones be used against?
AE?
What pathogens resistant against fluoroquinolones?
What pathogens can carbapenems be used against?
AE?
What pathogens resistant against carbapenems?
What is the recommendation for using NSAIDs?
What are the typoes of NSAIDs and COX2 inhibitors?
What is moa of NSAID?
Cell membrane phospholipid –> arachidonic acid –> leukotrienes + COX1/COX2
COX1 –> prostaglandins thromboxane (stomach, intestine, kidney, platelets): mucosal protection, renal blood flow and haemostasis
COX2 –> prostaglandins (inflammatory sites, macrophages, synovocytes) inflammation, pain and fever
What is AE of NSAIDs?
What is AE of COX2 inhibitors?
What are the short acting, medium acting and long acting steroids?
MoA
What is the consequence of corticosteroid withdrawal?
What is AE of corticosteroids
What are adjuncts for admin of corticosteroids?
What are the calcineurin inhibitors?
MoA
AE
What are the antimetabolites used for anti-cancer
What are there MoA
AE?
What IL2 receptor antagonist used for anticancer
Moa
What are the antimetabolites that are S phase specific?
MoA
AE
What are the mitotic inhibitors that are M phase specific
MOA
AE
What are topoisomerase inhibitors (anti cancer chemo)?
Moa
AE
What are cell cycle non specific drugs?
MoA
AE
Alkylating agents
What are the antitumor antibiotics used in cancer?
MoA
AE
What is normal range of Na+
What is classification of hypernatremia?
normal range = 135-145 mmol/L
Serum osmolality = 2Na+ + urea + glucose (normal: 285-295mmol/kg)
What are the causes of hypernatremia?
What are the signs and symptoms of hyper vs hyponatremia?
What is the diagnostic algorithm for hypernatremia?
What are the 2 steps in assessing hypernatremia?
What is the treatment principles for hypernatremia?
Maximum rate of correction in 24 hour period?
What is the treatment of hypervoemic/isolvemic/hypovolemic hypernatremia?
What is the severity of hypoantremia based on electrolyte level?
What is the etiology of hyponatremia?
What is the diagnostic algorithm for hyponatremia?
What are the 2 steps to assess hyponatremia?
What is the treatment objectives of hyponatremia
What complications of hyponatremia must you prevent
What is max correction and complication if overload?
What is the treatment of hyponatremia?
What is the rationale for using hypertonic saline, desmopressin and furosemide in managing hyponatremia?
What is normal range of K
Acid base status
Na+K+ ATP pump affected by what drug
Normal range = 3.6-5mmol/L
HyperK associated with acidosis, hypoK associated with alkalosis
Na+K+ ATPase pump inhibited by drugs such as digoxin –> inhibition of pump leads to failure of active transport of K+ from extracellular space into intracellular compartment
What are the causes of hyperK?
What are SS of hyperK?
What are SS of hypoK?
What is the diagnostic algorithm for hyperK?
What are the steps involved in finding out dx for hyperK?
Step 1: exclusion of pseudohyperkalemia, drug induced hyperK and other rrare causes
Repeat K+ once if in suspiciion
PseudohyperK: hemolysis of aged sample, thrombocytosis, leukocytosis, EDTA contamination, drug induced hyperK (IV/oral K+ supplement, K+ sparing diuretics), rare cuases (tumor lysis syndrome, hyperkalemic periodic paralysis)
Step 2: assess plasma HCO3- leve. decreased HCO3-. test for anion gap (Na++K+ -CL- -HCO3-). Increased anion gap: diabetic ketoacidosis, renal failure. Normal anion gap –> go step 3
Step 3: assess plasma creatinine level. Increased plasma creatinine: renal failure. normal plasma creatinine: go step 4
Step 4: assess ACTH stimulation test by short synacthen test
blunted or absent response: addisons disease, congenital adrenal hyperplasia (21hydroxylase deficiency)
Normal response –> Go step 5
Step 5: spot renin and aldosterone
What is the treatment modalities for hyperkalemia?
What is treatment of urgent hyperkalemia?
- 10% calcium gluconate 10ml IV oer 2-3 mins. Repeat if no effect in 5 mins. Onset = 1-3 mins, duration =30-60 mins
MoA: calcium antagonizes the membrane actions of hyperK and prevents hypocalcemia which increases cardiotoxicity of hypoerK - Dextrose insulin infusion: 250ml D10 or 50ml D50 along with 8-10 units Actrapid HM (short acting regular human insulin) over 30 mins and repeat every 4-6 hours if necessary, Onset = 30mins; duration = 4-6 hours
Insulin shifts K+ into cells by enhancing Na+K+ATPase pump in skeletal muscle. Glucose is given with insulin to precent hypoglycemia. Insulin can be given alone if serum glucose is high. - Sodium bicarbonate: 100-150ml of 8.4% NaHCO3 over 30-60 mins. Onset = 5-10 mins, duration = 2 hours
MoA: shift K+ into cells. Raise systemic pH with NaHCO3 results in H+ released from cells as part of buffering reaction - B-adrenergic agonists. 10-20mg salbutamol in 3ml NS by nebulizer. Onset = 15-30 mins, duration = 2-3 hours.
MoA: increases activity of Na+K+ ATpase pump in skeletal muscle (shifts k+ into cells0 - Loop diuretics: furosemide 40-80mg IV bolus
Increased urinary K+ loss –> inhibits Na+K+2Cl- cotransporter in the apical membrane which decreases Na+ K+ reabsorption - GI cation exchange resins: resonium A/C 15-50mg oral Q4-6h or as retention enema
Increases GI k+ loss. Binds K+ in the GIT in exchange for other cations such as Na+ or Ca2+ before the resin is passed from the body - Haemodialysis preferred (over peritoneal dialysis): indicated in hyperK patients with severe renal impairment and preferable over GI cation exchange resins if patient has functioning vascular access for dialysis
What is treatment of chronic hyperK?
Low K+ diet < 2 g/day
Diuretics = Furosemide/ Hydrochlorothiazide
Correction of metabolic acidosis with sodium bicarbonate 300 – 900 mg tds (10 – 30 mmol/day)
Fludrocortisone 0.1 – 0.2 mg daily for Type IV RTA
What is definition of hypoK
What is normal range
- Normal range = 3.6 – 5.0
- Plasma K+ < 3.0 mmol/L
- Serum K+ < 3.5 mmol/L
What are the causes of hypoK?
What is the diagnostic algorithm for hypoK?
What are the steps to assess hypoK and ddx?
What is the treatment principle of hypoK
What dosage form
Premixed K+ containing solutions for maintenance IV infusion
What is the treatment regimen of hypoK based on serum and ECG changes?
What are the treatment choices for hypoK?
- KCL
2 reasons: patients with hypoK and metabolic alkalosis are often Cl- depleted
Faster rate of correction compared with other preparation - KHO3-/potassium citrate: indicated in patients with hypoK and metabolic acidosis –> RTA and diarrhea
- K+ sparing diuretics: indicated in patients in which hypoK due to renal K+ wasting in which K+ supplement may not be sufficiently effective.
Aldosterone antagonist: spironolactone
Renal epithelial Na+ channel inhibitors = amiloride/triamterene
