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MBBS VI Medicine > General medicine knowledge > Flashcards

General medicine knowledge Flashcards

1
Q

What are normal CBC values?

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2
Q

What are normal clotting profile values?

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3
Q

What are normal electrolyte profile

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4
Q

What is normal LFT?

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5
Q

What is normal renal function test?

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5
Q

What is normal arterial blood gas values?

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6
Q

What is normal blood total protein, globulin, CK, LDH ESR?

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7
Q

What is the classification of gram+ve bacteria (cocci, bacilli –> aerobic, anaerobic)

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8
Q

What is the classification of gram-ve bacteria (cocci, bacilli, coccobacilli)?

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9
Q

How to differentiate gram+ve cocci?

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10
Q

How to differentiate gram+ve bacilli?

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11
Q

Differentiating aerobic gram-ve bacilli

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12
Q

Differentiating gram-ve coccobacilli

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13
Q

What can the groups of penicillins be used for?

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14
Q

What can the groups of cephalosporins be used for?

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15
Q

What pathogens can macrolides be used against?
What are its AE?

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16
Q

What pathogens can tetracyclines be used against?

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17
Q

What pathogens can aminoglycosides be used against?
AE?
What pathogens resistant against aminoglycosides?

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18
Q

What pathogens can fluoroquinolones be used against?
AE?
What pathogens resistant against fluoroquinolones?

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19
Q

What pathogens can carbapenems be used against?
AE?
What pathogens resistant against carbapenems?

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20
Q

What is the recommendation for using NSAIDs?

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21
Q

What are the typoes of NSAIDs and COX2 inhibitors?
What is moa of NSAID?

A

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

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22
Q

What is AE of NSAIDs?

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23
Q

What is AE of COX2 inhibitors?

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24
Q

What are the short acting, medium acting and long acting steroids?
MoA

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25
Q

What is the consequence of corticosteroid withdrawal?

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26
Q

What is AE of corticosteroids
What are adjuncts for admin of corticosteroids?

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27
Q

What are the calcineurin inhibitors?
MoA
AE

A
28
Q

What are the antimetabolites used for anti-cancer
What are there MoA
AE?

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29
Q

What IL2 receptor antagonist used for anticancer
Moa

A
30
Q

What are the antimetabolites that are S phase specific?
MoA
AE

A
31
Q

What are the mitotic inhibitors that are M phase specific
MOA
AE

A
32
Q

What are topoisomerase inhibitors (anti cancer chemo)?
Moa
AE

A
33
Q

What are cell cycle non specific drugs?
MoA
AE

A

Alkylating agents

34
Q

What are the antitumor antibiotics used in cancer?
MoA
AE

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35
Q

What is normal range of Na+
What is classification of hypernatremia?

A

normal range = 135-145 mmol/L
Serum osmolality = 2Na+ + urea + glucose (normal: 285-295mmol/kg)

36
Q

What are the causes of hypernatremia?

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37
Q

What are the signs and symptoms of hyper vs hyponatremia?

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38
Q

What is the diagnostic algorithm for hypernatremia?

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38
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A
39
Q

What are the 2 steps in assessing hypernatremia?

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40
Q

What is the treatment principles for hypernatremia?
Maximum rate of correction in 24 hour period?

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41
Q

What is the treatment of hypervoemic/isolvemic/hypovolemic hypernatremia?

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42
Q

What is the severity of hypoantremia based on electrolyte level?

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43
Q

What is the etiology of hyponatremia?

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44
Q

What is the diagnostic algorithm for hyponatremia?

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45
Q

What are the 2 steps to assess hyponatremia?

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46
Q

What is the treatment objectives of hyponatremia
What complications of hyponatremia must you prevent
What is max correction and complication if overload?

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47
Q

What is the treatment of hyponatremia?

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48
Q

What is the rationale for using hypertonic saline, desmopressin and furosemide in managing hyponatremia?

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49
Q

What is normal range of K
Acid base status
Na+K+ ATP pump affected by what drug

A

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

50
Q

What are the causes of hyperK?

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51
Q

What are SS of hyperK?

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52
Q

What are SS of hypoK?

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53
Q

What is the diagnostic algorithm for hyperK?

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54
Q

What are the steps involved in finding out dx for hyperK?

A

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

55
Q

What is the treatment modalities for hyperkalemia?

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56
Q

What is treatment of urgent hyperkalemia?

A
  • 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
57
Q

What is treatment of chronic hyperK?

A

 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

58
Q

What is definition of hypoK
What is normal range

A
  • Normal range = 3.6 – 5.0
  • Plasma K+ < 3.0 mmol/L
  • Serum K+ < 3.5 mmol/L
59
Q

What are the causes of hypoK?

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60
Q

What is the diagnostic algorithm for hypoK?

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61
Q

What are the steps to assess hypoK and ddx?

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62
Q

What is the treatment principle of hypoK
What dosage form
Premixed K+ containing solutions for maintenance IV infusion

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63
Q

What is the treatment regimen of hypoK based on serum and ECG changes?

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64
Q

What are the treatment choices for hypoK?

A
  • 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

MBBS VI Medicine (93 decks)

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