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6th Year PSA > Data Interp > Flashcards

Data Interp Flashcards

1
Q

do you always need to stop NSAIDs in asthmatics

A

NO - only if q suggests pts asthma is NSAID sensitive ie. they have a wheeze then you should stop (it causes bronchoconstriction)

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2
Q

causes of microcytic anaemia TAILS

A 
Thalassaemia
ACD
IDA 
Lead poisoning 
Sideroblastic anaemia (congenital)
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3
Q

causes of normocytic anaemia 3As & 2Hs

A

ACD
Acute blood loss
Aplastic anaemia

Haemolytic anaemia
Hypothyroidism

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4
Q

causes of macrocytic anaemia ‘Alcoholics may have liver failure’ - AMHLF

A 
Alcoholism
Myelodysplastic syndrome, Multiple myeloma
Hypothyroidism, Haemolytic anaemia
Liver failure
Folate + B12 deficiency
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5
Q

WCC + differentials - HIGH neutrophils - causes

A

BACTERIAL, tissue damage, steroids (reactive neutrophilia)

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6
Q

WCC + differentials - LOW neutrophils - causes

A

VIRAL, chemo/radiotherapy, clozapine, carbimazole

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7
Q

WCC + differentials - HIGH lymphocytes - causes

A

VIRAL, lymphoma, CLL

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8
Q

HIGH platelets - two types + causes

A

REACTIVE - Bleeding, tissue damage, post-splenectomy

PRIMARY - Myeloproliferative disorders

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9
Q

LOW PLATELETS - due to increased destruction - causes

A 
HEPARIN (induced thrombocytopaenia) 
hypersplenism
DIC
ITP
HUS/TTP
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10
Q

LOW PLATELETS - due to reduced production - causes

A

infection (viral)
DRUGS (PENICALLIMINE) eg in RhA pts
MDS/MF/MYELOMA

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11
Q

hyponatraemia assessment of what determines causes

A

fluid status

  • hypovolaemia: D, V, Diuretics, Salt losing nephropathy
  • euvolaemic: endocrine - hypothyroidism, Adrenal insufficiency, SIADH
  • hypervolaemic: 3x failures: HF, liver failure, renal F
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12
Q

euvolaemic hyponatraemia due to SIADH causes (pnemonic SIADH) x5

A 
SCLC + surgery
Infections
Abscess
Drugs - CARBAMAZEPINE, ANTIPSYCHOTICS
Head Injury

CNS pathology - stroke, haemorr, T
Lung pathology - pneumonia (Legionella), pneumothorax
Drugs - SSRI, TCA, PPI, Carbamazepine, opiates
Tumours
SURGERY

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13
Q

hypernatraemia causes - all begin with d’s (4)

A

dehydration
drips ie. too much saline
drugs - with too much sodium
diabetes insipidus - opposite of SIADH

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14
Q

hypernatraemia due to primarily - INCR in SODIUM +/OR LOSS OF WATER & secondaryily - LOW WATER INTAKE

A 
INCR in SODIUM: 
Medical high intake
Dietary high intake
Conn's Syndrome 
RAS
Cushing's Syndrome (overactivation of MR by cortisol --> aldosterone like effect) 
LOSS OF WATER: 
Renal losses 
-Osmotic diuresis
-DI 
NON- renal losess
-GI loss
-Sweat loss

LOW WATER INTAKE

  • child/elderly/dementia
  • fasting for surgery
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15
Q

Hypokalaemia (DIRE)

<3.5

A

DRUGS (LOOP + THIAZIDE diuretics)
Inadeq intake or GI loss (D/V)
RTA
Endocrine (Cushings + Conns)

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16
Q

Hyperkalaemia (DREAD)

>5.3

A

DRUGS (potassium sparing diuretics+ ACEi)
Renal F
Endocrine (Addisons)
Artefact (v.common - due to clotted sample)
DKA tx with insulin drops K+

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17
Q

raised urea with normal creatinine what should you look at next and what will it show

A

haemoglobin

-likely to be low as urea raised due to UGI bleed

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18
Q

3 cauess of a raised urea

A

AKI, UGI haemorrhage, eat a big steak

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19
Q

PRE-RENAL causes of AKI

A

= 70% of AKIs
UREA rise&raquo_space; Creatinine rise

Dehydration / shock
RAS (precipitated by ACEi or NSAIDs)

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20
Q

POST-RENAL causes of AKI

A

=20% of AKIs
Creatinine rise > Urea rise

OBSTRUCTION 
-bladder/hydronephrosis may be palpable
Luminal: Stones
Mural: TCC, renal cell carcinoma
Extra-mural: BPH
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21
Q

INTRINSIC RENAL causes of AKI

A

= 10% of AKIs
Creatinine rise > Urea rise

Ischaemia (pre-renal --> ATN)
Nephrotoxic ABx
Tablets (ACEi, NSAIDs)
Radiological contrast
Injury (rhabdo)
Negatively birefringent crystals (gout)
Syndromes (GN)
Inflammation (vasculitis)
Cholesterol emboli

-bladder/hydronephrosis NOT palpable

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22
Q

how can you assess liver ftn x 2 broad categories

A

HEPATOCTYE INJURY or CHOLESTASIS eg

  • BR
  • ALT + AST
  • ALP

SYNTHETIC FTN (ie. the protein it makes)

  • ALBUMIN
  • VIT K DEP CLOTTING F’S (2,7,9,10) meas via PT/INR
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23
Q

what does solitary raised BR often mean

A

HAEMOLYSIS - as BR is a break down product of Hb

-this is a cause of Pre-hepatic J NOT due to liver problems

24
Q

causes of raised ALP (ALKPHOS)

A 
Any fracture
Liver damage
K (for kancer)
Pagets disease of bone, Pregnancy
Hyperparathyroidism
Osteomalacia
Surgery
25
Q

where can ALP be found

A

placenta, bone, liver, bowel wall

26
Q

AST>ALT in what

A

Alcoholic hepatitis - because Ash Sahota drinks alcohol

27
Q

ALT>AST

A

Other hepatitis

28
Q

which TB drugs cause Drug induced liver injury

A

Isoniazid, Pyrazinimide

29
Q

name 5 cholestatic drugs

A 
flucloxacillin 
CO-AMOXICLAV
nitrofurantoin
steroids
sulphonylureas
30
Q

what is a PRE-hepatic pattern of LFTs + some causes

A

Pattern: BR increase
Cause: HAEMOLYSIS, Gilberts, Crigler-Najjar Syndrome

31
Q

what is an INTRA-hepatic pattern of LFTs + some causes

A

Pattern: BR & ALT/AST increase
Causes: Hepatitis, Cirrhosis, Fatty Liver, Malignancy (1’ or 2’), Metabolic: Wilsons disease/haemochromatosis, HF (causing hepatic congestion)

32
Q

what is a POST-HEPATIC (Obstructive) pattern of LFTs + some causes

A

Pattern: BR & ALP increased
Causes:
-luminal: stone (GS), drugs causing cholestasis
-mural: tumour (cholangiocarcinoma), PBC, PSC
-extramural: pancreatic or gastric C, LN

33
Q

Q on changing levothyroxine dose according to TFT result - what should you be guided by

A

TSH level 0.5-5 = target
-change by the SMALLEST increment offerred
IF <0.5 –> DECR DOSE
IF >5 –> INCR DOSE

34
Q

on what CXR view can you assess the size of the heart

A

ONLY on PA (NORMAL)

on AP the heart automatically appears larger

35
Q

how is rotation on a cxr assessed

A

distance between spinal processes and clavicles equidistant

36
Q

what happens to trachea in lung collapse + pneumothorax

A

COLLAPSE - TOWARDS affected side

PNEUMOTHROAX - away

37
Q

widened mediastinum on CXR (2)

A

Aortic dissection

RUL collapse with tracheal deviation

38
Q

triangle behind heart on CXR

A

sail sign

-LEFT LOWER LOBE COLLAPSE

39
Q

A-E of P.Oedema

A 
ALVEOLAR SHADOWING (bat wing)
Kerley B-lines (interstitial oedema)
Cardiomegaly
Diversion of the upper lobe
Effusions
40
Q

LVH criteria

A

QRS deflection of V1 ADDED to QRRS deflection of V6 (in terms of LARGE SQUARES) >= 3.5 = LVH

41
Q

ST segment depression due to what (3)

A 
Ischaemia
Infarction
 - check trop to distinguish - will be in some leads
DIGOXIN
- will be downsloping in ALL leads
42
Q

in what leads is T WAVE INVERSION NORMAL

A

Leads I & aVR (top middle two)

-in other leads TWI = OLD INFARCT/LVH

43
Q

what type of drugs require monitoring

A

NARROW TI drugs

44
Q

how to change drug doses of narrow TI drugs

A

If low serum drug level AND inadequate clinical response – INCREASE drug level
If low serum drug level BUT adequate clinical response – do NOT increase drug
If high serum drug level AND adequate clinical response – DECREASE drug level
-Except GENTAMICIN – the FREQ of administration is decreased, not the amount (by 12h, so instead of drug every 24h give every 36h)

45
Q 
Features of toxicity of drugs with narrow TI:
Digoxin
Lithium
Phenytoin
Theophylline
Gentamicin
Vancomycin
A

Digoxin - confusion, nausea, visual haloes, arrythmias
Lithium - early: tremor, intermed: tired, late: arrythmias, seizure, coma, ARF, DInsipidus
Phenytoin - gum hypertrophy, ataxia, nystagmus, periph neuropathy, teratogenicity
Theophylline - N/A
Gentamicin - ototoxic, nephrotoxic
Vancomycin - ototoxic, nephrotoxic

46
Q

Gentamicin dosing - based on what 2 things + what is usual

A

Dose by patient WEIGHT and RENAL FTN (serum creatinine)
· Usual dose (high-dose regimen) = 5-7mg/kg, OD (24-hourly)
· Renal failure (<20mL/min CrCl) = 1mg/kg, BD (12-hourly)
· IE = 1mg/kg, TDS (8-hourly)

47
Q

Gentamicin dosing - OD regimen monitoring + divided daily dosing

A

OD REGIMEN MONITORING:

  • Measure levels at particular times (6-14 HRS after last infusion)
  • Plot on a NORMOGRAM (see below)
  • Use nomogram to determine FREQUENCY of dosing (every 24, 36 or 48 hours)

DIVIDED DAILY DOSING:
-normogram exists but usually, daily peaks + troughs are used to guide tx

48
Q

Paracetamol OD <1 hr + >1 hr

A

<1hr –> activated charcoal–> Ix: paracetamol level ≥4hr after ingestion –>? NAC
If below the treatment line at 4 hours post-ingestion, no NAC is required
o If staggered overdose taken or time not known of ingestion, use NAC

> 1hr –> Ix: paracetamol level ≥4 hours after ingestion –>? NAC
o Use NAC graph to decide whether to administer

49
Q

what happens to LFTs in para OD

A

o ALT, AST: very high [peak at 72 hours post-ingestion]
o ALP: normal
o PT: if >180 seconds on day 4 will need transplantation

50
Q

when to stop warfarin before surgery

A

5 days

51
Q

warfarin INR targets

A

AF, DVT, cardioversion, cardiomyopathy, MI –> 2-3

Recurrent VTE on warfarin, mechanical heart valve –>3-4

52
Q

warfarin OD

A

Major bleed (–>hypotension OR bleed in a confined space – i.e. skull, eye)
o Stop warfarin
o IV vitamin K (5mg, slow IV) – Phytomenadione
o IV PCC – Beriplex

53
Q

warfarin + INR>8 + minor bleeding

A

Stop warfarin, IV VIT K (1-3mg; repeat in 24hrs if still high), restart warfarin when INR <5

54
Q

warfarin + INR>8 + no bleeding

A

Stop warfarin, PO VIT K (repeat in 24hrs if still high), restart warfarin when INR <5

55
Q

warfarin + INR 5-8 + minor bleeding

A

Stop warfarin, IV vitamin K (1-3mg), restart warfarin when INR <5

56
Q

warfarin + INR 5-8 + no bleeding

A

Withhold 1-2 doses of warfarin, consider reducing maintenance dose

57
Q

neutropenic sepsis mx

A

IV meds always (30% mortality so need to be aggressive)

- IV Piperacillin with Tazobactam + Gentamicin

6th Year PSA (11 decks)

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