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Pass The PSA > 3. Data interpretation > Flashcards

3. Data interpretation Flashcards

1
Q

What are the causes of microcytic anaemia?

A

Microcytic: TAILS
Thalassaemia, Anaemia of chronic disease, Iron-deficiency, Lead poisoning, Sideroblastic)

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2
Q

What are the causes of normocytic anaemia?

A

Normocytic: Anaemia of chronic disease, acute blood loss, haemolytic, renal failure

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3
Q

What are the causes of macrocytic anaemia?

A

Macrocytic: B12/folate, alcohol, hypothyroidism, myelo- conditions

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4
Q

What are the causes of high neutrophils?

A

Bacterial infection
Tissue damage (inflammation, infarct, malignancy)
Steroids

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5
Q

What are the causes of low neutrophils?

A

Viral infection
Clozapine
Carbimazole
Chemo/radiotherapy

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6
Q

What are the causes of high lymphocytes?

A

Viral infection
Lymphoma
CLL

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7
Q

What are the causes of high platelets?

A

Reactive: Bleeding, tissue damage
Primary: Myeloproliferative disorders

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8
Q

What are the causes of low platelets

A

Reduced production: Drugs (penicillamine), infection, myelo issues
Increased destruction: Heparin, DIC/ITP/TTP/HUS/TTP

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9
Q

What are the causes of hypovolaemic hyponatraemia?

A

Fluid loss (inc D+V)
Diuretics
Addison’s Disease

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10
Q

Causes of euvolaemic hyponatraemia?

A

SIADH
Psychogenic polydipsia
Hypothyroidism

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11
Q

Causes of hypervolaemic hyponatraemia?

A

Heart failure
Renal failure
+ liver/nutritional/thyroid failure

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12
Q

What are the causes of SIADH?

A

SCLC
Infections
Abscess
Drugs (antipsychotics, carbamazepine)
Head injury

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13
Q

Causes of hypokalaemia?

A

DIRE
Drugs (loop and thiazide)
Intestinal loss (D+V)
RTA
Endocrine (Cushings and Conns)

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14
Q

Causes of hyperkalaemia?

A

DREAD
Drugs (ACEIs, K+-sparing)
Renal failure
Endocrine (Addison’s)
Artefact (clotted sample)
DKA (can go hypo once insulin given)

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15
Q

How can you distinguish between pre, intra and post renal AKI?

A

Prerenal: rise urea > creatinine
Intra: rise creat > urea
Post: rise creat > urea + palpable bladder/hydronephrosis

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16
Q

Causes of pre-renal AKI

A

Dehydration (inc RAS)

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17
Q

Causes of intrinsic AKI

A

INTRINSIC
Ischaemia
Nephrotoxics
Radiological contrast
Injury (rhabdomyolysis)
Negative crystals (gout)
Syndromes (glomerulonephritis)
Inflammation
Cholesterol emboli

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18
Q

Causes of post-renal AKI?

A

Obstructions in lumen, wall or externally

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19
Q

How can severe pre-renal AKI be differentiated from intrinsic/post?

A

If urea x 10 > creat = severe pre-renal

20
Q

How can AKI and UGI bleed be differentiated?

A

UGI bleed will have low Hb

21
Q

What are the common nephrotoxics?

A

Renal drugs
NSAIDs
Antibiotics: gent, vanc, tetracylcines

22
Q

How do you assess hepatic function

A

Albumin, PT, bilirubin and gluocse

23
Q

How can pre, intra and post-hepatic jaundice be determined from LFTs

A

Raised bilirubin for all with
Pre: insignificant rises in both ALT and ALP
Intra: ALT rises > 10x and ALP rises < 3x
Post: ALT rises < 10x and ALP rises >3x

24
Q

How can LFTs distinguish between pathological and drug induced intrahepatic jaundice?

A

ALT associated with liver disease
AST associated with alcohol

25
Q

Causes of pre-hepatic jaundice?

A

Haemolysis

26
Q

Causes of intrahepatic jaundice

A

Damage within the liver (hepatitis, cirrhosis, malignancy)

27
Q

Causes of post-hepatic jaundice

A

Obstruction in lumen, wall or surrounding

28
Q

Distinguish between primary and secondary
a) hypothyroidism
b) hyperthyroidism

A

a) Low T4 with raised / low TSH
b) High T4 with low / raised TSH

29
Q

What causes primary and secondary hypothyroidism?

A

1: Hashimoto’s, drug induced
2: Pituitary pathology

30
Q

What causes primary and secondary hyperthyroidism?

A

1: Graves, toxic nodular goitre, drugs
2: Pituitary tumour

31
Q

What TSH dictates an increase or decrease in levothyroxine

A

decrease < 0.5-5.5 < increase

32
Q

How is CXR quality assessed>

A

PRIM
Projection: AP heart size > PA
Rotation: Distance between clavicles
Inspiration: Is the 7th anterior rib visible?
Markings: additional things the radiographer has seen

33
Q

Outline the ABCDE approach for CXR interpretation

A

Airway: trachea, carina, bronchi, hilar
Breathing: Lungs and pleura
Cardiac: Heart size and borders
Diaphragm: inc costophrenic angles
Everything else: bones, soft tissues, tubes, pacemakers etc

34
Q

How does a normal airway look on CXR?

A

Trachea central/slightly right
Bronchi division visible, right bronchus stockier than left

35
Q

What problems can be seen with airways on CXR?

A

Tracheal deviation: Pushed away (cancer, effusion), towards (tension pneumothorax)
Hilar enlargement: Unilateral (malignancy), bilateral (sarcoidosis)

36
Q

How do you assess the lung fields?

A

Check upper middle and lower zones have lung markings throughout
Pleura should be non visible (thickening suggests mesothelioma, reduced extension suggests pneumothorax

37
Q

How do you assess the heart on CXR

A

<50% thoracic width on PA, if not then consider congestive, structural or effusion

38
Q

How do you assess the diaphragm on CXR?

A

Should be indistinguishable from liver
If separated, free gas could be present so urgent senior review (likely perforation)
Blunted costophrenic angles mean fluid or consolidation

39
Q

What are the features of pulmonary oedema?

A

Alveolar oedema
B-lines
Cardiomegaly
Diversion to upper zones (vessels bigger here)
Effusions

40
Q

How can you differentiate between oedema and pneumonia?

A

ABCDE and bilateral for oedema, unilateral (usually) for pneumonia

41
Q

How do you account for Pa02 for someone on O2 therapy?

A

% O2 -10 = normal kPa
(if on 50% then kPa should be 40)

42
Q

How can you distinguish between T1 and T2 resp failure?

A

T1: low/Normal PaCO2 (fast/shallow breathing so blowing off CO2)
T2: High PaCO2 (slow breathing: blue bloaters, NM failure)

43
Q

Outline how PaCO2, HCO3- and pH are interpreted for acid-base status

A

Raised PaCO2: resp
Raised HCO3: metabolic
Both up/down + normal pH: compensation

44
Q

Causes of
Resp acidosis
Metabolic acidosis
Resp alkalosis
Metabolic alkalosis

A

Resp acidosis: T2RF
Metabolic acidosis: Lactic acidosis, DKA, renal failure
Resp alkalosis: rapid breathing, anxiety
Metabolic alkalosis: vomiting, diruretics, Conn’s Syndrome

45
Q

How do you manage a paracetamol overdose

A

Acute: Check normogram after 4hrs + administer NAC if above/fluids if below line
Staggered: NAC

46
Q

What is INR? What does it indicate?

A

Patient PT/population PT
Higher means longer clotting time .’. bleed risk

47
Q

Treat the following INRs for patients on warfarin
<6
6-8
>8
Major bleed (low BP, confined space eg brain, eye)

A

<6: reduce dose
6-8: Omit 2 days then reduce
>8: Omit + give 1-5mg oral vitamin K
Major: omit + 5-10 vit K IV + PT complex

Pass The PSA (5 decks)

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