Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PSA > Chapter 3: Data Interpretation > Flashcards

Chapter 3: Data Interpretation Flashcards

1
Q

Causes of anaemia (categorised by MCV)

A

Red blood cells:

  • Microcytic (low MCV) = iron deficiency anaemia, thalassaemia, sideroblastic anaemia.
  • Normocytic (normal MCV) = anaemia of chronic disease, acute blood loss, haemolytic anaemia, renal failure (chronic).
  • Macrocytic (high MCV) = B12/folate deficiency (megaloblastic anaemia), excess alcohol, liver disease (including non-alcoholic causes), hypothyroidism, “M” haematological causes (myeloproliferative, myelodysplastic, multiple myeloma).
    • B12 deficiency includes pernicious anaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of neutrophilia

A

Neutrophilia (high) :

  • bacterial infection
  • tissue damage (inflammation/infarct/malignancy)
  • *steroids*.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of Neutropenia

A

Neutropenia (low neutrophils)

  • viral infection
  • chemotherapy/radiotherapy (may become neutropenic in response to infection, neutropenic sepsis)
    • If neutropenic sepsis, must give urgent IV broad-spectrum antibiotics (hospital-specific).
  • clozapine (antipsychotic)
  • carbimazole (antithyroid).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Causes of lymphocytosis

A

Lymphocytosis (high lymphocyts)

  • viral infection
  • lymphoma
  • CLL.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Causes of Thrombocytopenia

A

Thrombocytopenia (low platelets)

  • reduced production
    • viral infection
    • drugs especially penicillamine in RA
    • myelodysplasia, myelofibrosis, myeloma
  • increased destruction
    • heparin
    • hypersplenism
    • DIC
    • ITP
    • HUS/TTP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Causes of thombocytosis

A

Thrombocytosis (high platelets)

  • reactive
    • bleeding
    • tissue damage e.g. infection/inflammation/malignancy
    • post-splenectomy
  • primary
    • myeloproliferative disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of hyponatraemia

Na+ 135-145 mmol/L

A

Hyponatraemia: assess fluid status first.

  • Hypovolaemic
    • fluid loss (D&V)
    • Addison’s
    • any diuretic.
  • Euvolaemic
    • SIADH
      • small cell lung tumours, _i_nfection, abscess, drugs (carbamazepine + antipsychotics), head injury.
    • psychogenic polydipsia
    • hypothyroidism.
  • Hypervolaemic
    • heart failure
    • renal failure
    • liver failure (hypoalbuminaemia)
    • nutritional failure (hypoalbuminaemia)
    • thyroid failure (hypothyroidism – can be euvolaemic too).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of SIADH

A

SIADH

  • small cell lung tumours
  • infection
  • abscess
  • drugs (carbamazepine + antipsychotics)
  • head injury.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of Hypernatraemia

A

Hypernatraemia: Causes all begin with “D”…

  • Dehydration.
  • Drips i.e. too much IV saline.
  • Drugs e.g. effervescent tablet preparations or IV preparations with high Na+ content.
  • Diabetes insipidus – opposite of SIADH.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Causes of Hypokalaemia (3.5-5mmol/L)

A

Hypokalaemia: DIRE

  • drugs (loop + thiazide diuretics)
  • inadequate intake or intestinal loss (D&V)
  • renal tubular acidosis
  • endocrine (Cushing’s + Conn’s syndrome).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of Hyperkalaemia (3.5-5mmol/L)

A

Hyperkalaemia: DREAD

  • drugs (K+-sparing diuretics + ACE-i)
  • renal failure
  • endocrine (Addison’s disease)
  • artefact (clotted sample)
  • DKA (when insulin given to treat DKA, K+ drops so needs monitoring + replacement).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Link between urea and Hb

A

Ur rise = AKI or upper GI haemorrhage

Hb broken down by gastric acid into Ur, then absorbed into blood

In an upper GI H’gge you may fine a low Hb, Ur rise.

nb isolated urea rise (without Creatinine rise may be seen in pre-renal causes of renal failure e.g. DEHYDRATION)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of pre-renal AKI

A

Pre-renal = U rise > C rise (U x 10 > C).

  • Dehydration (or if severe, shock) e.g. sepsis, blood loss.
  • Renal artery stenosis (often triggered by drugs e.g. ACEi or NSAIDs; renal hypoperfusion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of renal AKI

A

Intrinsic = U rise < C rise, no bladder or hydronephrosis.

INTRINSIC

  • ischaemic (prerenal AKI → ATN)
  • nephrotoxic antibiotics
    • gentamicin, vancomycin + tetracyclines
  • tablets
    • ACE-i, NSAIDs
  • radiological contrast
  • injury; rhabdomyolsis
  • negatively birefringent crystals (gout)
  • syndromes; glomerulonephridites
  • inflammation; vasculitis
  • cholesterol emboli.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of post renal AKI

A

Post-renal = U rise < C rise, bladder or hydronephrosis.

  • In lumen = stone or sloughed papilla.
  • In wall = tumour (renal cell, transitional cell), fibrosis.
  • External pressure = benign prostatic hyperplasia, prostate cancer, lymphadenopathy, aneurysm.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

LFT:

  1. Markers of hepatocellular injury or cholestasis
  2. Synthetic function
A
  1. bilirubin, ALT, AST, ALP.
  2. Albumin, vit K dependent clotting factors (2,7,9,10) measure PT/INR
17
Q

Causes of raised bilirubin (3 categories)

A
  • Bilirubin rise only = pre-hepatic e.g.
    • haemolysis
    • Gilbert’s syndrome
    • Crigler-Najjar syndrome
  • Bilirubin + AST/ALT rise = hepatic e.g.
    • fatty liver
    • hepatitis
    • cirrhosis
      • Hepatitis + cirrhosis = alcohol, viruses (hepatitis A-E, CMV + EBV), drugs (paracetamol overdose).
    • malignancy; 1⁰ or 2⁰
    • metabolic; Wilson’s, haemochromatosis
    • HF
  • Bilirubin + ALP rise = post-hepatic i.e. obstruction…
    • In lumen = gallstones, drugs (flucloxacillin, co-amoxiclav, nitrofurantoin, steroids + sulphonylureas).
    • In wall = cholangiocarcinoma, PBC, PSC.
    • External pressure = pancreatic or gastric cancer, lymph nodes.
18
Q

Causes of raised ALP

A

ALKPHOS

  • any fracture
  • liver damage (post-hepatic)
  • k for kancer
  • Paget’s + pregnancy
  • hyperparathyroidism
  • osteomalacia
  • surgery.
19
Q

Thyroid Fynction tests: and Changing levothyroxine!

A

Check TSH (0.5-5mIU/L), and change by smallest increment offered (unless grossly hypo/hyperthyroid).

  • <0.5 = decrease dose
  • 0.5-5 = nil action
  • >5 = increase dose.
20
Q

Abnormal TFTs: Hypothyroidism

A

Primary hypothyroidism = ↓T4 from thyroid so ↑TSH from pituitary = Hashimoto’s, drug-induced.

Secondary hypothyroidism = ↓TSH, so ↓T4 = pituitary tumour or damage.

21
Q

Abnormal TFTs: Hyperthyroidism

A

Primary hyperthyroidism = ↑T4, so ↓TSH = Grave’s, toxic nodular goitre, drug-induced.

Secondary hyperthyroidism = ↑TSH, so ↑T4 = pituitary tumour.

22
Q

Quick review of CXR:

PIPRA + ABCDEFGH

PSA=?pneumonia/pulmonary oedema

A

PIPRA:

  • Projection: PA (N, PA if no markings) or AP (can’t comment on heart) – should see from above clavicles to below diaphragm.
  • Inspiration: 7th anterior (down-sloping) rib transects diaphragm.
  • Penetration: vertebral bodies behind heart.
  • Rotation: distance between spinous processes + clavicles equal.
  • Artefact: if present.

ABCDEFGH:

  • Airways: trachea central – if not, consider collapse (towards) or pneumothorax (away).
  • Bone: rib fractures or lytic lesions.
  • Cardiac: cardiothoracic ratio <50% on PA film.
  • Diaphragm: air under diaphragm – bowel perforation or recent surgery; under L side is gastric bubble (N).
  • Edges: costophrenic + cardiophrenic angles sharp or blunt (effusion).
  • Fields: white area = effusion (unilateral + solid), pneumonia (unilateral + fluffy), oedema (bilateral + fluffy), fibrosis (bilateral + honeycomb).
    • Oedema, ABCDE = alveolar oedema, kerley B lines, cardiomegaly, diversion of blood to upper lobes, effusions.
    • Sail sign (triangle shape) behind heart = L lower lobe collapse.
  • Gynaecomastia + other soft-tissues.
  • Hila.
23
Q

Quick review of ABG

A
  • Check inspired oxygen concentration (FiO2):
    • Calculate N PaO2 for patient on oxygen: subtract 10 from FiO2, and if PaO2 exceeds this number, then patient not hypoxic.
      • E.g. On 60% oxygen with FiO2 of 30kPa actually hypoxic. Accurately done via arterial-alevolar gradient.
  • Check for respiratory failure: if PaO2 low or inappropriately N.
    • Type 1 = low or N PaCO2 (fast breathing) → heart/lung damage causing SOB.
    • Type 2 = high PaCO2 (slow breathing) → ‘blue-bloaters’ of COPD, NM failure or restrictive chest wall abnormalities.
  • Check acid-base status:
    • Low pH = acidosis; high pH = alkalosis.
    • PaCO2 abnormal = respiratory. HCO3 abnormal = metabolic. Both = compensation (fully if pH normal, otherwise partial). Both abnormal in opposite directions = mixed.
24
Q

Causes of the 4 acid base abnormalities

A

Respiratory alkalosis = rapid breathing – disease or anxiety.

Respiratory acidosis = same causes as T2RF. (COPD, blue bloaters, + neuromuscular failure + restrictive chest wall abn)

Metabolic alkalosis = vomiting, diuretics + Conn’s syndrome.

Metabolic acidosis = multiple causes e.g. lactic acidosis, DKA, renal failure, ethanol/methanol/ethylene glycol intoxication → narrow cause by using anion gap.

25
Q

Quick review of ECG interpretation

A

Rate: divide 300 by # of large squares between each QRS complex; N = 60-100bpm.

Rhythm: p-waves present before QRS = sinus; PR interval not constant or >1 square = heart block → 1st degree = constant but >1 square, 2nd degree type 1 = increasing PR then misses a QRS, 2nd type 2 = 2/3 p waves for every QRS, 3rd/complete = no relationship; no p waves + irregular QRS complexes = AF.

Axis: look at direction of I and II. If I +ve and II +ve = N; If I +ve and II –ve = LAD; If I –ve and II +ve = RAD.

QRS: width <3 small squares = N, narrow-complex; >3 = BBB – WiLLiaM = LBBB, rSR (M shape) in V6, MarRRoW = RBBB, rSR in V1.

V-waves: Add largest deflection in V1 to V6; >3.5 large squares = LVH (Sokolov-Lyon); small complexes throughout = pericardial effusion.

ST segment: elevated = infarction (flat + some leads) or pericarditis (convex + all leads); depressed = ischaemia (flat + some leads) or digoxin (down-sloping, all leads).

T-waves: height > 2/3rd QRS height throughout ECG = hyperkalaemia; inversion = N in aVR + I, other leads = old infarction/LVH

26
Q

What criteria would suggest the need for monitoring

name 6 common drugs that require monitoring

A

Drug with narrow therapeutic index; small difference in blood concentration for therapeutic + toxic effects require monitoring

  1. digoxin
  2. theophylline
  3. lithium
  4. phenytoin
  5. ABx: gentamicin
  6. ABx: vancomycin
27
Q

What does drug monitoring entale (2 part)

A

Monitoring

  1. assess clinical state
    • response to drug
    • evidence of toxicity
  2. measure serum drug levels

→ adjust dose/frequency accordingly

28
Q

For what reasons is the dose/freq of a drug altered (4)

A

Inadequate response + low serum drug level = increase dose – in general by smallest possible increment, especially if 0-order kinetics (e.g. phenytoin).

Adequate response + N/low serum drug level = no change – clinical response more important, as already therapeutic dose!

Adequate response + high serum drug level = decrease dose – if toxicity, then can omit for few days (except gentamicin).

  • gent: pre-emptive decrease in frequency by 12hrs (e.g. 36 rather than 24hrs)

Toxicity + any serum drug level = (1) stop dose (+ alternative); (2) supportive measures (usually IV fluids); (3) give antidote

29
Q

Common signs of drug toxicity

  • Digoxin
  • Lithium
  • Phenytoin
  • Gentamicin
  • Vancomycin
A
  • Digoxin
    • confusion
    • nausea
    • visual halos
    • arrythmia
  • Lithium
    • early: tremor
    • intermediate: tiredness
    • Later: arrhythmias
    • seizures
    • coma
    • renal failure
    • diabetes insipidus
  • Phenytoin
    • gum hypertrophy
    • ataxia
    • nystagmus
    • peripheral neuropathy
    • teratogenicity
  • Gentamicin
    • ototoxicity
    • nephrotoxicity
  • Vancomycin
    • ototoxicity
    • nephrotoxicity
30
Q

Gentamicin normal dosing (&2 exceptions)

A

Gentamicin monitoring: IV aminoglycoside antibiotic used in severe infections.

Doses calculated via weight + renal function.

  • Most treated with high-dose regimen of 5-7mg/kg once-daily;
  • Renal failure patient recieve divided daily dosing (1mg/kg) 12-hourly
  • Endocarditis patients recieve divided daily dosing (1mg/Kg) 8-hourly

Must monitor as high risk of nephrotoxicity + ototoxicity.

31
Q

Gentamicin: Normal once daily regime monitoring

A

Risk of ototoxicity and nephrotoxicity

  • Measure gentamicin levels at particular times e.g. 6-14h after last gentamicin infusion started.
  • Use nomogram (specific to dose). If point on graph falls within 24h area, continue at same dose. If above 24h area, then change dosing:
    • If in 36h area, change to 36-hourly dosing.
    • If in 48h area, change to 48-hourly dosing.
    • If above 48h area, repeat gentamicin level and only re-dose when concentration <1mg/L.
  • Change frequency over dose as need sufficient dose to hit peak to hit minimum inhibitory concentration of organism.
32
Q

Gentamicine: divided daily dosing regimes + monitoring

A

Divided daily dosing: Nomogram exists, but daily peak and trough levels usually used instead.

  • Peak (1hr post dose) if outside of normal range (3-5mg/L (endocarditis) 5-10mg/L (all else)) adjust the dose
  • Trough (just before next dose) if outside of normal range (<1mg/L (endocarditis) <2mg/L (all else)) adjust the interval
33
Q

Management of paracetamol overdose (2)

A
  • Specific = N-acetyl cysteine (NAC) if appropriate.
    • Paracetamol metabolised by liver; relies on glutathione which is quickly depleted so toxic NAPQI accumulates. NAC replenishes it.
  • Supportive = particularly IV fluids.
34
Q

Warfarin Mechanism of action

A

Inhibits synthesis of vitamin K-dependent clotting factors (2, 7, 9 + 10) – prolongs PT from which INR derived.

35
Q

What is INR?

A

INR = ratio of patient PT to N population.

Normal INR = 1. INR

Only used to monitor warfarin – use PT for liver disease/ DIC

36
Q

Target INRs

A

Target INR for most = 2.5

if recurrent thromboembolism while on warfarin or metal replacement heart valves INR = 3.5.

37
Q

If major bleed i.e. causing hypotension or bleeding in confined space (brain or eye):

A
  1. Stop warfarin
  2. give 5-10mg IV vitamin K
  3. give prothrombin complex (e.g. Beriplex).
38
Q

How to manage over coagulation

A

If not bleeding, then look at INR to judge next step:

  • INR <6 = reduce warfarin dose.
  • INR 6-8 = omit warfarin for 2 days then reduce dose.
  • INR >8 = omit warfarin + give 1-5mg oral vitamin K.
  • If minor bleeding, with INR >5, give IV instead of oral vitamin K.

PSA (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions