Data interpretation Flashcards
Q3.1
Stop
- clozapine - agranulocytosis
- propanolol and ibuprofen - CI in asthmatics
Causes of microcytic anaemia
1. Most common
2. TAILS
Most common - IDA
T – Thalassaemia
A – Anaemia of chronic disease
I – Iron deficiency anaemia
L – Lead poisoning
S – Sideroblastic anaemia
Causes of normocytic anaemia
1. Most common
2. 3A2H
Most common: anaemia of chronic disease and acute blood loss
A – Acute blood loss
A – Anaemia of Chronic Disease
A – Aplastic Anaemia
H – Haemolytic Anaemia
H – Hypothyroidism
Macrocytic anaemia
1. Most common
2. Megaloblastic
3. Normoblastic
- B12 deficiency/ folate deficiency
Excess alcohol
Liver disease (non-alcoholic causes included) - B12 deficiency/ folate deficiency
- Alcohol
Reticulocytosis (usually from haemolytic anaemia or blood loss)
Hypothyroidism
Liver disease
Drugs such as azathioprine
Neutrophilia causes
MC: Bacterial infection
- tissue damage
- steroids
Neutropenia
MC: Viral infection, clozapine, carbimazole
- chemo/radiotherapy
Lymphocytosis
MC: Viral infection
- Lymphoma
- Chronic lymphocytic leukemia
Neutropenic sepsis
Patient on anti-cancer or immunosuppressant treatment gets neutropenia <1
Thrombocytopenia
M/C: Drugs e.g. penicillamine and heparin
- Reduced production: infection, drugs e.g. penicillamine, myelodysplasia, myelofibrosis, myeloma
- Reduced destruction: heparin, hypersplenism, DIC, ITP, haemolytic uremic syndrome
Hyponatraemia
1. Hypovolaemic
2. Euvolaemic
3. Hypervolaemic
- M/C: fluid loss (esp. diarrhoea and vomiting) + diuretics (any type)
- Addison’s - SIADH, psychogenic polydipsia, hypothyroidism
- M/C: HF, renal failure
- liver failure, nutritional failure (both causing hypoalbuminaemia)
- Thyroid failure (hypothyroidism, can be euvolaemic too)
Causes of SIADH
S mall cell lung tumours
I nfection
A bscess,
D rugs (especially carbamazepine and antipsychotics)
H ead injury
Causes of hypernatraemia (4Ds)
Dehydration
Drips (too much saline)
Drugs
Diabetes insipidus
Hypokalaemia (DIRE)
M/C: Drugs (loop and thiazide diuretics)
Inadequate intake or intestinal loss (e.g. vomiting/diarrhoea)
Renal tubular acidosis
Endocrine (Cushing’s and Conn’s)
Hyperkalaemia (DREAD)
M/C: Drugs (K+ sparing diuretics and ACE-i)
Renal failure
Endocrine (Addison’s disease)
Artefact (v common, due to clotted sample
DKA
What can a raised urea be a sign of?
AKI and upper GI bleed
Why is urea raised in upper GI bleed
Urea is a breakdown product
of amino acids (such as globin chains in haemoglobin) (blood broken down by gastric juice and urea absorbed)
- What to do if raised urea but normal creatinine in a patient who is not dehydrated (i.e. does not have prerenal failure)
Check Hb –> if low, possible GI bleed
Types of AKI
- Pre-renal (70%)
- Intrinsic (10%)
- Post-renal (i.e. obstructive, 20%)
Pre-renal AKI (70%)
1. Biochemical disturbance
2. Causes
- Urea rise»_space; creatinine rise
- Dehydration (or if severe, shock) of any cause, e.g. sepsis, blood loss.
- Renal artery stenosis (RAS)∗
- Dehydration (or if severe, shock) of any cause, e.g. sepsis, blood loss.
Intrinsic AKI (10%)
1. Biochemical disturbance
2. Causes (INTRINSIC)
- Urea rise «creatinine rise, bladder or hydronephrosis not palpable
- M/C: N + T
I schaemia (due to prerenal AKI, causing acute tubular necrosis)
N ephrotoxic antibiotics ∗∗
T ablets (ACEI, NSAIDs)
R adiological contrast
I njury (rhabdomyolysis)
N egatively birefringent crystals (gout)
S yndromes (glomerulonephridites)
I nflammation (vasculitis)
C holesterol emboli
Post-renal AKI (20%)
1. Biochemical disturbance
2. Causes (lumen, wall, external pressure)
- Urea rise «creatinine rise, bladder or hydronephrosis may be palpable
- In lumen: stone or sloughed papilla
In wall: tumour (renal cell, transitional cell), fibrosis
External pressure: benign prostatic hyperplasia, prostate cancer, lymphadenopathy, aneurysm
Note regarding differentiating severe pre-renal AKI with high creatinine and intrinsic/obstructive AKI
multiply the urea by 10; if it exceeds the creatinine (showing a relatively greater increase in urea compared to creatinine) then this suggests a pre-renal aetiology.
Nephrotoxic antibiotics
Gentamicin, vancomycin and tetracyclines
How is AKI usually triggered in renal artery stenosis
ACE-i or NSAIDs
Liver function: markers of hepatocyte injury or cholestasis
- bilirubin
- alanine aminotransferase (ALT) and the less commonly measured
aspartate aminotransferase (AST) - alkaline phosphatase (alk phos or ALP).
Liver function: synthesis markers
- albumin
- vitamin K-dependent clotting factors (II, VII, IX and X) measured via prothrombin time (PT)/international normalized ratio (INR).
What would a raised bilirubin on its own indicate?
A raised bilirubin on its own indicates prehepatic jaundice
(Same as single raised urea indicates pre-renal injury)
bilirubin is a breakdown product of haemoglobin, think haemolysis
Common causes of a raised Alk Phos (ALKPHOS)
Any fracture
Liver damage (posthepatic)
K (for kancer)
Paget’s disease of bone and Pregnancy
Hyperparathyroidism, Osteomalacia, and Surgery.
Deranged LFTs: pre-hepatic
1. Biochem
2. Causes
- Single raised bilirubin
- M/C: Haemolysis
- Gilbert’s and Crigler-Najjar syndromes
Deranged LFTs: intra-hepatic
1. Biochem
2. Causes
- Raised bilirubin AND raised AST/ALT
- M/C: hepatitis, cirrhosis, malignancy
- Fatty liver
- Metabolic (Wilson’s disease/haemochromatosis)
- HF (causing hepatic congestion)
Deranged LFTs: post-hepatic (obstructive)
1. Biochem
2. Causes (in lumen, in wall, ext pressure)
- Raised bilirubin AND raised ALP
2.M/C: Gallstones, drugs causing cholestasis, gastric/pancreatic cancer
In lumen: gallstones, drugs causing cholestasis
In wall: tumour (cholangiocarcinoma), PBC, sclerosing cholangitis
Ext pressure: pancreatic or gastric cancer, lymph node
Common causes of hepatitis and cirrhosis
(1) alcohol
(2) viruses (Hepatitis A–E, CMV, and EBV)
(3) drugs (paracetamol overdose, statins, rifampicin)
(4) autoimmune (primary biliary cirrhosis, primary sclerosing
cholangitis, and autoimmune hepatitis).
Drugs causing cholestasis
Flucloxacillin
CO-AMOXICLAV
nitrofurantoin
steroids
sulphonylureas
TFTs: Low T4, high TSH
1. Type of hypothyroidism
2. Cause
- Primary hypothyroidism (low T4 causes high TSH)
- Hashimoto’s thyroiditis, drug-induced hypothyroidism
TFTs: Low T4, low TSH
1. Type of hypothyroidism
2. Cause
- Secondary hypothyroidism (low TSH from pituitary causes low T4)
- Pituitary tumour or damage
TFTs: High T4, low TSH
1. Type of hypothyroidism
2. Cause
- Primary hyperthyroidism (high T4 causes low TSH)
- Grave’s disease, toxic nodular goitre, drug-induced
TFTs: high T4, high TSH
1. Type of hypothyroidism
2. Cause
- Secondary hyperparathyroidism (high TSH from pituitary causes high T4)
- Pituitary tumour
How to interpret and change levothyroxine dose following TFT results (TSH range mIU/L)
<0.5 Decrease dose
0.5–5 Nil action – same dose
> 5 Increase dose
Digoxin toxicity
Confusion, nausea, visual halos, and arrhythmias
Lithium toxicity
Early: tremor
Intermediate: tiredness
Late: arrhythmias, seizures, coma, renal failure, and diabetes insipidus
Phenytoin toxicity
Gum hypertrophy, ataxia, nystagmus, peripheral neuropathy, and teratogenicity
Gentamicin/vancomycin toxicity
Ototoxicity and nephrotoxicity
Paracetamol metabolism and overdose
Metabolised by glutathione
In excess, glutathione is depleted and NAPQI builds up (toxic) –> acute liver damage
Which are the vitamin K-dependent clotting factors
II, VII, IX, and X
Warfarinised patients: what to do in major bleed
- stop warfarin
- give 5–10 mg IV phytomenadione (vitamin K)
- give prothrombin complex (e.g. Beriplex®)
https://bnf.nice.org.uk/treatment-summaries/oral-anticoagulants/#vitamin-k-antagonists
Drugs that cause hyponatraemia
Carbamazepine, diuretics, SSRIs (esp citalopram), Antipsychotics (esp
