Revision 1 Flashcards
Stages of AKI
Stage 1
Increase in creatinine to 1.5-1.9 times baseline, or
Increase in creatinine by ≥26.5 µmol/L, or
Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours
Stage 2
Increase in creatinine to 2.0 to 2.9 times baseline, or
Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours
Stage 3
Increase in creatinine to ≥ 3.0 times baseline, or
Increase in creatinine to ≥353.6 µmol/L or
Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2
Stages of CKD
grade 1 - eGFR >90 with other evidence of damage
grade 2 - eGFR 60-89
grade 3a - eGFR 45-59
grade 3b - eGFR 30-44
grade 4 - eGFR 15-29
grade 5 - eGFR <15
Causes of CKD
Diabetes
Glomerulonephritis
Unknown
Hypertension and vascular disease
Pyelonephritis and reflux
Hepatocellular damage - LFT results
bilirubin - normal or raised ALT - very very very high ALP - normal to high albumin - normal GGT - normal to high
Cholestatic/obstructive pattern - LFT results
bilirubin - high to very very very high ALT - normal to high ALP - very very very high (indicates obstruction) albumin - normal GGT - high to very very very high
COPD stages
Based on the FEV1 (FEV1/FVC always <70% in COPD)
Stage 1 (mild) >80%
Stage 2 (moderate) 50-79%
Stage 3 (severe) 30-49%
Stage 4 (very severe) <30%
Management of COPD
- stop smoking
- SAMA (ipratropium) /SABA (salbutamol)
- if still symptomatic but no asthmatic features - offer LAMA (tiotropium) and LABA (salmetarol)
- if still symptomatic but with asthmatic features - offer LABA and ICS
- step up to triple therapy if severe exacerbation (>2 moderate exacerbations/year)
- long term O2 therapy
Resp drugs - SABA, SAMA, LAMA, LABA, ICS
SABA = salbutamol
SAMA = short acting muscarinic antagonist e.g. Ipratropium (1st line)
LAMA = long-acting muscarinic antagonist e.g. tiotropium bromide
LABA = long-acting beta-2 agonist e.g. salmeterol (2nd line)
ICS = inhaled corticosteroids e.g. beclomethasone, fluticasone
Asthma chronic management
- exclude the obvious
- SABA reliever
- if still uncontrolled or asthma causes waking at night or sx >3x per week - add low dose ICS
- add leukotriene receptor antagonist (montelukast)
- add LABA and consider stopping LTRA
- adjust doses into maintenance and reliever therapy (MART)
- increase ICS dose within MART or switch to fixed ICS, LABA and SABA
- increase ICS to fixed high dose or consider additional drug (LAMA) or refer to specialist
Diagnosing diabetes by WHO criteria
- Sx of hyperglycaemia (polydipsia, polyuria, fatigue, weight loss) AND raised blood glucose (fasting >7, random >11.1)
- raised blood glucose on 2 occasions (fasting, random, positive oral glucose tolerance test)
- HbA1c >48 (but shouldn’t use this test for diagnosis)
Features of T1DM
Absolute insulin deficiency - due to immune destruction of beta cells
Autoantibodies to GAD, insulin or IA-2
Present with features of DKA - abdo pain, polyuria, polydipsia, dehydration, Kaussmaul respiration, sweet smelling breath
Presents in childhood
5-10% of diabetic patients
Features of T2DM
Progressive - proceeded by pre diabetes or impaired glucose tolerance
Deficiency in the ability to secrete or for it to have action - insulin resistance
Seen in older ages groups - associated with obesity and FHx
Management for T2DM
- lifestyle - diet and exercise modifications
- [1st line] metformin (standard release) - gradually increase the dose over several weeks (if GI effects consider modified release)
- [2nd line] metformin + DPP-4 inhibitor OR pioglitazone OR sulfonylurea OR SGLT-2 inhibitor (is sulf CI)
- [3rd line] triple therapy metformin + DPP4-inhibitor/pioglitazone + sulfonylurea OR metformin + pioglitazone/sulfonylurea + SGLT-2 inhibitors
potentially consider insulin-based treatment - if the above is ineffective/not tolerated or CI - consider combination treatment with metformin + sulfonylurea + GLP-1 receptor agonist
Benzodiazepine - routes
Rectal diazepam
Buccal midazolam
IV lorazepam
What is the target HbA1c for T1DM?
<= 48 mmol/mol
Complications of T2DM
Macrovascular - atherosclerotic CVD (storke, MI, PAD, HF)
Microvascular - diabetic kidney disease, CKD 5, retinopathy, peripheral neuropathy, autonomic neuropathy
Foot - diabetic foot
Metabolic - dyslipidaemia, DKA, HHS
Psychosocial - depression, anxiety
What are the NICE weight classes according to BMI?
Healthy weight — BMI of 18.5-24.9 kg/m2 Overweight — BMI of 25-29.9 kg/m2 Obesity l — BMI of 30-34.9 kg/m2 Obesity ll — BMI of 35-39.9 kg/m2 Obesity lll — BMI of 40 kg/m2 or more
What hormones are involved in the anorexic response (decreased feeding)?
Leptin -> release aMSH and CART acts on LH to inhibit feeding
Also activates the PVN hypothalamus -> release of ACTH and TSH -> stimulates sympathetic NS -> increases metabolic rate
What hormones are involved in the orexigenic response (increased feeding)?
Leptin levels low so aMSH and CART decreased
Other neurones NPY and AgRP stimulates -> project to AN -> stimulate feeding
Projects to PVN and inhibits release of ACTH and TSH -> stimulation of PSNS -> decreases metabolic rate
Clinical features of hypothyroidism
- Weight gain
- Cold intolerance
- Dry (anhydrosis), cold, yellowish
- Hoarseness or deepening of voice, goitre (if Hashimoto’s)
- Slow HR
- Non pitting oedema
- Dry coarse scalp hair
- Constipation
- Menorrhagia
- Depressed
- Decreased deep tendon reflexes
- Carpal tunnel
What is the most common cause of hypothyrodisim (in developing world and developed world)
Developed world = Hashimoto’s thyroiditis (gotire, associated with T1DM, Addision’s and pernicious anaemia)
Developing world = iodine deficiency (iodine needed for thyroid hormone production in the follicular cells)
Describe the HPT axis
- Normally, the hypothalamus detects low levels of thyroid hormones and releases TRH as a response
- Anterior pituitary releases TSH as a response
- Thyroid gland makes T3 and T4 in response to TSH (mainly T4)
- In cells T4 is converted to T3 (more biologically active) to exert its effects (speed up basal metabolic rate)