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)
What are the hormone levels in primary hypothyroidism
- lack of T3 and T4 production from the thyroid gland - slows down metabolic processes
- high TSH as there is no negative feedback from T3 and T4 - the pituitary gland tries to stimulate the thyroid gland by secreting more TSH
- therefore high TSH, low T4
What are the hormone levels in secondary hypothyroidism?
- pathology in the pituitary gland leads to low TSH production and as a result low T3 and T4 too
- therefore low/normal TSH, low T4
What TFT results would we expect in primary, secondary and a patient poorly compliant with thyroxine?
- In primary: TSH high, free T4 low
- In secondary: TSH low, free T4 low
- In patient poorly compliant with thyroxine: high TSH, normal free T4
What autoantibodies can be seen in 90% of Hashimoto’s patients?
anti-TPO
What is the management for hypothyroidism?
Thyroxine (levothyroxine) which is a synthetic T4
What are the effects of thyroid hormone (T3)?
- increases cardiac output
- stimulates bone resorption - thinning out the bones
- activates the sympathetic nervous system
Clinical features of hyperthyroidism
- Weight loss, increased appetite
- Manic, restlessness
- Palpitations
- Increased sweating, heat intolerance
- Clubbing
- Pretibial myxoedema - lesions above lateral malleoli
- Diarrhoea
- Oligomenorrhoea
- Anxiety, tremor
- Reduced libido
- Gynaecomastia in men
- Thyroid eye disease
Describe primary hyperthyroidism
- Due to thyroid pathology (Graves’, toxic multinodular goitre, thyroid adenoma
- thyroid produces excessive TH (T4 and T3)
- High TH exerts negative feedback on the hypothalamus and pituitary to reduce TRH and TSH release
- Overall high T4, low TSH
Describe secondary hyperthyroidism
- caused by a pathology in hypothalamus or anterior pituitary (TSH secreting tumour in AP)
- leads to overproduction of TSH
- thyroid gland overstimulated -> excessive TH
- high TSH and high T4
What is Graves’ disease
- primary hyperthyroidism
- B cells produce ab against thyroid proteins (autoantibodies)
- TSH-R autoantibodies which bind to the TSH receptor on the follicular cells
- Results in the growth of the thyroid gland and stimulates production of excess TH
What is a thyroid storm/thyrotoxic?
- body enters a state of severe hypermetabolism - normal sx become exaggerated
- triggered by acute infection, trauma, pregnancy, surgery, stroke, acute iodine load (contrast), abruptly stopping antithyroid medication
- clinical features = fever, tachycardia, agitation, hyperthermia, hypertension, AF, HF, jaundice, delirium, coma
- treat sx with paracetamol, IV propanalol, dexamethasone, anti-thyroids
Where does pancreatitis pain radiate to?
The back (due to it being a retroperitoneal organ)
Where does acute cholecystitis pain radiate to?
Tip of the right shoulder
Pain made worse by eating FATTY FOODS
What are the clinical signs of hyperlipidaemia?
- Xanthomas - fatty deposits in the skin
- Xanthalasma - skin around eyes
- Corneal arcus - brown ring of fat around cornea
- Fatty liver disease (hepatic steatosis)
- Atherosclerotic CVD - coronary artery disease, stroke, PVD, carotid artery stenosis
- Xanthomata
Palmar xanthoma
Eruptive xanthoma causes: FH, lipoprotein lipase deficiency = red/yellow vesciles on extensor surfaces (elbows, knees)
Tendon xanthoma, tuberous xanthoma, xanthelasma
Describe the absorption of fats
- After eating a fatty meal, cholesterol and fatty acids enter the intestinal cells
- FA are assembled into TGs and are packaged together with cholesterol and lipoproteins to form chylomicrons
- Chylomicrons enter the lymphatic vessels and eventually enter the right and left subclavian veins (where they empty into the blood
- LPL breaks down chylomicrons → TGs break down → FAs which can be taken up by nearby cells (muscle cells and adipose tissue)
- Remains of the chylomicrons head to the liver to deposit left over lipid molecules
- The liver also produces FAs and glycerol which get combined with chylomicron remnants → packaged into VLDLs
- VLDLs enter the blood and LPL in the capillaries break them down to release TGs for nearby tissues to use
- As TGs leave the VLDL it becomes an IDL
- then as cholesterol predominates, it becomes an LDL again
- LDLs travel around in he blood - they are endocytose by cells with DLD receptors (liver or peripheral tissues that need cholesterol)
What is the QRISK2?
CVD risk assessment tool for patients aged <= 84 years. Patients >= 85 years are at high risk of CVD due to their age -defined as a 10-year risk of 10% or greater
estimating the 10‑year risk of having a cardiovascular event, in people who do not already have heart disease
NICE now recommend we offer a statin to people with a QRISK2 10-year risk of >= 10%
How much atorvastatin do we give to a patient with >= 10% QRISK, T1DM, CKD eGFR <60?
20mg
How much atorvastatin do we give to a patient with known IHD, cerebrovascular disease or peripheral artery disease?
80mg
What are the layers of the adrenal gland from out to in - what does each layer produce?
Cortex
zona glomerulosa - makes mineralocorticoid /aldosterone (RAAS increases Na, decrease K, increase BP)
zona fasiculata - makes glucocorticoids (cortisol) - promotes gluconeogenesis to keep BG high
zona reticularis - makes androgens (testosterone)
Medulla - catecholamines (adrenaline)
What is addison’s disease and what are the hormone levels?
Primary adrenal insufficiency=destruction of the adrenal cortex overtime
Low glucocorticoids (such as cortisol)
Low mineralocorticoids (such as aldosterone)
Low adrenal androgens (such as dehydroepiandrosterone)
Therefore, high ACTH but low cortisol
What is the most common cause of addison’s in the developed and undeveloped worlds?
autoimmune destruction
TB
How might someone with addison’s present - refer to each layer of the adrenal gland
Zona glomerulosa - low aldosterone
- Low sodium hyponatraemia
- Hyperkalaemia
- Low BP
- Hypovolaemia
- Acidosis (metabolic)
- Craving for salt foods
- N&V, vomiting, dizziness
Zona fasiculata - low cortisol
- Low blood glucose in times of stress (hypoglycaemia)
- Weak tired disoriented
- hyperpigmentation (in palmar creases), vitiligo
- Cause pituitary gland to be overactive due to negative feedback
- Pituitary gland produces pro-opiomelanocortin which is a precursor for ACTH and melanocyte stimulating hormone, leading to hyperpigmentation in joints and sun exposed areas
- Secondary adrenal insufficiency not associated with hyperpigmentation
Zona reticularis - low androgens
- Doesn’t affect men as testes are major source of T
- Women loss of pubic and arm hair and decreased sex drive
Describe the HPA (cortisol) axis
- Corticotropin-releasing hormone (CRH) is secreted by the hypothalamus. The release of CRH is influenced by stress levels, time of day and serum cortisol levels
- CRH travels in the blood and binds to specific receptors on the pituitary gland. This binding causes increased production of adrenocorticotropic hormone (ACTH)
- ACTH is released into the bloodstream and travels to the adrenal glands, where it binds to specific receptors on the adrenal cortex
- The binding of ACTH to the receptors on the adrenal cortex stimulates the release of cortisol into the bloodstream, where it has a wide range of effects
- Increased serum cortisol levels inhibit the production of CRHandACTHvianegative feedback, preventing the overproduction of cortisol
- Cortisol is important as it promotes gluconeogenesis in the liver, increases muscle breakdown to AA and breaks down adipose tissue into FFA for liver
- Overall, it opposes insulin and increases blood glucose levels
What hormone does cortisol oppose?
insulin (decreases BG) whereas cortisol increases BG
How do we investigate someone with suspected addison’s disease?
- ACTH stimulation test (short Synacthen test)
- Give synthetic ACTH (IM) to stimulate the adrenal gland to produce cortisol
- Measure cortisol (and aldosterone) before and 30 mins after
- normally in response to ACTH, there would be an increase in cortisol
- however, in addison’s, the adrenal glands are too damaged to respond to ACTH therefore cortisol remains low (high ACTH, low cortisol)
What 2 medications are patients with addison’s disease given?
both glucocorticoids (hydrocortisone) and mineralocorticoids (fludrocortisone) replacement therapy
What is an addisonian crisis?
occurs when a person with Addison’s disease experiences severe physical stress
The adrenal glands are unable to supply the extra cortisol needed to cope with the stress so life threatening sx develop
How would someone with an addisonian crisis present?
- severely dehydrated
- hypotension
- hypovolaemic shock
- altered consciousness
- seizures
- stroke
- cardiac arrest
What is the management for addisonian crisis?
- hydrocortisone 100 mg IM or IV
- 1L normal saline over 30-60 mins
- with dextrose (if hypoglycaemic)
- continue hydrocortisone 6 hourly until pt stable
- stop fludrocortisone (high cortisol exerts weak mineralocorticoid action)
What score is used for patients with AF to decide if anticoagulation therapy is required?
CHADVASC
What does high and low INR mean?
high INR = increased risk of bleeding
low INR = increased risk of clotting
What does rivaroxabam and apixabam inhibit?
factor Xa
what does dabigatran inhibit?
directly thrombin
has reversal agent - monoclonal antibody
What can partially reverse the effects of LMWH?
reversed by protamine sulphate, although this only partially reverses the effect of LMWH
