Block 1: Public health and obesity Flashcards
1
Q
BMI equation and what causes diabetes
A
BMI= Weight / Height^2
What causes T2D: decreased beta cell function, decreased insulin action in muscle and liver
2
Q
Metformin
A
- MoA: reduces hepatic glucose output, increases insulin sensitivity
- Advantages: weight loss/weight neutral, no hypos, less expensive
- Side effects: gastric upset, lactic acidosis (rare)
3
Q
Sulfonylurea
A
- For example Gliclazide
- MoA: stimulates insulin secretion from beta cells
- Advantages: quicker reduction of blood glucose
- Problems: weight gain, hypoglycaemia
4
Q
Thiazolidinediones (Pioglitazone)
A
- MoA: improves sensitivity of tissues to insulin
- Problems: fluid retention, weight gain, heart failure
- Contraindications: heart failure, type 1 diabetes, bladder cancer
5
Q
SGLT-2 inhibitos
A
- For example: Dapagliflozin, Canagliflozin, Empagliflozin
- Blocks the reabsorption of glucose back into the blood in the kidneys, more is excreted in urine
- Advantages: weight reduction, cardiovascular risk reduction
- Side effects: genital/ urinary tract infection
6
Q
Incretin
A
- Two drugs: GLP 1 analogue and DPP-4 inhibitor
- GLP-1 analogue increases insulin secretion by beta cells. DPP-4 inhibitor stops the destruction of GLP-1
- Advantages: reduces appetite causing weight reduction, cardiovascular risk reduction, better then insulin for HGV drivers as less hypos (dont have to stop work)
- Problems: injectable, GI side effects
- GLP-1 example: Liraglutide, Exenatide and Semaglutide. Injectable medication
7
Q
Insulin
A
- Advantages: effect on blood glucose, improvement in glycaemic control
- Problems: injectable, weight gain, Hypoglycaemia, occupational concern (HGV driver stop work till achieve good glycaemic control)
- Types: animal insulin, Human insulin, Analogue insulin
- How long: Intermediate acting (Humilin I), Long acting (Glargine), Short acting (Actrapid), Mixed insulin (Novomix 30)
8
Q
Reversing T2D principle
A
A reduction in weight of 15kg or more can cause remission of T2D.
Physiology: in T2D higher levels of intrahepatic fat cause liver insulin resistance. In T2D glucose output is high
9
Q
How you can reverse T2D
A
- More effective in patients who’ve had T2D for less time
- Step 1 (low calorie diet): 600kcal/day liquid formula diet + nonstarchy vegetables. Or 800kcal in liquid formula only
- Step 2 (step wise return to normal eating): replace liquid formula with normal food, one meal at a time. Aiming for 1500 kcal/day
- Step 3: Long term support to limit calorie ingestion and encourage increased physical activity
10
Q
Recommended practise for measuring blood pressure
A
- Use a calibrated and validated instrument
- Quiet room
- No smoking, exercise or caffeine for 30 mins
- Measure after 5 mins in a seated position, feet on floor
- Arm should be free of tight clothing and at heart level
- Cuff bladder covers >80% of arm circumference
- Take 3 measurements, 1 min apart and average last 2
- Check both arms, use arm with higher reading
- Check standing blood pressure to detect drug induced postural hypotension
11
Q
Blood pressure screening
A
> 60 year olds should have an annual blood pressure check
Lifestyle changes (DASH diet, weight loss, low salt, physical activity) in a 9 week trial reduces blood pressure on average by 12 mmHg systolic.
12
Q
Hypertension: WHO priority action
A
- Public health initiative i.e. alcohol and weight reduction, salt
- Integrated programmes to treat hypertension and other NCD’s (diabetes, atherosclerosis and cardiovascular disease)
- Education and encouragement of population to get tested and treatment, and to maintain treatment
- Promote workplace wellness programmes i.e. smoking restriction, healthy food options
13
Q
Assessment post hypertension diagnosis
A
- Measurement of height and weight (BMI or waist circumference
- Examination of the heart for left ventricular hypertrophy (ECG)
- Examine lungs for heart failure
- Examine abdomen for pulsatile masses, renal enlargement or bruits
- Examine fundi for signs of retinopathy (fundoscopy)
- Auscultate for carotid and femoral arterial bruits: start antiplatelets
- Examine peripheral pulses (to exclude co-arctation or PVD)
- Urinalysis: microalbuminuria (renal disease)
- Bloods: serum electrolytes (secondary causes), U&E’s (calculate eGFR), HbA1c, fasting blood lipid profile
- Chest x-ray of echocardiogram to confirm left ventricular hypertrophy if suspected from ECG
- Referral to specialist if possible secondary cause or stage 3/4
14
Q
The Juxtaglomerular apparatus
A
The macula densa cells in the distal tubule are responsible for activating the renin-angiotensin system.
15
Q
Renal artery stenosis
A
- Unilateral: can be due to fibromuscular hyperplasia in younger people and atherosclerosis in older.
- Bilateral: When giving ACEi can cause an AKI as they are dependent on RAS to maintain GFR
16
Q
When to investigate for possible renal hypertension
A
Consider renal imaging with ultrasound ± doppler :
- Isolated hypertension in young women
- Reduced eGFR or acute reduction following treatment with RAS blockers (ace inhibitor)
- Abnormal urinalysis with proteinuria/haematuria
- Hypertension resistant to 3 or more agents
- Presentation with acute (flash) pulmonary oedema with no known CVD
- Coincident atherosclerotic vascular disease( absent peripheral pulse) ± renal artery bruits
- Should be screened by doppler ultrasound along the renal arteries
17
Q
Management of renal hypertension
A
- Primary renal disease: treat underlying cause if possible, manage hypertension as per guidelines for CKD
- Renovascular disease: stenting of renal artery stenosis if possible, medication avoiding RAAS blocking agents
18
Q
Hypertension: Mineralocorticoid excess
A
- Aldosterone excess promotes sodium/potassium exchange in distal tubule
- Consider in hypokalaemia or drug resistant hypertension. Bicarb will rise but sodium normal. Metabolic alkalosis
- Causes: Adrenocortical adenoma (benign tumour,often unilateral), Bilateral adrenocortical hyperplasia
- Investigate with plasma aldosterone:renin ratio (NB correct hypokalaemia and withdraw agents that affect RAS) Diagnostic Values ≥ 300 pmol/L per mg/(L.h). Renin will be suppressed
- If positive then further imaging with CT ± selective venous sampling
- Manage with surgery (single adenoma) or receptor blockers
- NB Cushing’s may also present as a syndrome of mineralocorticoid excess
19
Q
Catecholamine excess: Phaeochromocytoma
A
- The three catecholamines: Dopamine, Norepinephrine (noradrenaline), Epinephrine (adrenaline- increases systolic, decreases diastolic). Normally one is released in excess
- Secreted from adrenal medulla under autonomic NS
- Increase in heart rate and force via beta1 receptors,
- Increased venous return and peripheral resistance via alpha receptors
- Symptoms: headache, excess sweating, palpitations. anxiety/nervousness, tremor, pain in lower chest, nausea, weight loss. Autonomic symptoms
- Can present with diabetes, hypertension resistant to >3 agents, paroxysmal postural hypotension
- Tumour in adrenal gland
20
Q
Secondary cause of hypertension- Phaeochromocytoma: investigations and management
A
- Plasma or 24 hour urinary metanephrines or catecholamines
- Avoid beta blocking agents and TCA’s – result in unopposed a adrenergic activity
- Imaging by CT – approx. 15% outside adrenal glands, can be in the sympathetic nervous chain along the spinal cord, overly the distal aorta/major vessels, ureters, bladder
- Surgical removal best (adrenalectomy) but preparation with alpha and beta blockade essential- can resolve diabetes and hypertension but will need cortisol replacement
- Tumours often unilateral
