unit 2 Flashcards
(271 cards)
1
Q
What is an arrhythmia (dysrhythmia)?
A
An abnormal heart rhythm that can range from harmless irregularities to life-threatening conditions.
2
Q
How are arrhythmias classified?
A
- By Site of Origin: Supraventricular (Atrial) or Ventricular.
- By Rate Change: Tachycardia (>100 BPM) or Bradycardia (<60 BPM).
3
Q
What are common causes of arrhythmias?
A
Electrolyte imbalances, ischemic heart disease, heart failure, hypertension, drug effects, congenital heart defects.
4
Q
What are common symptoms of arrhythmias?
A
Palpitations, dizziness, shortness of breath, chest pain, syncope (fainting), fatigue.
5
Q
What are examples of supraventricular arrhythmias?
A
Atrial fibrillation, atrial flutter, supraventricular tachycardia (SVT), sinus arrhythmia.
6
Q
What are examples of ventricular arrhythmias?
A
Ventricular tachycardia (VT), ventricular fibrillation (VF), premature ventricular contractions (PVCs).
7
Q
What are possible complications of arrhythmias?
A
Stroke, heart failure, cardiac arrest, sudden death.
8
Q
A
9
Q
A
10
Q
What are the two main causes of dysrhythmias?
A
- Disturbance in impulse formation
- Disturbance in impulse conduction
- Both (impulse formation & conduction abnormalities)
11
Q
What are the causes of abnormal impulse formation?
A
- Increased automaticity (abnormal pacemaker areas)
- After-depolarization (triggered impulses during repolarization)
12
Q
What causes abnormal pacemaker activity (automaticity- rhythm)?
A
- Increased sympathetic stimulation
- Excess catecholamines
- Ischaemia (most common cause)
- Increased β-adrenoreceptor activation
- Reduced Na⁺/K⁺ ATPase pump activity, leading to depolarization
13
Q
Example of a dysrhythmia caused by increased automaticity?
A
Atrial fibrillation
14
Q
What is after-depolarization?
A
New impulses triggered after a normal action potential during repolarization, linked to arrhythmias.
15
Q
Conditions leading to after-depolarization?
A
- Digitalis (Digoxin) overdose
- Myocardial ischaemia
- Excess catecholamines
16
Q
What are the two types of abnormal impulse conduction?
A
- Heart block (conduction failure or delay)
- Re-entry (circular conduction pathway leading to tachycardia)
17
Q
What is heart block?
A
A conduction defect involving the AV node, leading to delayed or absent impulses reaching the ventricles.
18
Q
Causes of heart block?
A
- Myocardial infarction (MI)
- Fibrosis
- Diphtheria
- Rheumatic fever
- Congenital defects
19
Q
Types of heart block?
A
- Complete heart block – No impulses conducted from atria to ventricles.
- Partial heart block – Some impulses are blocked (e.g., 2:1 or 3:1 conduction).
20
Q
What is re-entry in dysrhythmias?
A
A conduction defect where an area of myocardium (often damaged after MI) has a longer refractory period, creating a circular electrical loop that sustains tachycardia.
21
Q
Examples of re-entry arrhythmias?
A
- Atrial flutter
- Atrial fibrillation
- Supraventricular tachycardia (SVT)
- AV nodal re-entrant tachycardia (AVNRT)
22
Q
What is the cause of atrial flutter?
A
A re-entrant electrical impulse looping in the right atrium.
23
Q
What is the atrial rate in atrial flutter?
A
250-400 bpm
24
Q
What is the ventricular rate in atrial flutter?
A
Usually regular and slower due to the AV node blocking some impulses. Example: 3:1 heart block (only 1 out of 3 atrial impulses reach the ventricles).
25
ECG characteristic of atrial flutter?
Sawtooth pattern due to flutter waves, with the absence of normal P waves.
26
What causes atrial fibrillation (the science)?
Multiple random electrical impulses from ectopic sites in and around the atria, commonly near the pulmonary veins.
27
What happens to the atria during atrial fibrillation?
The atria fibrillate (quiver) instead of contracting properly due to unsynchronized, chaotic electrical signals.
28
How does atrial fibrillation affect the ventricular rate?
- Most atrial impulses do not pass through the AV node due to its refractory properties.
- The ventricular rate is irregular and can range from bradycardia (<60 bpm) to tachycardia (>100 bpm).
29
What are the ECG characteristics of atrial fibrillation?
- Absence of P waves
- Irregularly irregular rhythm
- Narrow QRS complexes
- Undulating or flat baseline (depending on the number of ectopic sites)
30
How does the number of ectopic sites affect the ECG baseline?
- More ectopic sites → Flatter baseline
- Fewer ectopic sites → More undulating baseline
31
What is a dysrhythmia (arrhythmia)?
An abnormal heart rhythm, ranging from harmless to fatal.
32
What are the classifications of dysrhythmias?
Based on the site of origin (atrial or ventricular) and rate (tachycardia >100 bpm, bradycardia <60 bpm).
33
What are 2 the causes of dysrhythmias?
1. Disturbance in impulse formation 2. Disturbance in impulse conduction 3. Both
34
What is abnormal impulse formation?
Due to automaticity (abnormal pacemaker sites) or after-depolarization (new impulses triggered after a normal action potential).
35
What is abnormal impulse conduction?
Includes heart block (conduction defect at AV node) and re-entry (common after MI due to damaged myocardium).
36
What is atrial flutter?
A rapid, regular atrial rhythm (250-400 bpm) caused by a re-entrant electrical loop, often in the right atrium.
37
What is atrial fibrillation (AF)?
An irregular, chaotic atrial rhythm due to multiple ectopic impulses, often near the pulmonary veins.
38
How is AF identified on an ECG?
No P waves, irregular ventricular response, narrow QRS complexes, undulating or flat baseline.
39
What are the symptoms of AF?
Irregular pulse, breathlessness, palpitations, chest discomfort, dizziness, fatigue, reduced exercise tolerance.
40
What are the types of AF?
1. Paroxysmal (self-terminating within 48 hrs) 2. Persistent (>7 days, needs treatment) 3. Permanent (>1 year).
41
How is AF diagnosed?
Manual pulse palpation, ECG, echocardiogram, chest X-ray, and blood tests (e.g., thyroid, kidney function).
42
What are the risks associated with AF?
Increased risk of stroke and heart failure.
43
How is stroke risk assessed in AF patients?
Using the CHA2DS2-VASc score.
44
What does the CHA2DS2-VASc score assess?
Risk of thromboembolism based on factors like age, gender, heart failure, hypertension, diabetes, and stroke history.
45
When should anticoagulation be considered for AF patients?
Males with CHA2DS2-VASc score ≥1, and all patients with a score ≥2.
46
What is used to assess bleeding risk in AF patients?
The ORBIT bleeding risk score.
47
What anticoagulants are recommended for AF patients?
DOACs (Dabigatran, Apixaban, Rivaroxaban, Edoxaban); if contraindicated, Vitamin K antagonists (Warfarin, Acenocoumarol).
48
Why are ventricular arrhythmias dangerous?
They can lead to cardiac arrest and sudden death.
49
What is Ventricular Tachycardia (V-Tach)?
A rapid, abnormal rhythm originating from the ventricles, caused by a single strong firing site or circuit.
50
What causes V-Tach?
Structural heart problems like scarring from a heart attack or abnormalities in heart muscles.
51
How does V-Tach appear on an ECG?
Wide and bizarre QRS complexes, absent P-waves.
52
What is the heart rate range in V-Tach?
100-250 bpm.
53
What are the types of V-Tach?
1. Non-sustained V-Tach – Lasts <30s, few or no symptoms. 2. Sustained V-Tach – Lasts >30s, needs immediate treatment to prevent cardiac arrest.
54
What can V-Tach progress into?
Ventricular Fibrillation (V-Fib).
55
What is Ventricular Fibrillation (V-Fib)?
A chaotic, disorganized electrical activity in the ventricles, causing them to quiver instead of contracting.
56
What happens to blood circulation in V-Fib?
The heart pumps little or no blood, leading to cardiac arrest.
57
How does V-Fib appear on an ECG?
Irregular random waveforms of varying amplitude, no identifiable P, QRS, or T waves.
58
What happens if V-Fib is not treated?
It progresses from coarse V-Fib to fine V-Fib and ultimately to a flatline (asystole).
59
What are the advantages of Warfarin?
- Long-term safety (used for 60+ years) - Antidote available (Vitamin K) - Cheap (generic available) - Long half-life
60
What are the disadvantages of Warfarin?
- Requires frequent INR monitoring - Many drug interactions (CYP450 metabolism) - Food interactions (e.g., cranberry juice, grapefruit juice, alcohol) - Slow onset of action (48-72 hours) - Variable dosing
61
What are the advantages of NOACs?
- No INR monitoring required - Fewer drug interactions - No food interactions - Fixed dosing - Rapid onset of action (1.5-3 hours)
62
What are the disadvantages of NOACs?
- Expensive - Short half-life - No widely available antidote (for some NOACs) - Limited long-term safety data
63
What are the two main strategies for AF management?
Rate control and Rhythm control
64
When is rate control preferred over rhythm control?
First-line choice for most patients, except when: - AF has a reversible cause - AF is causing heart failure - New-onset AF - Atrial flutter (ablation preferred)
65
What is the first-line treatment for rate control?
- Beta-blocker (except sotalol) - Calcium channel blocker (Diltiazem, Verapamil)
66
When is Digoxin monotherapy used for rate control?
- Patients who do little/no exercise - If other drugs are unsuitable due to comorbidities/preferences
67
What is second-line treatment for rate control?
Combination of two of the following: - Beta-blocker - Diltiazem - Digoxin
68
When is rhythm control considered?
- If symptoms persist despite HR control - If rate control fails
69
What is first-line treatment for rhythm control?
Standard Beta-blocker (not sotalol)
70
What is second-line treatment for rhythm control?
Dronedarone (after successful cardioversion)
71
What is the "Pill in the Pocket" strategy?
- Used for infrequent paroxysmal AF with mild symptoms - Taken only when an episode starts - Often triggered by alcohol or caffeine
72
What is Ventricular Tachycardia (V-Tach)?
A fast, regular rhythm originating from the ventricles, often due to structural heart problems like heart attack scarring.
73
What is a key ECG finding in V-Tach?
Wide and bizarre QRS complexes with absent P-waves.
74
What is Ventricular Fibrillation (V-Fib)?
A chaotic, unsynchronized ventricular rhythm where the heart quivers instead of contracting, leading to cardiac arrest.
75
How does V-Fib appear on an ECG?
Irregular random waveforms with no identifiable P, QRS, or T waves.
76
What is a major advantage of Warfarin over NOACs?
It has an available antidote (Vitamin K) if bleeding occurs.
77
Why do NOACs have an advantage over Warfarin?
They require no INR monitoring and have fewer drug and food interactions.
78
What is a major disadvantage of NOACs?
They are expensive and currently lack a widely available antidote for bleeding.
79
What is the first-line treatment for rate control in AF?
β-Blockers (except sotalol) or Calcium Channel Blockers (Diltiazem, Verapamil).
80
When is rhythm control considered in AF?
If symptoms persist despite controlled heart rate.
81
What is the "Pill in the Pocket" strategy?
Using Flecainide or Propafenone only when an episode of AF starts, for infrequent cases.
82
What is anaemia?
A decrease in red blood cells (RBCs) or haemoglobin content, leading to reduced oxygen-carrying capacity of the blood.
83
What are the three main types of anaemia?
1. Microcytic – Small, pale RBCs (e.g., iron deficiency, anaemia of chronic disease). 2. Macrocytic – Large RBCs (e.g., folate or vitamin B12 deficiency). 3. Normocytic – Normal-sized RBCs but reduced numbers (e.g., sickle cell, thalassaemia).
84
What are common causes of iron deficiency anaemia?
Dietary deficiency, malabsorption (e.g., coeliac disease), blood loss (menstruation, GI bleeding), increased requirements (pregnancy, growth spurts).
85
What are the haemoglobin (Hb) reference ranges?
- Men (>15 years): 13.5–17.5 g/dL (135–175 g/L) - Women (>15 years): 11.5–15.5 g/dL (115–155 g/L) - Children (12–14 years): ~12.0 g/dL (120 g/L)
86
What are the diagnostic thresholds for iron deficiency anaemia?
- Men: <130 g/L - Women: <120 g/L - Pregnant women: <110 g/L (1st trimester), <105 g/L (2nd & 3rd trimester), <100 g/L (postpartum)
87
What are common symptoms of iron deficiency anaemia?
Tiredness, shortness of breath, heart palpitations, pale skin.
88
What are less common symptoms of iron deficiency anaemia?
Tinnitus, altered taste, itchy skin, sore tongue, hair loss, pica (craving non-food items), dysphagia, spoon-shaped nails, restless legs syndrome.
89
What is the most reliable test for diagnosing iron deficiency anaemia?
Serum ferritin level (<30 µg/L confirms iron deficiency).
90
What are the limitations of serum ferritin testing?
Can be falsely high in infections/inflammation, less reliable in pregnancy.
91
What additional tests confirm iron deficiency anaemia?
- Complete blood count (CBC) – Low haemoglobin, microcytosis - Iron studies – Low serum iron, high total iron-binding capacity (TIBC)
92
When should urgent referral for iron deficiency anaemia be considered?
- People >60 years with iron deficiency anaemia - Women >55 years with postmenopausal bleeding - People <50 years with rectal bleeding
93
When should a diagnostic trial of iron be considered?
- Premenopausal women with menorrhagia (if no suspicion of coeliac disease) - Pregnant women - NOT recommended for men or postmenopausal women without excluding GI bleeding
94
What is the risk of iron toxicity?
Giving iron to someone without deficiency can be harmful.
95
Why should folate not be given alone in suspected B12 deficiency?
Folate can correct anaemia symptoms but does not treat B12 deficiency, which can cause neuropathy (nerve damage).
96
Why should combinations of iron, B12, and folic acid be avoided unless the cause of anaemia is clear?
Treating one deficiency can mask another, leading to improper treatment.
97
What dietary advice should be given alongside iron treatment?
- Eat iron-rich foods (e.g., red meat, spinach, lentils, fortified cereals). - Take with vitamin C (e.g., citrus fruits) to enhance absorption. - Avoid tea, coffee, and calcium around iron intake, as they inhibit absorption.
98
What is the usual dose for oral iron supplements?
100–200 mg daily (divided doses).
99
What is the most commonly used oral iron supplement?
Ferrous sulfate.
100
What are common side effects of oral iron supplements?
GI issues such as nausea, epigastric pain, constipation, and diarrhoea.
101
What are alternatives for patients who cannot tolerate ferrous sulfate?
Ferrous fumarate or ferrous gluconate (lower iron content = fewer side effects).
102
When is parenteral (IV) iron used?
- Unsuccessful oral therapy - Inability to take oral iron reliably - Continued blood loss or malabsorption
103
What are common types of IV iron?
Iron dextran (CosmoFer), iron sucrose (Venofer), ferric carboxymaltose (Ferinject), iron isomaltoside 1000 (Monofer).
104
How long should iron treatment continue after haemoglobin normalises?
3 months.
105
When should haemoglobin levels be rechecked after starting iron treatment?
After 2–4 weeks.
106
When should a patient be referred to a specialist during iron therapy?
If haemoglobin does not increase by >2 g/dL.
107
What is dyslipidaemia?
Abnormal lipid and/or lipoprotein levels in the blood, including elevated cholesterol, triglycerides, or lipoproteins.
108
What is the role of lipoproteins?
They help distribute lipids and sterols in the bloodstream.
109
How does dyslipidaemia impact health?
It promotes endothelial dysfunction and atherogenesis, increasing the risk of cardiovascular diseases.
110
How is dyslipidaemia managed?
Through dietary changes and medications that affect lipid metabolism.
111
What is primary dyslipidaemia?
Dyslipidaemia caused by genetic factors and diet.
112
What is familial hypercholesterolaemia (FH)?
A common genetic disorder leading to high cholesterol levels and early cardiovascular disease.
113
How common is heterozygous FH?
It affects about 0.2% of the UK population.
114
How common is homozygous FH, and how severe is it?
It is rare (1 in 300,000) and can cause cardiovascular disease in childhood.
115
What is secondary dyslipidaemia?
Dyslipidaemia caused by medical conditions or drugs (up to 40% of cases) and can be reversed.
116
What are common medical causes of secondary dyslipidaemia?
Diabetes mellitus, hypothyroidism, chronic kidney disease, chronic liver disease.
117
Which drugs can influence lipid profiles?
Alcohol, sex hormones, corticosteroids, thiazide diuretics, beta-blockers, antipsychotics, antiretroviral drugs.
118
Who is eligible for an NHS cardiovascular risk assessment?
Individuals aged 40-74 years in England (free).
119
What is measured in a blood lipid assessment?
Total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides.
120
Why is LDL ("bad cholesterol") harmful?
It causes plaque build-up in arteries.
121
Why is HDL ("good cholesterol") beneficial?
It removes LDL from the blood, reducing heart disease risk.
122
What guidelines does NICE (2016) provide for primary prevention?
Identify high-risk individuals, prioritizing those with a 10-year CVD risk of 10% or more.
123
Who should not use risk calculators?
Patients with established CVD, chronic kidney disease (stage 3+), familial hypercholesterolaemia, or type 1 diabetes.
124
What are two risk assessment tools for CVD?
QRISK®2 (England & Wales) and JBS3 (estimates lifetime risk).
125
What is the first-line treatment for dyslipidaemia?
Statins.
126
What if statins alone are not enough?
Ezetimibe may be added as a second-line lipid-lowering drug.
127
What is inclisiran and how does it work?
A small interfering RNA drug that reduces PCSK9 production, increasing LDL cholesterol uptake and lowering its blood levels.
128
When is inclisiran used?
With statins or alone if statins are contraindicated/poorly tolerated.
129
What are alirocumab and evolocumab used for?
Patients with primary heterozygous familial hypercholesterolaemia or those whose LDL levels remain high despite maximum tolerated lipid-lowering therapy.
130
Is aspirin recommended for primary prevention of CVD?
No, due to limited benefits and increased bleeding risk.
131
Who is offered antihypertensive therapy for primary prevention?
High-risk patients with sustained hypertension.
132
What is the first-line lipid-lowering therapy for primary prevention?
Statins (low-dose atorvastatin) for patients with ≥10% 10-year CVD risk (QRISK2), chronic kidney disease, or type 1 diabetes with risk factors.
133
What is the target cholesterol reduction in primary prevention?
>40% reduction in non-HDL cholesterol (annual review needed).
134
What are alternatives if statins are not tolerated?
| primary prev
Ezetimibe or bile acid sequestrants; fibrates for high-risk patients with hypertriglyceridemia and low HDL.
135
What is recommended for secondary prevention of CVD? anit platelet
Low-dose daily aspirin (or clopidogrel if aspirin is intolerable).
136
Who is offered antihypertensive therapy for secondary prevention?
Patients with CVD and sustained high blood pressure.
137
What is the preferred lipid-lowering therapy for secondary prevention?
High-dose atorvastatin, unless contraindicated.
138
What is used for lipid-lowering in chronic kidney disease?
| prevention
Low-dose atorvastatin (high-dose simvastatin is avoided unless necessary).
139
What is the goal of lipid-lowering therapy in secondary prevention?
>40% reduction in non-HDL cholesterol, with annual review of adherence, lifestyle, and cholesterol levels.
140
What are additional options if statins fail?
| 2 prevention
Ezetimibe or bile acid sequestrants (rarely used). Icosapent ethyl for elevated triglycerides and LDL-cholesterol in specific ranges.
141
Why are psychological risk factors considered in secondary prevention?
Mood and anxiety disorders can impact CVD risk; SSRIs are preferred for depression in coronary heart disease. Complex cases should be referred.
142
What should be addressed before starting drug treatment for dyslipidaemia?
Secondary causes (e.g., thyroid disorders, diabetes) and provide dietary/lifestyle advice alongside medications.
143
What are key lifestyle recommendations for both primary and secondary prevention?
Dietary changes, exercise, and smoking cessation.
144
What are the main dietary recommendations?
Eat at least 5 portions of fruit & veg per day, increase omega-3 fatty acids (oily fish), and fiber (whole grains, legumes, veg).
145
What is the recommended salt intake for blood pressure management?
Less than 6g per day.
146
How much physical activity is recommended per week?
150 minutes of moderate-intensity or 75 minutes of vigorous-intensity activity.
147
What are common side effects of statins?
Mild muscle pain, stomach upset, headaches.
148
What are serious but rare side effects of statins?
Severe muscle pain, dark urine, jaundice, severe tiredness.
149
What tests are required before starting statins?
Blood tests to check cholesterol and liver function.
150
How often should cholesterol and liver function be monitored after starting statins?
At 3 months, then annually.
151
What food should be avoided when taking statins?
Grapefruit juice (increases drug levels and side effects).
152
Why is it important to inform healthcare providers about other medications?
Statins can interact with other drugs and supplements.
153
What is an alternative if statins are not tolerated in prevention?
Ezetimibe or other lipid-lowering options.
154
What is ischaemia and what causes it?
Ischaemia is a lack of oxygen and nutrients due to inadequate blood flow, often caused by narrowing of blood vessels.
155
What conditions can ischaemia lead to?
It can cause cardiovascular diseases such as angina and myocardial infarction (heart attack).
156
What are the three main causes of ischaemia?
1. Arteriosclerosis (stiffened, thickened arteries).
2. Atherosclerosis (fatty plaque build-up in arteries).
3. Thrombosis (blood clot inside a vessel).
157
How do atherosclerosis and thrombosis contribute to ischaemia?
Atherosclerosis narrows arteries gradually due to plaque build-up. Thrombosis forms a clot, which can block arteries or break off and cause an embolism.
158
What are risk factors for atherosclerosis and thrombosis?
Endothelial damage (e.g., high cholesterol, surgery), abnormal blood flow, high fibrinogen levels, and certain oral contraceptives.
159
How do symptoms differ based on the affected artery?
| ischeamis
Coronary arteries: Chest pain (angina).
Brain arteries: Stroke symptoms (weakness, slurred speech).
Limb arteries: Pain while walking (peripheral artery disease).
Renal arteries: High BP, kidney failure.
160
What is angina, and what causes the pain?
Angina is chest pain from heart muscle ischaemia. Pain is caused by hypoxia-induced release of substances like K+, H+, bradykinin that stimulate pain receptors.
161
What are key triggers of angina?
Physical exertion, emotional stress, cold exposure, and heavy meals. Pain resolves with rest (~3 mins after stopping exercise).
162
What are the different types of angina?
Stable Angina: Pain on exertion, no symptoms at rest.
Unstable Angina: Sudden, worsening pain, occurs at rest, risk of infarction.
Variant (Prinzmetal’s) Angina: Occurs at rest due to coronary artery spasm, often at the same time daily.
163
How is angina diagnosed?
Based on history, ECG (ST depression), coronary angiogram, stress test (exercise ECG/MRI), echocardiogram, and blood tests.
164
How can you distinguish angina from a heart attack?
Angina: Temporary pain, improves with rest.
Heart attack: Severe, prolonged pain that doesn’t improve with rest.
165
What are first-line treatments for stable angina?
Beta blockers or calcium channel blockers, depending on patient preference and contraindications.
166
What is the preferred combination if monotherapy fails?
| angina
Beta blocker + dihydropyridine calcium channel blocker (e.g., amlodipine, nifedipine).
167
When is a third drug added, and what are the options?
| angina
If angina is uncontrolled on two drugs and revascularisation is not an option, consider long-acting nitrates, ivabradine, nicorandil, or ranolazine.
168
When should monotherapy with alternatives be considered?
| angina
If beta blockers and calcium channel blockers are contraindicated or not tolerated.
169
What safety concerns exist for certain angina medications?
MHRA warnings apply to ivabradine and nicorandil, which should be used cautiously.
170
What is hypertension?
Persistently high blood pressure.
171
What are the two types of hypertension?
Primary Hypertension: No identifiable cause.
Secondary Hypertension: Due to an underlying condition (e.g., kidney disease, endocrine disorders).
172
What are the hypertension stages?
Stage 1: 140/90 – 159/99 mmHg (Clinic) or 135/85 – 149/94 mmHg (ABPM/HBPM).
Stage 2: 160/100 – 179/119 mmHg (Clinic) or ≥ 150/95 mmHg (ABPM/HBPM).
Stage 3 (Severe): ≥ 180/120 mmHg (Clinic).
173
What are the main risk factors for hypertension?
Age: Increases with age.
Gender: Women have lower BP until 65, then higher.
Ethnicity: Higher in Black African/Caribbean populations.
Genetics: Family history increases risk.
Social deprivation: Higher risk in deprived areas.
Co-existing conditions: Diabetes, kidney disease.
Lifestyle: Smoking, alcohol, high salt, poor diet, obesity, inactivity.
Stress: Anxiety and stress can elevate BP.
174
What are the general principles for antihypertensive treatment?
1. Stepwise approach: Start with one drug, titrate to max tolerated dose before adding another.
2. Isolated systolic hypertension: Treat similarly if systolic BP ≥ 160 mmHg.
3. Ethnicity: Prefer ARBs over ACE inhibitors in Black African/Caribbean patients.
4. Pregnancy: Avoid ACE inhibitors & ARBs.
5. Cost efficiency: Use generic drugs when possible.
175
What is Step 1 treatment for hypertension?
- ACE Inhibitor/ARB: < 55 years or Type 2 diabetes (prefer ARB for Black African/Caribbean patients).
- Calcium Channel Blocker (CCB): ≥ 55 years or Black African/Caribbean descent without diabetes.
- Thiazide-like diuretics (e.g., Indapamide): Used if other treatments aren’t tolerated or for heart failure.
176
What is Step 2 treatment?
Add CCB or Thiazide-like diuretic to Step 1 drug if BP isn’t controlled.
177
What is Step 3 treatment?
Triple therapy: ACE/ARB + CCB + Thiazide-like diuretic.
178
What is Step 4 treatment (Resistant Hypertension)?
If BP remains uncontrolled:
- Add spironolactone (if potassium ≤ 4.5 mmol/L).
- Add alpha- or beta-blocker (if potassium > 4.5 mmol/L).
- Refer to a specialist if BP is still uncontrolled.
179
How is chronic hypertension managed in pregnancy?
- ACE Inhibitors/ARBs: Avoid, stop within 2 days of pregnancy confirmation.
- Thiazide diuretics: Discuss risks of congenital abnormalities & neonatal complications.
- Target BP: 135/85 mmHg.
- Preferred antihypertensives: Labetalol or Nifedipine; Methyldopa if others are unsuitable.
- Aspirin: 75–150 mg daily from 12 weeks to prevent pre-eclampsia.
- PLGF Testing: Offered between 20–36 weeks if pre-eclampsia is suspected.
180
What are causes of drug-induced hypertension?
1. Sodium retention & volume expansion (e.g., NSAIDs, corticosteroids).
2. Sympathetic nervous system activation (e.g., decongestants, stimulants).
3. Arteriolar smooth muscle constriction (e.g., calcineurin inhibitors).
4. Discontinuation of BP-lowering drugs.
181
How is drug-induced hypertension managed?
1. Discontinue the causative agent.
2. Adjust specific therapy or drug dose.
182
What is the endocrine system?
A system of ductless glands that release hormones directly into the blood, regulating long-term processes.
183
What are key functions of the endocrine system?
Regulates metabolism, growth, reproduction, and stress responses. Works alongside the nervous system but controls slower, long-term processes.
184
What are common endocrine-related diseases?
1. Diabetes (insulin deficiency/resistance).
2. Obesity (appetite/hormone imbalance).
3. Hypothyroidism (low thyroid hormone).
4. Inflammatory conditions (treated with corticosteroids).
185
What are key drugs for endocrine disorders?
- Insulin: Diabetes management.
- Appetite regulators: Obesity treatment.
- Thyroid hormone replacement: Hypothyroidism.
- Corticosteroids: Inflammation control.
186
key diabetes comparasion
187
188
What is Diabetes Mellitus (DM)?
A disorder characterized by hyperglycemia (high blood glucose levels). Normal range: 4–8 mmol/L.
189
What are the two types of diabetes?
Type 1 DM: Autoimmune destruction of pancreatic beta cells → no insulin.
Type 2 DM: Insulin resistance + reduced insulin secretion (more common in obesity).
190
What are the key symptoms of diabetes?
Polydipsia: Excessive thirst.
Polyuria: Excessive urination (osmotic diuresis).
Fatigue, weight loss (T1DM), blurred vision, recurrent infections.
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Why does hyperglycemia cause polydipsia & polyuria?
Excess glucose exceeds renal threshold → glucose in urine draws water with it → polyuria → dehydration → polydipsia.
192
How is diabetes diagnosed?
FPG: ≥7.0 mmol/L
RPG: ≥11.1 mmol/L
OGTT (2h post-load): ≥11.1 mmol/L
HbA1c: ≥48 mmol/mol (6.5%).
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Why is HbA1c useful?
Measures 2–3 month glucose control, used for diagnosis and monitoring (not suitable for T1DM).
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Why are diabetics prone to infections & blurred vision?
Infections: Glucose in urine promotes Candida growth.
Blurred vision: Osmotic swelling of the eye lens.
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What are the two types of complications in diabetes?
Acute metabolic: Ketoacidosis (T1DM), Hyperosmolar hyperglycemic state (T2DM), Hypoglycemia. Long-term: Microvascular (retinopathy, neuropathy, nephropathy) & Macrovascular (CVD, stroke, gangrene).
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Why is cardiovascular risk high in diabetes?
Hypertension, obesity, and hyperlipidemia contribute to heart attacks and strokes. Managing these is more important than glucose control in T2DM.
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What are the key goals in diabetes management?
1. Control symptoms 2. Prevent acute complications 3. Prevent long-term complications
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Why is patient education important?
Patients must learn self-care and attend structured education programs (e.g., DAFNE, DESMOND).
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What is the role of diet in diabetes?
A balanced diet helps control glucose. Alcohol doesn’t raise glucose but can cause hypoglycemia in insulin users.
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What is the first-line drug for T2DM?
Metformin (Biguanide) – improves insulin sensitivity, reduces hepatic glucose production.
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What are the side effects of Metformin?
GI upset, weight loss, lactic acidosis, B12 deficiency. Avoid if eGFR <45.
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How do Sulfonylureas (e.g., Gliclazide) work?
Stimulate insulin secretion from beta cells but can cause hypoglycemia & weight gain.
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What do SGLT2 inhibitors (e.g., Empagliflozin) do?
Block glucose reabsorption in kidneys → glucose excreted in urine. Used in CVD & heart failure. Risk of DKA & infections.
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What is the main benefit of GLP-1 receptor agonists (e.g., Liraglutide)?
Weight loss, glucose-dependent insulin release
inhibitglucagon, delayed gastric emptying. Side effects: Nausea, vomiting, diarrhea.
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Why is insulin required for T1DM?
Absolute insulin deficiency. Insulin types: Rapid, short, intermediate, long-acting.
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What are the risks of insulin therapy?
Hypoglycemia, weight gain, lipodystrophy. Somogyi effect = rebound hyperglycemia due to overnight hypoglycemia.
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What is the purpose of blood glucose monitoring in diabetes?
Prevents hypoglycemia and reduces long-term complications.
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How is blood glucose monitored daily?
Capillary self-monitoring using a glucose meter and test strips.
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What does HbA1c measure?
Average blood glucose over 2-3 months (RBC lifespan = 120 days).
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Why is HbA1c important?
It is the gold standard for monitoring chronic glycemia and predicting long-term complications.
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How is HbA1c reported?
Previously %, now in mmol/mol.
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Who should NOT rely on HbA1c results?
Patients with hemoglobin disorders (e.g., anemia, hemolysis).
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Can urine glucose testing diagnose diabetes?
No. It only detects sugar presence, not its amount or cause.
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Why are urine ketone tests useful?
Detects diabetic ketoacidosis (DKA), mainly in T1DM.
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What other factors should be monitored in diabetes?
Obesity, blood pressure, lipids, smoking – all increase CVD risk.
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What is obesity & why is it important?
Excess body fat negatively affects health; linked to 80-85% of T2DM cases and metabolic syndrome (obesity, insulin resistance, high BP → ↑CVD, stroke, diabetes risk).
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What are the causes of obesity?
Caloric surplus (more intake than burn) + complex factors (genetics, metabolism, hormones, age, diet, neuroendocrine regulation).
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Which brain region regulates appetite & metabolism?
Hypothalamus via nervous & endocrine systems using >50 hormones.
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What are major health risks of obesity?
Hypertension, hyperlipidemia, CVD, T2DM, cancer, sleep apnea, infertility, osteoarthritis, mobility issues.
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How is obesity measured?
1) BMI (kg/m²) – general fatness 2) Waist circumference – better for visceral fat 3) Waist-to-hip ratio – better predictor of metabolic disease 4) Skinfold thickness – subcutaneous fat 5) Bioelectrical impedance (BIA) – electrical current to estimate body fat %.
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What is the first-line treatment for obesity?
Diet + exercise (0.5-1 kg/week weight loss) with long-term support.
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How does Orlistat help with weight loss?
GI lipase inhibitor → prevents fat absorption → excreted in stools. Used if BMI ≥30 (or BMI ≥28 w/ comorbidities).
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What are common Orlistat side effects & precautions?
Oily stools, urgency, gas, vitamin deficiencies (A, D, E, K) → take multivitamins before bed.
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What other drugs help with obesity?
Liraglutide, Semaglutide (GLP-1 agonists) → reduce appetite & increase satiety.
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When is bariatric surgery considered & what are the options?
BMI >40 or BMI >35 with obesity-related conditions. 1) Gastric band (adjustable, reversible, early satiety) 2) Gastric bypass (permanent, reduces stomach size & absorption).
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Why do post-op bariatric patients need supplements?
Reduced absorption → lifelong multivitamin supplements needed.
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What are the two main thyroid hormones?
Thyroxine (T4) and Triiodothyronine (T3).
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Which is the active thyroid hormone?
T3 (Triiodothyronine).
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Where are thyroid hormones stored?
In thyroglobulin inside thyroid follicles.
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What is the role of C-cells in the thyroid?
They produce calcitonin, which helps regulate calcium balance.
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What are the steps of thyroid hormone synthesis?
1. Iodide uptake 2. Iodide oxidation & binding to thyroglobulin 3. Coupling to form T3 & T4 4. Release into circulation.
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How much iodine do we need daily?
150 mcg.
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How does the thyroid use iodine?
The thyroid absorbs iodide from the blood and converts it into T3 & T4.
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Which hormone regulates iodine uptake in the thyroid?
Thyroid-Stimulating Hormone (TSH).
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Where does most of the T3 in the body come from?
80% of T3 comes from the conversion of T4 (mainly in the liver).
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What are the main proteins that transport thyroid hormones in the blood?
1. Thyroxine-binding globulin (TBG) 2. Thyroxine-binding prealbumin (TBPA) 3. Albumin.
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What is the half-life of T4?
6-7 days.
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What is the half-life of T3?
1 day.
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What is the primary function of thyroid hormones?
Regulate metabolism, growth, and development.
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Which organs are key in maintaining body temperature via thyroid hormones?
Heart, muscles, liver, and kidneys.
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What happens to metabolism in hypothyroidism?
It slows down, leading to cold intolerance, weight gain, and fatigue.
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What happens to metabolism in hyperthyroidism?
It speeds up, causing weight loss, heat intolerance, and increased heart rate.
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What is goitre?
Thyroid enlargement, which can occur in both hypo- and hyperthyroidism.
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What is the most important test for diagnosing thyroid dysfunction?
TSH (Thyroid-Stimulating Hormone) test.
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What happens to TSH levels in primary hypothyroidism?
TSH is high, but T3 & T4 are low.
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What happens to TSH levels in hyperthyroidism?
TSH is low, but T3 & T4 are high.
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What is the main treatment for hypothyroidism?
Levothyroxine (T4), taken orally.
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How long does it take for levothyroxine to reach a stable level?
4-5 weeks, with dosage adjustments every 3-4 weeks.
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What is an alternative treatment for severe hypothyroidism?
Liothyronine (T3), but it causes fluctuations in hormone levels.
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What are the treatment options for hyperthyroidism?
1. Antithyroid drugs (e.g., Carbimazole, Propylthiouracil). 2. Beta-blockers (for symptom relief). 3. Radioactive iodine therapy. 4. Thyroidectomy (surgery).
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What are the two main diseases caused by adrenal gland dysfunction?
Addison’s Disease (adrenal insufficiency) and Cushing’s Syndrome (excess cortisol).
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What hormones are primarily affected in adrenal dysfunction?
Cortisol (a glucocorticoid) and Aldosterone (a mineralocorticoid).
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What is Addison’s disease?
A condition where the adrenal glands do not produce enough cortisol and aldosterone.
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What are the causes of Addison’s disease?
Autoimmune destruction (most common), infections (TB, HIV), adrenal haemorrhage, congenital adrenal hyperplasia, or long-term steroid use.
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What are the early symptoms of Addison’s disease?
Fatigue, muscle weakness, weight loss, low BP, dizziness, dark patches on the skin (hyperpigmentation).
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What are the red flag symptoms of Addison’s disease?
Severe abdominal/back/leg pain, vomiting, diarrhoea, dehydration, confusion, and low BP (Addisonian crisis).
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How is Addison’s disease diagnosed?
Blood tests (low cortisol, high ACTH), ACTH stimulation test, low sodium, high potassium, low glucose levels.
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What is the treatment for Addison’s disease?
Hormone replacement therapy: Hydrocortisone for cortisol and Fludrocortisone for aldosterone.
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What is an Addisonian crisis?
A life-threatening emergency due to a severe cortisol deficiency, causing low BP, dehydration, and shock.
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How is an Addisonian crisis treated?
IV hydrocortisone, IV fluids, glucose, and electrolyte correction (sodium, potassium).
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What is Cushing’s syndrome?
A condition caused by excess cortisol production due to adrenal tumours, pituitary tumours (Cushing’s disease), or long-term steroid use.
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What are the causes of Cushing’s syndrome?
Tumours (adrenal or pituitary), ectopic ACTH production (lung cancer), or long-term corticosteroid use (iatrogenic Cushing’s).
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What are the symptoms of Cushing’s syndrome?
Weight gain (moon face, buffalo hump), high BP, muscle weakness, diabetes, thin skin, purple stretch marks, osteoporosis.
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How is Cushing’s syndrome diagnosed?
Dexamethasone suppression test, 24-hour urine cortisol test, midnight salivary cortisol test.
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What is the treatment for Cushing’s syndrome?
Surgery (tumour removal), medications (metyrapone, ketoconazole, aminoglutethimide), or stopping/reducing steroid use if iatrogenic.
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What is iatrogenic Cushing’s syndrome?
Cushing’s caused by long-term corticosteroid use (e.g., prednisone, dexamethasone).
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How can long-term steroid use cause adrenal suppression?
Exogenous steroids suppress ACTH production, leading to adrenal gland atrophy. If stopped suddenly, adrenal insufficiency can occur.
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How can adrenal suppression be prevented when using steroids?
Use the lowest dose possible, take in the morning, consider alternate-day therapy, taper steroids gradually.
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What are the key side effects of long-term corticosteroid use?
Cushingoid features, osteoporosis, diabetes, hypertension, increased infection risk, adrenal suppression.
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Why should patients on long-term steroids carry a steroid emergency card?
In case of illness or stress, they may need extra steroids to prevent adrenal crisis.
