Med 3000 Week 1

Front 1

Define hypertension

Back 1

Elevated BP where either systolic > 140mmHg or diastolic > 90mmHg

Front 2

DDx elevated blood pressure reading

Back 2

Alcohol
Baby Pregnancy (preeclampsia)
Coarctation of aorta
Drugs
Endocrine disease
Renal disease
Physiological

Front 3

Pathogenesis essential HTN

Back 3

Multifactorial - kidneys -> renin elevation increase aldosterone neg feedback loop -> increase BP
Sympathetic overactvity->increase TPR
Genetics
Environmental - diet, alcohol, obesity, lack exercise
Consequence of specific disease causing sodium retention and/or peripheral vasoconstriction

Front 4

Describe and draw histological structure of the aorta and how it is altered by HTN

Back 4

Internal elastic lamina is thickened
Hypertrophy of SM
fibrous tissue deposition
Dilation of vessels become tortuous and walls become less compliant

Front 5

How are smaller arteries histologically altered by HTN?

Back 5

hyaline arteriosclerosis, lumen narrows, aneurysms develop, widespread atheroma develops coronary and/or cerebrovascular disease esp if other risk factors present

Front 6

Describe the symptoms high blood pressure can cause

Back 6

Hypertensive encephalopathy (transient disturbance speech/vision, paraesthesiae, disorientation, fits and LOC, papilloedema, hemorrhage in and around basal ganglia causing neurological deficit), phaeochromocytoma (paroxysmal headache, palpitation, sweating), coronary artery disease (angina, breathlessness)

Front 7

Key features history for HTN

Back 7

FHx, lifestyle (exercise, salt intake, drugs, smoking & alcohol)
other risk factors
Symptoms of other causes of secondary HTN, Sx indicating effects of high BP on target organ damage, cerebral effects (TIA, headaches, dizziness), CVS effects (dyspnoea, chest pain, angina, claudication, ankle oedema), renal effects (haematuria), medications (NSAIDs, OCP, steroids)

Front 8

Keey features examination for HTN

Back 8

Signs of 2ndry HTN, signs of target organ damage.
Radio-femoral delay (coarctatation)
Abdomen - enlarged kidneys (polycystic kidney disease)
bruits (renal artery stenosis)
Cushing syndrome (characteristic facies and habitus causes of 2ndry HTN)
Risk factors eg obesity, hyperlipidaemia
CVS examination - LVH, accentuation 2nd heart sound, fourth heart sound, abnormal optic fundi, evidence generalised atheroma, specific complications such as AA or peripheral vascular disease

Front 9

Describe the routine investigations in a patient with HTN

Back 9

Urinalysis (blood, protein, glucose)
UEC, BSL, serum total and HDL cholesterol
12-lead ECG
CXR, ambulatory BP recording, echocardiogram, renal US, renal angiography, urinary catecholamines, urinary cortisol and dexamethasone suppresion test (detect Cushing syndrome)

Front 10

Management HTN

Back 10

lifestyle modifications (weight loss, exercise, diet, smoking cessation), drugs (diuretic, aspirin, B-blocker, CCB, ACEi, ARB), monitoring

Front 11

MOA ACEi

Back 11

inhibits conversion of angiotensin I to angiotensin II

Front 12

MOA ARB

Back 12

blocks angiotensin receptor

Front 13

MOA CCB

Back 13

Relax smooth muscles -> vasodilation

Front 14

MOA thiazide

Back 14

inhibit reabsorption of Na and Cl from DCT by blocking Na/Cl symporter

Front 15

B-Blocker

Back 15

blocks cardiac B1-adrenoceptors
negative chronotropic effect -> reduce CO, reduce renin and sympathetic activiity

Front 16

Common causes of treatment failure

Back 16

non-adherence with drug therapy, inadequate therapy, failure to detect renal artery stenosis and phaeochromocytoma, compliance, lack of doctor communication and education

Front 17

Describe the key aspects of the coronary circulation

Back 17

Major vessels -left main coronary that divides into left anterior descending and circumflex arteries, and right main coronary artery. The left and right coronary arteries originate at the base of the aorta from openings called the coronary ostia located behind the aortic valve leaflets.

Front 18

Features characteristic of cardiac pain

Back 18

Central, diffuse, radiating to jaw/neck/shoulder/arm, tight, squeezing, choking, precipitated by exertion and/or emotion, relieved by rest and quick response to nitrates, breathlessness

Front 19

Features characteristic of non-cardiac chest pain

Back 19

Peripheral, localised, other or no radiation, sharp, stabbing, catching, spontaneous, not related to exertion, provoked by posture, respiration or palpation, not relieved by rest, slow or no response to nitrates, respiratory, gastrointestinal, locomotor or psychological associated features

Front 20

List common causes of chest pain

Back 20

Myocardial ischaemia (angina), MI, GERD, aortic dissection, AA, oesophageal spasm, gall bladder disease, indigestion, stomach ulcer, anxiety, gallstone

Front 21

Pathology, clinical features and risk assessment of stable angina

Back 21

Fixed stenosis
Demand-led ischaemia, related to effort, predictable, symptoms over long term
Symptoms on minimal exertion, exercise testing-duration of exercise, degree of ECG changes, abnormal BP response

Front 22

Pathology, clinical features and risk assessment of unstable angina

Back 22

Dynamic stenosis
Supply-led ischaemia, symptoms at rest, unpredictable, symptoms over short term
Frequent or nocturnal symptoms, ECG changes at rest, ECG changes with symptoms, elevation of troponin

Front 23

Acute management of cardiac chest pain

Back 23

Airway
Breathing (high flow O2)
Circulation (BP, pulse, ECG, bloods [cardiac markers, CK, myoglobin, troponin])
Drugs (PAIN) - Pain management, Aspirin, Inhibit platelet aggregation, Nitroglycerin
Evaluation-CXR, echocardiography, myocardial perfusion, angiography, MIBI technetium scanning

Front 24

Changes on ECG suggesting acute angina?

Back 24

Normal between attacks, changes if interruption of oxygen to myocardium.
During attacks - transient ST depression, symmetrical T wave inversion or talll, pointed, upright T wave
Angina provided by stress test
ST elevation in Prinzmetal angina
Exercise ECG testing-abnormal in 85% patients with angina

Front 25

Cardiovascular causes of acute dyspnoea

Back 25

Ischaemic disease (eg heart failure)
Valvular disease
Septal defects
Cardiomyopathy
Myxoma
Pericardial disease (effusion & pericarditis)
Arrythmias

Front 26

Respiratory causes acute dyspnoea

Back 26

Airway obstruction (foreign body, tumor, secretion, oedema, inflammation, acute exacerbation of COPD)
Parenchymal disease (infection/malignancy/atelectasis/vascular disease eg thromboembolus/pulmonary oedema)
Pleural disease (effusion/pneumothorax)

Front 27

Other causes of dyspnoea

Back 27

Respiratory muscles/thoracic cage (systemic neuromuscular disease/phrenic nerve dysfunction)
Anaemia/haemoglobinopathy
Metabolic acidosis
Hyperthyroidism
Ascites
GERD
Anxiety/Psychogenic
Drugs (eg aspirin intoxication)
Fever/sepsis

Front 28

Describe systolic heart failure and its underlying pathophysiology

Back 28

Most common, due to reduced systolic contraction (heart unable to pump effectively). May result from MI, myocarditis, dilated cardiomyopathy

Front 29

Describe diastolic heart failure and its underlying pathophysiology

Back 29

More common in elderly & patients with LVH. Due to impaired ventricular relaxation & filling with normal systolic contraction. May result from impaired ventricular relaxation (an active process), increased ventricular stiffness, valvular disease, or constrictive pericarditis.

Front 30

Left ventricular heart failure

Back 30

Due to LV dysfunction, CO decreases and pulmonary venous pressure increases.

Front 31

Right ventricular heart failure

Back 31

Due to RV dysfunction, systemic venous pressure increases, causing fluid extravasation and consequent oedema, primarily in dependent tissues (feet, ankles) & abdominal viscera

Front 32

Acute vs chronic heart failure

Back 32

Rapid onset vs long term.

Front 33

Low output vs high output heart failure

Back 33

Cardiac output reduced (associated with cardiovascular disease) vs cardiac output remaining high (eg anaemia, emphysema)

Front 34

Clinical assessment of dyspnoea

Back 34

Hx - pulmonary & cardiac disease
SOCRATES
Fever, chills, night sweats, weight loss, change in appetite, recent trauma, symptoms of gastroesophageal reflux
Detailed medication Hx and PMHx

Front 35

Findings for cardiac disease

Back 35

Dyspnoea on exertion, PND, orthopnoea, associated chest pain eg angina, palpitations.
JVP, peripheral oedema, ascites, pleural effusions, pulmonary oedema, cardiomegaly, S3 gallop, crepitations

Front 36

Findings for pulmonary disease

Back 36

Dyspnoea with rest & exertion
Tobacco use
Cough
Sputum
Wheezing
Pleuritic chest pain
Recent URTI
Expieratory wheezes
Decreased air movement
Resonance to percussion
Barrel-chested physique

Front 37

CXR

Back 37

Size & shape of heart & lungs, lung congestion/oedema, other causes of oedema

Front 38

ECG

Back 38

Heart conductivity, MI, cardiac hypertrophy, arrhythmia

Front 39

Echocardiography, including doppler studies

Back 39

Heart structure & function, valve incompetence, ejection fraction, wall motion abnormalities, LV hypertrophy, pericardial effusion

Front 40

Haematology tests/biochemistry

Back 40

FBC - anaemia
EUC - preexisting metabolic abnormalities, electrolyte imbalance
BNP - biomarker heart failure
Lipids - high HDL & TGs correlated with CAD
Thyroid function test (if thyroid disease suspected)

Front 41

Cardiac enzymes

Back 41

If recent infarct suspected

Front 42

Other investigations

Back 42

Radionuclide imaging - assessment global LV and RV function
Cardiopulmonary exercise (stress) testing - exercise tolerance reduced in HF
CT/invasive coronary angiography - suspected IHD - confirms/excludes CAD as the cause
Myocardial biopsy - eg suspected myocarditis

Front 43

New York Classification of Heart Failure

Back 43

I - heart disease present, but no undue dyspnoea from ordinary activity
II - comfortable at rest, dyspnoea on ordinary activities
III - less than ordinary activity causes dyspnoea, which is limiting
IV - Dyspnoea present at rest; all activity causes discomfort

Front 44

Features on CXR suggesting diagnosis of HF

Back 44

Alveolar oedema, Kerley B lines, cardiomegaly, Dilated prominent upper lobe vessels, pleural Effusion

Front 45

Emergency Management HF

Back 45

Sit patient upright
100% O2 + continuous pulse oximetry
IV access & monitor ECG (treat any arrythmias)
Investigations while continuing management
Diamorphine (opioid) 2.5-5mg IV - for pain, reduce RR, HR, dilate blood vessels)
Furosemide - reduce fluid overload
GTN spray (dilate veins, decrease preload)
Further investigations, examination and Hx

Front 46

General measures in management of chronic HF

Back 46

Lifestyle changes - stop smoking, reduce EtOH, less salt, optimise weight & nutrition
Regular communication with healthcare practitioners
Medications eg diuretics, ACE-i, ARBs, B-blockers

Front 47

Discuss the EBM role for ACE-i

Back 47

ACE-i have consistently shown beneficial effects on mortality, morbidity, and QoL in large scale, prospective clinical trials - indicated in all stages symptomatic HF resulting from impaired LV systolic HF (no evidence for diastolic HF)

Front 48

Discuss the EBM for ARBs

Back 48

Used in patients who are unable to tolerate ACE-i. Similar survival benefit to ACE-i

Front 49

Discuss EBM for B-blockers

Back 49

Certain B-blockers shown to improve outcomes in systolic HF. When effective, reduce LV size & improve LV contraction (additional to benefits of ACE-i)

Front 50

When is heart transplant warranted?

Back 50

In severe HF unresponsive to other forms of Rx (ie medicine, implanted devices and surgery)
Contraindications - advanced age, malignancy, other co-morbidities

Front 51

Describe common causes of abnormal lipid profiles

Back 51

Primary hyperlipidaemia - gene mutations causing either overproduction or defective clearance of TG and LDL cholesterol, or underproduction or excessive clearance of HDL
Secondary hyperlipidaemia - sedentary lifestyle, diet, uncontrolled diabetes, nephrotic syndrome, renal failure, hypothyroidism, cholestatic liver diseases, alcohol or tobacco use, drugs
Pregnancy

Front 52

Predominant hyperglyceridaemia

Back 52

Elevated TG levels with elevated VLDL. When fasting TG >1.5mmol/L, risk CHD and stroke increases significantly. >1.9 compared to <1.5 increases risk CHD and stroke by >30%.
CVD risk particularly increased in setting of low HDL and/or elevated LDL levels

Front 53

Predominant hypercholesterolaemia

Back 53

Elevated cholesterol -> due to elevated LDL cholesterol.
Lowering LDL by 2.5mmol/L lowers risk coronary events by 25%, lowering below 2mmol/L reduces RR by 50%
2-3% reduction in CHD risk for each 1% increase in HDL

Front 54

mixed pattern

Back 54

elevation of both cholesterol and TG

Front 55

Hx of patient with CVD risk factors

Back 55

Diet, exercise, medications, alcohol abuse, existing medical conditions-diabetes, hypothyroidism, nephrotic syndrome, chronic renal failure, obstructive liver disease, FHx dyslipidaemia

Front 56

Examination of patient with CVD risk factors

Back 56

BMI, BP, peripheral vascular examination, CV examination (including evaluation of bruits, skin-xanthomas, eye-xanthelasmas/HTN changes)

Front 57

Investigations for patient with CVD risk factors

Back 57

Fasting glucose (diabetes mellitus)
Liver enzymes (liver function)
EUC (kidney function)
TSH/&3/T4 (thyroid function)
urinary protein (kidney function)

Front 58

Non-pharmacological management of dyslipidaemia

Back 58

Lifestyle advice - attain and maintain normal body weight
Low fat diet (<6% calories from saturated fat)
Increased fibre intake, fresh fruit & vegies, omega-3 fatty acids
Increase exercise (esp aerobic exercise for at least 30 mins on most and preferably all days of the week)
Avoidance tobacco products
Minimise alcohol intake

Front 59

Pharmacological management of dyslipidaemia

Back 59

Statins- decrease synthesis of cholesterol. Better at decreasing LDL
Fibrates - reduce TG levels
Cholesterol absorption inhibitors

Front 60

Other drugs for dyslipidaemia

Back 60

Nicotinic acid-reduces LDL increases HDL
Fish oil-helps reduce TGs
Bile acid binding resins

Front 61

EBM hypercholesterolaemia with statins

Back 61

Primary prevention-reduces risk coronary events with pravastatin by 31%.
Secondary prevention-16% overall mortality reduction

Front 62

Difference complex carbohydrate consumption between developing and developed countries

Back 62

Developed countries 40-45% caloric intake, 70-80% developing countries

Front 63

How the body responds to overnutrition

Back 63

Excess glucose and fat stored via utilisation insulin
Glucose -> glycogen in liver + muscles
Used by brain, RBCs, renal medulla for energy
Excess glucose taken up by adipocytes -> fat
Lipids -> TGs absorbed and stored by adipose tissue
May result in development of insulin resistance
ER insulin receptors stop responding to insulin
Over time, body no longer responds to insulin properly

Front 64

How the body responds to undernutrition

Back 64

First priority make glucose available to brain + RBCs
Firstly utilise glycogen stores
Gluconeogenesis
Lipolysis
Ketone bodies

Front 65

Role of insoluble dietary fibre

Back 65

Bulking effect in GIT
Absorbs water -> enlarges & softens faeces -> eases their elimination -> redues risk constipation, haemorrhoid & diverticulitis formation
Reduces gastric emptying -> promotes a feeling of fullness -> prevents surges in blood glucose levels
Protective effect against development of colon cancer

Front 66

Role of soluble dietary fibre

Back 66

Lower blood cholesterol
Bind to bile acids -> prevent cholesterol absorption -> promotes cholesterol excretion -> increases turnover of cholesterol

Front 67

Dietary requirement recommendations at rest, light work, heavy work

Back 67

Females:6.7, 8.4, 9.4MJ
Males 8.4, 11.3, 14.6MJ

Front 68

Complications of obesity and their outcomes

Back 68

Metabolic - type 2 diabetes, dslipidaemia, hyperuricaemia, insulin resistance
Immunological - lowgrade inflammatory state
Respiratory - Obstructive sleep apnoea, asthma
Cardiovascular - increased risk of IHD, HTN, stroke
Gastrointestinal - nonalcoholic steatohepatitis, reflux oesophagitis, gallstones
Orthopaedic - back pain, osteoarthritis
Dermatological - acanthosis nigricans, skin tags, intertrigo
Reproductive - polycystic ovary syndrome
Renal - proteinuria
Oncology - increased risk of cancers of breast and bowel
Psychosocial - depression, social discrimination, social isolation, binge-eating disorder, bulimia

Front 69

Complications of obesity

Back 69

Obesity doubles or can triple the risk of early death
The more severe the obesity, the higher the risk of an early death
Lead to psychosocial problems-discrimination, work disability, decreased participation in social activities, low self-esteem, decreased QoL

Front 70

Questions assessing how obesogenic home environment is

Back 70

What does your diet normally consist of?
Do you regularly eat fruit and vegetables?
Junk/fast food?
Do you eat/snack between set meal times? Frequency, type, amount
Any instances of binge eating?
triggers, frequency, type, amount
Any instances of waking up at night and eating? frequency, type, amount
What do you usually drink?
type, amount, frequency

Front 71

Questions to ask regards to energy expenditure

Back 71

Do you exercise? type frequency duration intensity
Do you currently play any sports? type duration frequency
What do you usually do when you are at home? watch tv computer daily chores
Do you drive/own a car?
Do you spend much time outdoors?
What do you do for a living?
details of occupation
hrs at work
desk job?

Front 72

Potentially reversible causes of weight gain

Back 72

Endocrine factors - hypothyroidism, hypothalamic tumors or injury, cushing's syndrome, insulinoma
Drug treatments - TCAs, corticosteroids, sulphonylureas, sodium valproate, oestrogen-containing contraceptive pill, B-blockers

Front 73

How would you manage obesity?

Back 73

Lifestyle advice-dietary habits, physical activity
Pharmacological therapy - consider in patients with BMI >30 (>27 + comorbidity)
Surgical/bariatric surgery