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GP core conditions Flashcards

1
Q

Asthma: patho physiology

A

Patho physiology:
• IgE mediated inflammatory response. This is the Ig dealing with allergens. If an allergen is encountered it can trigger response of:
• Bronchial muscle contraction
• Mast cell+ basophil degranulation (causing inflammation of airway)
• Increased mucus secretion

Non allergic asthma has similar symptoms but without allergen, can have other triggers such as:
Viral
Drugs (beta-blockers and NSAIDs)
Exercise and cold air- dries airways so can trigger inflame response

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2
Q

asthma: symptoms

A

Clinical triad:
• Dry chronic cough (worse at night)
• SOB
• Expiratory wheeze

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3
Q

asthma: acute signs

A 
Acute signs:
•	Tachypnoea 
•	Expiratory wheeze 
•	Hyperinflated chest
•	PEFR <33%
•	Paradoxical pulse (bp falls on inspiration)
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4
Q

Asthma:Investigations

A

spirometry: FEV1/ FVC < 70%

you can perform an FEV1 reversibility test

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5
Q

Asthma: Management

Under 5s

A
  1. Short acting B2 agonist
  2. +Regular low dose inhaled corticosteroid (ICS) for 8 weeks)
  3. +LTRA (leukotriene receptor antagonist) (montelukast)
  4. Increase dose of steroids
  5. Oral steroids
  6. Refer
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6
Q

Asthma: Management

Over 5s

A
  1. SABA (salbutamol or terbutaline)
  2. ICS (beclometasone or fluticasone) +oral LTRA
  3. ICS +inhaled LABA (salmeterol)
  4. Moderate dose ICS +LABA
  5. High dose ICS
  6. Add theophylline
  7. Oral steroids (prednisolone) + refer
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7
Q

Heart Failure: pathophysiology

A

CO= SV x HR. There is decreased SV.
systolic failure: more common, cannot contract fully –> causes like ishcaemic heart disease
Diastolic failure: due to hypertrophy, pericardium problems (pericarditis, tamponade)
RSHF: can come from a result of lung diseases causing increase in vascular resistance–> pulm. hypertension (cor pulmonale)

other causes:
hypertension (most common)
cardiomyopathies
Arrythmias (AF)
Mitral incompetence
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8
Q

Heart failure: Symptoms

A 
Cough (esp at night). pink frothy sputum
PND
decreased exercise tolerance
SOB
sweating and clammy
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9
Q

Heart failure: signs

A 
Pitting odoema in ankles
pulmonary odeoma- LSHF
Sacral odeoma and increased JVP-- RSHF
tachycardic
expiratory fine crackles
hepatomegaly (due to portal hypertension) - ascites
weight gain/ weight loss
displaced apex beat
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10
Q

Heart failure: Diagnosis

A

gold standard: use echocardiogram – measures Ejection fractions
in GP- BNP (relates to damaged heart muscle)
Framlingham criteria
New York Hear Association classification

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11
Q

Heart failure: investigation (1)

A

Echo
ECG
Chest X- ray
Bloods

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12
Q

Heart failure: investigations (2)

A

Ecg - can spot causes: AF, MI (inverted T waves- partial ischaemia, pathological Q waves- full ischaemia), can see axis deviation (due to hypertrophy), larger R waves
Bloods- FBC, UandEs, TFTs, LFTs, BNP
CXR- A- Alveolar odema
B- Kerley B lines
C- cardiomegaly
D- upper lobe deviation (vessels pointing up)
E- effusions- bilateral

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13
Q

HF, Management: acute

A

Oxygen
Morphine
Furosemide - 40-80 mg IV
GTN spray - vasodilator (if compensating HF, refer to senior to not tip person into cardiogenic shock)

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14
Q

HF, management: chronic

A

Diuretics: FUROSEMIDE, spironolactone
ACEi - lisinopril/ ramipril
B BLOCKER - bisoprolol
digoxin - decreases heart rate and increases heart contractility

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15
Q

Diabetes Mellitus: Pathophysiology (1)

A

Type 1: autoimmune destruction of beta cells in Islets of Langerhans in the pancreas –> this results in reduced production of insulin. As a result less glucose is taken from blood into cells and converted to glycogen.
Type 2: Beta cells are intact but secrete less insulin, other cells also become less insulin sensitive.

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16
Q

DM: Pathophysiology (2)

A

100% of filtered glucose in urine in kidneys should be reabsorbed. But due to large amount of glucose, the transport tubules are at full capacity so glucose remains in urine. This causes water to diffuse into urine as well. Meaning polyuria. This leads to dehydration causing polydipsia.

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17
Q

DM: signs and symptoms

A

Type 1: rapid onset of clinical triad over a few days
Polyuria, polydipsia and weight loss. may also be affected by other autoimmune diseases (such as coeliac, Grave’s Hashimotos)
Type 2: More gradual. Polyuria, Polydipsia, weight loss (though weight loss is v uncommon in type 2 compared to type 1). Blurred vision, lethargy and fatigue, genital thrush, recurrent infections
On exam: acanthosis nigracans (sign of insulin resistance), dyslipidaemia, high BP

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18
Q

DM: Investigations

A 
Blood glucose. Random venous glucose 
Fasting venous glucose
HbA1c >48. 42-48 - prediabetic. 
GOLD STANDARD: glucose tolerance test. ask patient to fast overnight, then give 75g of glucose. check after 2 hours
Urinalysis
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19
Q

DM: Investigations

A 
Blood glucose. Random venous glucose 
Fasting venous glucose
HbA1c. >48
GOLD STANDARD: glucose tolerance test. ask patient to fast overnight, then give 75g of glucose. 
Urinalysis
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20
Q

DM: Fundoscopy

A

Background diabetic retinopathy
Dot and blot haemorrhages in retina

Pre- proliferative diabetic retinopathy
cotton wool spots (resulting from ischaemic damage caused by capillary occlusion)

Proliferative retinopathy
Neovascularisation, but these are more unstable so get haemorrhages

Advanced diabetic retinopathy
Recurrent vitreous hameorrahages
retinal detachment

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21
Q

DM: management. drugs (type 2)

A

1st line: metformin
impairs hepatic production of glucose and increases peripheral insulin sensitivity. SE: abdo pain, flatulence and diarrhoea/ constipation
ALTERNATIVES
gliptin
pioglitazone
sulfonylurea
SGLT-2i
2nd line:
Metformin + pioglitazone/ sulfonylurea/ SGLT- 2i
3rd line:
Triple therapy: metformin + gliptin/ pioglitazone +sulfonylurea

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22
Q

DM: Management. Lifestyle and education

A

Type 1: DAFNE

Type 2: DESMOND

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23
Q

CHD: Pathophysiology

A 
foam cells (macrophages that have taken up LDLs) embed into the arterial wall damaged by HTN and form a plaque
Stenosis of the LAD is ass w/ greater risk and poorer prognosis
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24
Q

CHD: Symptoms

A

Angina (chest tightness that can radiate to shoulder or arm)
Typical/ stable: bought on by physical exertion, fades quickly at rest
Decubitus: occurs when lying down (impaired LV function)
Prizmental’s: Coronary artery spasm at rest. More frequent in women, ST elavationd during pain

25
CHD: Investigations
QRisk2: assessment tool to calculate 1o year risk of developing CHD. Age, sex, ethnicity, location, smoking status, PMHx, FHX, BMI etc. ECG: resting and exercise Bloods: glucose, cholesterol Echocardiogram
26
CHD: Management (1)
Lifestyle: Smoking, weight loss, dietry changes, exercise, stress management, DVLA: stop driving for 1 week if successful angioplasty, 4 weeks if unsuccessful angioplasty
27
CHD: Management (2) chronic
ACEi/ ARB for LV dysfunction, hypertension or diabetes need to monitor renal function B blocker: bisoprolol, this reduces myocardial oxygen demand (can use a CCB if cannot use BB. in HF - amlodipine, in no HF- dilitiazem or verapamil) Statin 80mg Dual anti platelet therapy: Aspirin Ticagrelor Surgery: CABG- bypass PCI - stent from an angioplasty
28
CHD: need to rule out
Need to rule out immediately life threatening: Acute coronary syndrome Pulmonary embolism Aortic dissection Tension pneumothorax Spontaneous rupture of the oesophagus (Boerhaave’s syndrome)
29
CHD: Management
Need to rule out immediately life threatening: Acute coronary syndrome Pulmonary embolism Aortic dissection Tension pneumothorax Spontaneous rupture of the oesophagus (Boerhaave’s syndrome)
30
Stroke: pathophysiology
disruption of blood supply to brain. Can either be as a result of ischeamia or haemorrhage. Ischaemia- (80%). caused by embolus or thrombus formation. Can also by systemic hypoperfusion secondary to cardiac arrest. Haemorrhagic- can get intracerebral, sub- arachnoid (usually due to burst berry aneurysm in circle of Willis)
31
Stroke: symptoms
sudden onset of CNS symptoms:
32
Stroke: diagnosis
sudden onset focal neuro symptoms from last 24 hrs. Confusion, headache (sudden/severe/ sentinel headaches in previous weeks), weakness in limbs, sensory loss, speech problems, visual problems, unilateral tongue weakness/ horner's syndrome (ptosis, miosis and anhydrosis) FAST can be used to screen: facial drooping, arm weakness, speech difficulty, time
33
Stroke: Management (chronic)
Lifestyle: smoking, alcohol, less salt, weight loss, exercise. Need to inform DVLA if problems after 1 month Now treat RF--- antiplatelet- Clopidogrel for life (+PPI) anticoag - Warfarin/ NOAC Use Cha2DS2VASC score to assess risk of stroke Use HASBLED to assess risk of bleed now on Anticoag can also give anti-HTN meds: ACEi +diuretics can also give statins Inform DVLA. Normal drivers if problems after a month HGV- must inform
34
Stroke: Management (chronic)
Lifestyle: smoking, alcohol, less salt, weight loss, exercise. Need to inform DVLA if problems after 1 month Now treat RF--- IF NO AF: antiplatelet (aspirin, dipyramidole) - Clopidogrel for life (+PPI) Statin anticoag - Warfarin/ NOAC Use Cha2DS2VASC score to assess risk of stroke (CHF (1), HTN (1), Age >75 (2), DM (1), stroke/TIA (2), Vascular disease (1), Age 65-74 (1), Sex- F (1) Use HASBLED to assess risk of bleed now on Anticoag (HTN (1), abnormal renal or liver function (1), stroke (1), Bleeding (1), Labile INR (1), Elderly (1), drugs or alcohol (1). can also give anti-HTN meds: ACEi +diuretics can also give statins
35
CKD: pathophysiology
GFR <60 mL/min for >3 MONTHS also loss of hormonal function of kidneys. All causes disturbance of electrolytes, increased BP and excess fluid
36
CKD: Aetiology
Vascular - HTN, renal artery stenosis, heart failure Inflam/ infective- glomerulonephritis, pyelonephritis, interstitial nephritis AI: SLE Metabolic: DM (diabetic nephropathy - this is most common cause), renal stones, urinary tract obstruction, hypercalacaemia Neoplastic: renal cancer Envionment/ endocrine: parathyroid bone disease, malnutrition
37
CKD: symptoms
early: begins with generalised symptoms: tiredness, loss of appetite and headaches Later: increased tiredness, paleness, headaches, visual disturbance, loss of appetite and nausea, pruritis, cafe-au-lait spots final stages: renal failure leads to oliguria or anuria, dyspnoea, vomiting, bibasal crackles,
38
CKD: investigations
urinalysis: microalbuminuria (urine albumin: creatinine ratio), RBCs, glucose Bloods: Uand Es, creatinine, eGFR, glucose, calcium, phosphate, protein, FBC, ESR, PTH (GFR- measures how many ml of waste fluid kidneys can excrete per minute. Difficult to measure directly so is estimated to give eGFR. Estimate is based on lebel of creatinine and the patients demographics.
39
CKD, response:
lifestyle: smoking, alc, reduced sodium diet Meds: stop all nephrotoxic drugs- NSAIDs, nicotine, aminoglycosides, X-ray contrast Manage the risk factors by: HTN - ACEi/ARB Hypercholesterloaemia: statin, clotting: antiplatelet
40
Hypertension: Pathophysiology
cardiac output remains the same but systemic resistance is increased. This is because large vessels show structural changes- deposition of calcium and increase in collagen. LV hypertrophy. Reduced renal perfusion and greater GFR - may then activate the RAAS
41
Hypertension: Types
Essential - primary. Idiopathic Secondary hypertension renal disease - most common. Mostly due to renal disease like glomerulonephritis endocrine - Cushing's/ Conn's (primary hyperaldosternoism)/ acromegaly Malignant hypertension - URGENT. rapid rise in BP. 200/130/ Bilateral retinal haemorrhage and exudate
42
Hypertension: Symptoms
usually asymptomatic. On examination: tachycardia, a third heart sound and (if severe HTN) retinopathy
43
HTN: investigations
Ambulatory monitoring BP (over 24 hours) ECG Urine dip: test for protein and blood Fasting blood for lipid profile Fundoscopy - Grad 1: subtle, generalised arteriolar narrowing Grade 2: areas of focal narrowing, and compression of venules at sites of arteriovenous crossing (AV nipping) Grade 3: development of features similar to diabetic retinopathy- retinal haemorrhages, hard exudates and cotton wool spots Grade 4 (malingnant HTN): all features of grade 3 + optic disc swelling.
44
HTN: management
<55 >55 or black A C A+C A+C+D A+C+B
45
AF: Pathophysiology
Disorganised electrical activity in atria Rapidly firing impulses cause disorganised depolarisation and ineffective atrial contraction. AV node receives impulses more frequently than it can conduct so only some get through and results in irregular ventricular rhythm. Atrial rhythm of 300-600 bpm, v. rhythm of 160-180
46
AF: symptoms
may cause palpatations, chest pain, dyspnoea, fatigue, light- headedness, syncope Polyuria (found in all supraventricular arrhythmia like AF) on exam: Tachycardic, irregular irregular pulse
47
AF: Investigations
ECG- absent p waves, irregular QRS complex. irregular RR intervals, chaotic baseline Bloods: TFTs, FBC (anaemia), U and Es (infection), BNP (HF), cardiac enzymes (MI) CXR- HF
48
AF: Management
First line - rate control (monotherapy). B Blocker (atenolol), CC-b (verapamil/ dilitiazem) (cannot give both BB and CCbas can casue AV block) Digoxin Second line: rhythm control. <48 hrs- anticoagulation +rate/rhythm >48 hrs- DC cardioversion (consider amiodarone 4 weeks before- 12 months after cardioversion)
49
AF: CHA2DS2VASC
CHF or LVSD (1), HTN (1), Age >75 (2), DM (1), Stroke/TIA/ thromboembolism (2), Vascular disease (1), Age 65-74 (1), sex(f) (1) Consider Anticoag to anyone with score of 2 or above Warfarin- Vit K antagonist. NOACs (rivaroxaban) inhibits factor Xa. Less interactions and monitoring required But monitor their HASBLED score for 1 year risk of major bleeding in patients anticoag w AF
50
COPD: pathophysiology
chronic bronchitis + emphysema. non reversible airway obstruction Chronic bronchitis- inflammation of the bronchi emphysema - damage to smaller airways and alveoli, loss of elasticity. leads to hyperinflated lungs unlikely to develop in under 10 pack years
51
Pink Puffers
EmPhysema mostly no CO2 retention - no cyanosis reduced lung compliance, destruction of capillary bed . but as both ventilation and perfusion are reduced, there isn't a V/Q mismatch. So no hypoxaemia Body compensates by increased work of breathing Normal/ low CO2 and normal O2 Pursed lips breathing maintains PEEP, tripod position will develop heart disease and resp acidosis later than blue bloaters
52
Blue Bloaters
Chronic Bronchitis Will get air trapping and retain CO2 Obstruction leads to decreased ventillation but normal perfusion, so VQ mismatch = hypoxaemia. Fail to maintain resp. effort so high CO2 and low O2 patients become reliant on hypoxaemic drive, not on CO2 levels Get pulmonary hypertension, to try and cope with VQ mismatch This can lead to RSHF- cor pulmonale
53
COPD: Symptoms
``` productive cough, white or clear sputum EXPIRATORY wheeze (if insp then it is an exacerbation) SOB No pain/ blood OE: barrel chested- hyperinflated SOB at rest accessory muscles for breathing pursed lip breathing Coarse crackles, prolonged exp. phase ```
54
COPD: complications
Resp infections: Haem. influenzae Moraxella catarrhalis Strep. pneumoniae sputum changes colour to yellow/green increased in SOB pleuritic pain
55
COPD: Investigations
``` MRC dyspnoea scale (3- walks slower than others, 4- SOB at 100m, 5- too SOB to leave house) Spirometry FEV1 <80% of predicted FVC normal or slightly reduced FEV1/ FVC <0.7 Serum alpha 1 antitrypsin - ```
56
COPD: treatment chronic
1. SABA and SAMA (iprotropium) 2. LABA (salmeterol) and LAMA (tiotropium) 3. ICS and LABA 4. Triple therapy- LABA + LAMA+ ICS
57
COPD: treatment acute
CO: controlled oxygen:venturi S: Salbutamol 5mg NEB I: Ipratropium 0.5mg NEB C: corticosteroids- prednisolone 30 mg PO/ Hyrdocortisone 200 mg IV A: Abx +aminophylline (similar to theophylline) R:Radiotherapy (CXR) + Resp support (BiPAP if high CO2) profilcaxis for osteoporosis (as corticosteroid induced and due to catabolic mechanisms due to increased work of breathing) - Calcium and vit D3
58
Stroke: management (acute)
If ischaemic: thrombolysis with alteplase and aspirin for 2 weeks If haemorrhagic: prothrombin and Vit K to nromalise clotting

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